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Reporter: Aviva Lev-Ari, PhD, RN

See on Scoop.it – Cardiovascular Disease: PHARMACO-THERAPY

FDA Adds Antinausea, Cardiac Drugs to Watch List
Medscape
The beta blocker metoprolol succinate (Toprol-XL, AstraZeneca) also landed on the list, posted on the FDA Web site last month, because of reports that suggested therapeutic ineffectiveness.

FDA Adds Cardiac Drugs to Watch List

Jun 25, 2013

Drug & Reference Information

The other drug on the latest watch list, metoprolol succinate, is used to treat angina, heart failure, and hypertension

The US Food and Drug Administration (FDA) has put a class of antiemetic drugs, including ondansetron (Zofran, GlaxoSmithKline, and Zuplenz, Par Pharmaceutical), on its latest quarterly list of products to monitor because of potential signals of an increased risk for serotonin syndrome.

The beta blocker metoprolol succinate (Toprol-XL, AstraZeneca) also landed on the list, posted on the FDA Web site last month, because of reports that suggested therapeutic ineffectiveness.

The agency received reports of possible adverse events for these products in the FDA Adverse Event Reporting System (FAERS) database during the first 3 months of 2013. The FDA cautions that an appearance on the watch list does not mean that the agency has concluded that the drug poses the health risk reported through FAERS. What it does mean is that the FDA will investigate whether there is a causal connection. If there is one, the agency would consider a regulatory action such as collecting more data to better characterize the risk, revising the drug’s label, or requiring a risk evaluation and mitigation strategy.

Likewise, by adding a drug to the list, the FDA is not implying that clinicians should cease prescribing it or that patients should stop taking it, the agency says.

The antiemetics on the watch list belong to a subtype of serotonin blockers that bind to the 5-HT3 receptor. Clinicians prescribe them to prevent nausea and vomiting in patients undergoing chemotherapy for cancer. Serotonin syndrome, which was reported to FAERS in conjunction with these antiemetics, is caused by excessive levels of the neurotransmitter. It can be fatal. Symptoms include confusion, agitation, dilated pupils, headache, rapid heart rate, and changes in blood pressure and temperature.

The other drug on the latest watch list, metoprolol succinate, is used to treat angina, heart failure, and hypertension.

Potential Signals of Serious Risks/New Safety Information Identified by FAERS, January 2013 to March 2013

Product name: active ingredient (trade) or product class Potential signal of a serious risk/new safety information Additional information (as of May 1, 2013)
Metoprolol succinate (Toprol-XL, AstraZeneca) extended-release products Lack of therapeutic effect, possibly related to product quality issues FDA is continuing to evaluate this issue to determine the need for any regulatory action.
Serotonin-3 (5-HT3) receptor antagonist products: ondansetron(Zofran, GlaxoSmithKline, andZuplenz, Par Pharmaceutical), palonosetron (Aloxi, Helsinn Healthcare), granisetron (Kytril, Hoffmann-La Roche) Serotonin syndrome FDA is continuing to evaluate this issue to determine the need for any regulatory action.

 SOURCE

http://www.medscape.com/viewarticle/806890

More information on FAERS and its quarterly watch list is available on the FDA Web site.

Potential Signals of Serious Risks/New Safety Information Identified by FAERS, January 2013 to March 2013

http://www.medscape.com/viewarticle/806890

Carvedilol superior to Metoprolol in MADIT-CRT analysis

APRIL 2, 2013 

Rochester, NY – Treatment with carvedilol is associated with a significant 30% reduction in the risk of hospitalization for heart failure (HF) or death when compared with patients treated metoprolol, according to a new analysis of the Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT) [1].

The benefit of carvedilol over metoprolol was more pronounced in the subgroup of patients with a cardiac resynchronization therapy defibrillator (CRT-D), where carvedilol was associated with a significant 39% reduction in the risk of hospitalization for HF or death, and in those with left bundle branch block (LBBB). In the LBBB patients with a CRT-D, treatment with carvedilol was associated with a 49% reduction in risk compared with metoprolol.

“Furthermore, we found a pronounced dosage-dependent relationship between outcome and dose in carvedilol, which was not found in metoprolol-treated patients,” write Dr Martin Ruwald (University of Rochester Medical Center, New York) and colleagues in the April 1, 2013 issue of the Journal of the American College of Cardiology.

Benefit follows results observed in COMET
The MADIT-CRT study was presented and published in 2009 and included patients with mild HF or left ventricular dysfunction without symptoms. Participants in the trial had NYHA class 1 and 2 disease, systolic dysfunction, and ventricular dyssynchrony (wide QRS complexes). As reported by heartwire, the study showed that the addition of resynchronization pacing in primary-prevention patients with an implantable cardioverter defibrillator (ICD) reduced the risk of HF events by approximately one-third over 2.5 years.

Both metoprolol and carvedilol have a class IA indication in the management of patients with HF, with choice of the drug left to the discretion of the physician. In the Carvedilol or Metoprolol European Trial (COMET), there was an absolute 5.7% survival benefit with carvedilol over metoprolol. Other studies and analyses have suggested that there are differences between the two beta-blockers, say Ruwald and colleagues.

In this analysis of MADIT-CRT, which included 1515 patients with left ventricular ejection fraction (LVEF)<30%, QRS duration >130 ms, and NYHA functional class 1 or 2, the primary end point of hospitalization for HF or death from any cause occurred in 132 patients (30%) taking metoprolol and 243 patients (23%) taking carvedilol. During the 3.4-year follow-up, 48 patients (11%) taking metoprolol and 104 patients (10%) taking carvedilol died.

In multivariate analysis, the reduction in the primary end point with carvedilol translated into a 30% reduction in risk compared with metoprolol, a benefit that was driven primarily by a reduction in HF hospitalizations. There was only a trend toward a reduction in the risk of ventricular tachycardia/ventricular fibrillation (VT/VF). The reduction in the risk of hospitalization for HF/death from any cause was more pronounced in patients receiving CRT-Ds.

Reduction in HF hospitalization/death (carvedilol vs metoprolol)

Study population and subgroups Hazard ratio (95% CI)
MADIT-CRT 0.70 (0.57-0.87)
CRT-D 0.61 (0.46-0.82)
ICD 0.81 (0.59-1.11)
CRT-D and LBBB 0.51 (0.35-0.76)
CRT and non-LBBB 0.79 (0.51-1.23)
ICD and LBBB 0.96 (0.66-1.39)
ICD and non-LBBB 0.55 (0.30-1.00)
LBBB 0.73 (0.56-0.95)
Non-LBBB 0.64 (0.45-0.91)

The researchers note that mean carvedilol and metoprolol doses in MADIT-CRT were 18 mg and 64 mg, respectively. These dosages are comparable to real-life dosages administered to patients in the clinical setting, although somewhat lower than in previous randomized controlled trials, according to the researchers.

“We speculate that low baseline resting heart rates in our study indicate that the patients generally were well titrated at baseline and that the rate may have contributed to a relatively low dose in both metoprolol and carvedilol compared with the beta-blocker dosage in clinical trials,” state Ruwald et al.

http://www.theheart.org/article/1524745.do

J Am Coll Cardiol. 2013 Apr 9;61(14):1518-26. doi: 10.1016/j.jacc.2013.01.020.

Effect of metoprolol versus carvedilol on outcomes in MADIT-CRT (multicenter automatic defibrillator implantation trial with cardiac resynchronization therapy).

Ruwald MH, Ruwald AC, Jons C, Alexis J, McNitt S, Zareba W, Moss AJ.

Source

Heart Research Follow-up Program, Cardiology Division, University of Rochester Medical Center, Rochester, NY 14642, USA. mruwald@hotmail.com

Abstract

OBJECTIVES:

This study sought to compare the effects of metoprolol and carvedilol in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial With Cardiac Resynchronization Therapy) study.

BACKGROUND:

The impact of beta-blockers in heart failure (HF) patients with devices is uninvestigated.

METHODS:

All patients receiving either metoprolol or carvedilol in the MADIT-CRT study were identified and compared. Time-dependent Cox proportional hazard regression analyses were performed to assess differences in hospitalization for HF or death and ventricular arrhythmias.

RESULTS:

Hospitalization for HF or death occurred in 30% of the patients on metoprolol and in 23% on carvedilol. Treatment with carvedilol was associated with a significantly decreased risk of hospitalization for HF or death when compared with metoprolol (hazard ratio [HR]: 0.70, [95% confidence interval (CI): 0.57 to 0.87], p = 0.001). This reduction in risk was further attenuated in the subgroup of cardiac resynchronization therapy with implantable cardioverter-defibrillator (CRT-D) patients (HR: 0.61 [95% CI: 0.46 to 0.82], p = 0.001) and CRT-D patients with left bundle branch block (LBBB) (HR: 0.51 [95% CI: 0.35 to 0.76], p < 0.001). Ventricular arrhythmias occurred in 26% and in 22%, respectively, of the patients receiving metoprolol or carvedilol (HR: 0.80 [95% CI: 0.63 to 1.00], p = 0.050). General use of beta-blockers and adherence in this study was high, and a clear dose-dependent relationship was found in carvedilol, but not in metoprolol.

CONCLUSIONS:

In HF patients in New York Heart Association functional class I and II and with wide QRS complexes, carvedilol was associated with a 30% reduction in hospitalizations for HF or death when compared with metoprolol. A novel beneficial and synergistic effect of carvedilol was seen in patients with CRT-D and LBBB. Furthermore, we found a pronounced dose-dependent relationship in carvedilol, but not in metoprolol.

http://www.ncbi.nlm.nih.gov/pubmed/23500269?dopt=Abstract

Extended-Release Metoprolol ( Toprol-XL) Must Be Combined With Alpha-Blocker in Pheochromocytoma

On February 12, the FDA approved safety labeling revisions for metoprolol succinate (Toprol-XL extended-release tablets; AstraZeneca LP) to provide recommendations regarding its use in the setting of pheochromocytoma.

Patients diagnosed with pheochromocytoma should only receive extended-release metoprolol in combination with an alpha-blocker and only after alpha-blocker therapy has been initiated. Administration of beta-blockers alone in this setting has been linked to a paradoxic increase in blood pressure because of the attenuation of beta-mediated vasodilation in skeletal muscle.

Metoprolol is a beta 1-selective (cardioselective) adrenoceptor-blocking agent indicated for the treatment of hypertension; angina pectoris; and stable, symptomatic heart failure of ischemic, hypertensive, or cardiomyopathic origin.

http://www.medscape.com/viewarticle/591151

Study Suggests Benefit For Beta Blockers During Noncardiac Surgery
The use of perioperative beta-blockade for noncardiac surgery has been declining as a result of the controversial POISE study, which turned up evidence for harm associated with extended-release metoprolol in this setting. Now a large new observational study published in JAMA offers a contrary perspective by suggesting that perioperative beta-blockade may be beneficial in low- to intermediate-risk patients. But without better evidence the debate about this topic is unlikely to be resolved. Martin London and colleagues performed a retrospective analysis of 136,745 patients who underwent noncardiac surgery at VA hospitals, 40…
Source: CardioBrief – April 23, 2013 Category: Cardiology Authors: Larry Husten Tags: Interventional Cardiology & Surgery Prevention, Epidemiology & Outcomes beta blockers JAMA Observational study Source Type: blogs

http://www.medworm.com/rss/search.php?t=Toprol&f=drugs&blogs=1

NDA 19-962/S-038 Page 3 Rx only

TOPROL-XL® 

(metoprolol succinate) 

EXTENDED-RELEASE TABLETS TABLETS: 25 MG, 50 MG, 100 MG, AND 200 MG

DESCRIPTION 

TOPROL-XL, metoprolol succinate, is a beta1-selective (cardioselective) adrenoceptor blocking agent, for oral administration, available as extended release tablets. TOPROL-XL has been formulated to provide a controlled and predictable release of metoprolol for once-daily administration. The tablets comprise a multiple unit system containing metoprolol succinate in a multitude of controlled release pellets. Each pellet acts as a separate drug delivery unit and is designed to deliver metoprolol continuously over the dosage interval. The tablets contain 23.75, 47.5, 95 and 190 mg of metoprolol succinate equivalent to 25, 50, 100 and 200 mg of metoprolol tartrate, USP, respectively. Its chemical name is (±)1-(isopropylamino)-3-[p-(2-methoxyethyl) phenoxy]-2-propanol succinate (2:1) (salt). Its structural formula is:

Metoprolol succinate is a white crystalline powder with a molecular weight of 652.8. It is freely soluble in water; soluble in methanol; sparingly soluble in ethanol; slightly soluble in dichloromethane and 2-propanol; practically insoluble in ethyl-acetate, acetone, diethylether and heptane. Inactive ingredients: silicon dioxide, cellulose compounds, sodium stearyl fumarate, polyethylene glycol, titanium dioxide, paraffin.

CLINICAL PHARMACOLOGY General 

Metoprolol is a beta1-selective (cardioselective) adrenergic receptor blocking agent. This preferential effect is not absolute, however, and at higher plasma concentrations, metoprolol also inhibits beta2adrenoreceptors, chiefly located in the bronchial and vascular musculature. Metoprolol has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at plasma concentrations much greater than required for beta-blockade. Animal and human experiments indicate that metoprolol slows the sinus rate and decreases AV nodal conduction.

Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. NDA 19-962/S-038 Page 4

The relative beta1-selectivity of metoprolol has been confirmed by the following: (1) In normal subjects, metoprolol is unable to reverse the beta2-mediated vasodilating effects of epinephrine. This contrasts with the effect of nonselective beta-blockers, which completely reverse the vasodilating effects of epinephrine. (2) In asthmatic patients, metoprolol reduces FEV1 and FVC significantly less than a nonselective beta-blocker, propranolol, at equivalent beta1-receptor blocking doses.

In five controlled studies in normal healthy subjects, the same daily doses of TOPROL-XL and immediate release metoprolol were compared in terms of the extent and duration of beta1-blockade produced. Both formulations were given in a dose range equivalent to 100-400 mg of immediate release metoprolol per day. In these studies, TOPROL-XL was administered once a day and immediate release metoprolol was administered once to four times a day. A sixth controlled study compared the beta1-blocking effects of a 50 mg daily dose of the two formulations. In each study, beta1-blockade was expressed as the percent change from baseline in exercise heart rate following standardized submaximal exercise tolerance tests at steady state. TOPROL-XL administered once a day, and immediate release metoprolol administered once to four times a day, provided comparable total beta1blockade over 24 hours (area under the beta1-blockade versus time curve) in the dose range 100–400 mg. At a dosage of 50 mg once daily, TOPROL-XL produced significantly higher total beta1-blockade over 24 hours than immediate release metoprolol. For TOPROL-XL, the percent reduction in exercise heart rate was relatively stable throughout the entire dosage interval and the level of beta1-blockade increased with increasing doses from 50 to 300 mg daily. The effects at peak/trough (ie, at 24-hours post-dosing) were: 14/9, 16/10, 24/14, 27/22 and 27/20% reduction in exercise heart rate for doses of 50, 100, 200, 300 and 400 mg TOPROL-XL once a day, respectively. In contrast to TOPROL-XL, immediate release metoprolol given at a dose of 50–100 mg once a day produced a significantly larger peak effect on exercise tachycardia, but the effect was not evident at 24 hours. To match the peak to trough ratio obtained with TOPROL-XL over the dosing range of 200 to 400 mg, a t.i.d. to q.i.d. divided dosing regimen was required for immediate release metoprolol. A controlled cross-over study in heart failure patients compared the plasma concentrations and beta1-blocking effects of 50 mg immediate release metoprolol administered t.i.d., 100 mg and 200 mg TOPROL-XL once daily. A 50 mg dose of immediate release metoprolol t.i.d. produced a peak plasma level of metoprolol similar to the peak level observed with 200 mg of TOPROL-XL. A 200 mg dose of TOPROL-XL produced a larger effect on suppression of exercise-induced and Holter-monitored heart rate over 24 hours compared to 50 mg t.i.d. of immediate release metoprolol.

The relationship between plasma metoprolol levels and reduction in exercise heart rate is independent of the pharmaceutical formulation. Using an Emax model, the maximum effect is a 30% reduction in exercise heart rate, which is attributed to beta1-blockade. Beta1-blocking effects in the range of 30– 80% of the maximal effect (approximately 8–23% reduction in exercise heart rate) correspond to metoprolol plasma concentrations from 30-540 nmol/L. The relative beta1-selectivity of metoprolol diminishes and blockade of beta2-adrenoceptors increases at plasma concentrations above 300 nmol/L.

Although beta-adrenergic receptor blockade is useful in the treatment of angina, hypertension, and heart failure there are situations in which sympathetic stimulation is vital. In patients with severely damaged hearts, adequate ventricular function may depend on sympathetic drive. In the presence of AV block, beta-blockade may prevent the necessary facilitating effect of sympathetic activity on conduction. Beta2-adrenergic blockade results in passive bronchial constriction by interfering with endogenous adrenergic bronchodilator activity in patients subject to bronchospasm and may also interfere with exogenous bronchodilators in such patients. NDA 19-962/S-038 Page 5

In other studies, treatment with TOPROL-XL produced an improvement in left ventricular ejection fraction. TOPROL-XL was also shown to delay the increase in left ventricular end-systolic and end-diastolic volumes after 6 months of treatment.

Pharmacokinetics 

Adults In man, absorption of metoprolol is rapid and complete. Plasma levels following oral administration of conventional metoprolol tablets, however, approximate 50% of levels following intravenous administration, indicating about 50% first-pass metabolism. Metoprolol crosses the blood-brain barrier and has been reported in the CSF in a concentration 78% of the simultaneous plasma concentration.

Plasma levels achieved are highly variable after oral administration. Only a small fraction of the drug (about 12%) is bound to human serum albumin. Metoprolol is a racemic mixture of R- and S- enantiomers, and is primarily metabolized by CYP2D6. When administered orally, it exhibits stereoselective metabolism that is dependent on oxidation phenotype. Elimination is mainly by biotransformation in the liver, and the plasma half-life ranges from approximately 3 to 7 hours. Less than 5% of an oral dose of metoprolol is recovered unchanged in the urine; the rest is excreted by the kidneys as metabolites that appear to have no beta-blocking activity. Following intravenous administration of metoprolol, the urinary recovery of unchanged drug is approximately 10%. The systemic availability and half-life of metoprolol in patients with renal failure do not differ to a clinically significant degree from those in normal subjects. Consequently, no reduction in dosage is usually needed in patients with chronic renal failure.

Metoprolol is metabolized predominantly by CYP2D6, an enzyme that is absent in about 8% of Caucasians (poor metabolizers) and about 2% of most other populations. CYP2D6 can be inhibited by a number of drugs. Concomitant use of inhibiting drugs in poor metabolizers will increase blood levels of metoprolol several-fold, decreasing metoprolol’s cardioselectivity. (See PRECAUTIONS, Drug Interactions.)

In comparison to conventional metoprolol, the plasma metoprolol levels following administration of TOPROL-XL are characterized by lower peaks, longer time to peak and significantly lower peak to trough variation. The peak plasma levels following once-daily administration of TOPROL-XL average one-fourth to one-half the peak plasma levels obtained following a corresponding dose of conventional metoprolol, administered once daily or in divided doses. At steady state the average bioavailability of metoprolol following administration of TOPROL-XL, across the dosage range of 50 to 400 mg once daily, was 77% relative to the corresponding single or divided doses of conventional metoprolol. Nevertheless, over the 24-hour dosing interval, ß1-blockade is comparable and dose-related (see CLINICAL PHARMACOLOGY). The bioavailability of metoprolol shows a dose-related, although not directly proportional, increase with dose and is not significantly affected by food following TOPROL-XL administration.

Pediatrics The pharmacokinetic profile of TOPROL-XL was studied in 120 pediatric hypertensive patients (6-17 years of age) receiving doses ranging from 12.5 to 200 mg once daily. The pharmacokinetics of metoprolol were similar to those described previously in adults. Age, gender, race, and ideal body weight had no significant effects on metoprolol pharmacokinetics. Metoprolol apparent oral clearance (CL/F) increased linearly with body weight. Metoprolol pharmacokinetics have not been investigated in patients < 6 years of age. NDA 19-962/S-038 Page 6

Hypertension 

The mechanism of the antihypertensive effects of beta-blocking agents has not been elucidated. However, several possible mechanisms have been proposed: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output; (2) a central effect leading to reduced sympathetic outflow to the periphery; and

(3) suppression of renin activity.

Clinical Trials

In a double-blind study, 1092 patients with mild-to-moderate hypertension were randomized to once daily TOPROL-XL (25, 100, or 400 mg), PLENDIL® (felodipine extended release tablets), the combination, or placebo. After 9 weeks, TOPROL-XL alone decreased sitting blood pressure by 6-8/47 mmHg (placebo-corrected change from baseline) at 24 hours post-dose. The combination of TOPROL-XL with PLENDIL has greater effects on blood pressure.

In controlled clinical studies, an immediate release dosage form of metoprolol was an effective antihypertensive agent when used alone or as concomitant therapy with thiazide-type diuretics at dosages of 100-450 mg daily. TOPROL-XL, in dosages of 100 to 400 mg once daily, produces similar ß1-blockade as conventional metoprolol tablets administered two to four times daily. In addition, TOPROL-XL administered at a dose of 50 mg once daily lowered blood pressure 24-hours post-dosing in placebo-controlled studies. In controlled, comparative, clinical studies, immediate release metoprolol appeared comparable as an antihypertensive agent to propranolol, methyldopa, and thiazide-type diuretics, and affected both supine and standing blood pressure. Because of variable plasma levels attained with a given dose and lack of a consistent relationship of antihypertensive activity to drug plasma concentration, selection of proper dosage requires individual titration.

Angina Pectoris 

By blocking catecholamine-induced increases in heart rate, in velocity and extent of myocardial contraction, and in blood pressure, metoprolol reduces the oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris.

Clinical Trials

In controlled clinical trials, an immediate release formulation of metoprolol has been shown to be an effective antianginal agent, reducing the number of angina attacks and increasing exercise tolerance. The dosage used in these studies ranged from 100 to 400 mg daily. TOPROL-XL, in dosages of 100 to 400 mg once daily, has been shown to possess beta-blockade similar to conventional metoprolol tablets administered two to four times daily.

Heart Failure 

The precise mechanism for the beneficial effects of beta-blockers in heart failure has not been elucidated. NDA 19-962/S-038 Page 7

Clinical Trials

MERIT-HF was a double-blind, placebo-controlled study of TOPROL-XL conducted in 14 countries including the US. It randomized 3991 patients (1990 to TOPROL-XL) with ejection fraction ≤ 0.40 and NYHA Class II-IV heart failure attributable to ischemia, hypertension, or cardiomyopathy. The protocol excluded patients with contraindications to beta-blocker use, those expected to undergo heart surgery, and those within 28 days of myocardial infarction or unstable angina. The primary endpoints of the trial were (1) all-cause mortality plus all-cause hospitalization (time to first event) and

(2) all-cause mortality. Patients were stabilized on optimal concomitant therapy for heart failure, including diuretics, ACE inhibitors, cardiac glycosides, and nitrates. At randomization, 41% of patients were NYHA Class II, 55% NYHA Class III; 65% of patients had heart failure attributed to ischemic heart disease; 44% had a history of hypertension; 25% had diabetes mellitus; 48% had a history of myocardial infarction. Among patients in the trial, 90% were on diuretics, 89% were on ACE inhibitors, 64% were on digitalis, 27% were on a lipid-lowering agent, 37% were on an oral anticoagulant, and the mean ejection fraction was 0.28. The mean duration of follow-up was one year. At the end of the study, the mean daily dose of TOPROL-XL was 159 mg.

The trial was terminated early for a statistically significant reduction in all-cause mortality (34%, nominal p= 0.00009). The risk of all-cause mortality plus all-cause hospitalization was reduced by 19% (p= 0.00012). The trial also showed improvements in heart failure-related mortality and heart failure-related hospitalizations, and NYHA functional class.

The table below shows the principal results for the overall study population. The figure below illustrates principal results for a wide variety of subgroup comparisons, including US vs. non-US populations (the latter of which was not pre-specified). The combined endpoints of all-cause mortality plus all-cause hospitalization and of mortality plus heart failure hospitalization showed consistent effects in the overall study population and the subgroups, including women and the US population. However, in the US subgroup (n=1071) and women (n=898), overall mortality and cardiovascular mortality appeared less affected. Analyses of female and US patients were carried out because they each represented about 25% of the overall population. Nonetheless, subgroup analyses can be difficult to interpret and it is not known whether these represent true differences or chance effects.

SOURCE

http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/019962s038lbl.pdf

Clinical Endpoints in the MERIT-HF Study 

CLINICAL ENDPOINT NUMBER OF PATIENTS RELATIVE RISK (95% CI) RISK REDUCTION WITH TOPROLXL NOMINAL P-VALUE
PLACEBO N=2001 TOPROLXL N=1990
ALL-CAUSE MORTALITY PLUS ALL-CAUSE HOSPITALIZATION* 767 641 0.81 (0.730.90) 19% 0.00012

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Trans-apical Transcatheter Aortic Valve Replacement in a Patient with Severe and Complex Left Main Coronary Artery Disease (LMCAD)

Writer: Larry H Bernstein, MD, FCAP

and

Curator: Aviva Lev-Ari, PhD, RN

Significant, defined as a greater than 50 percent narrowing, left main coronary artery disease (LMCAD) is found in 4 to 6 percent of all patients who undergo coronary arteriography [1]. When present, it is associated with multivessel coronary artery disease (MVCAD) about 70 percent of the time [2,3].

Most patients are symptomatic and at high risk of cardiovascular events, since occlusion of this vessel compromises flow to at least 75 percent of the left ventricle, unless it is protected by collateral flow or a patent bypass graft to either the left anterior descending or circumflex artery. Studies performed before revascularization with coronary artery bypass graft surgery (CABG) became the standard of care revealed a poor prognosis for these patients, with three-year survival as low as 37 percent [4]. CABG, when directly compared to medical therapy, is associated with significantly better cardiovascular outcomes, including mortality [5].

Percutaneous coronary intervention (PCI) with stenting has generally been restricted to such patients considered inoperable or at high risk for CABG, or with prior CABG and at least one patent graft to the left anterior descending or circumflex artery (so-called “protected” left main disease). Graft patency is important in this setting in the event of acute or late closure after PCI. However, evidence is increasing to support the use of PCI with stenting in some cases. (See ‘PCI versus CABG’ below.)

Asymptomatic patients with left main lesions felt to not be hemodynamically significant should be managed with preventative therapies. Patients with anginal symptoms attributable to lesions elsewhere should be managed with therapies similar to those used in other patients with coronary artery disease. (See “Overview of the care of patients with stable ischemic heart disease”.)

This topic will discuss most aspects of the management of patients with LMCAD. The approach to patients with multivessel coronary artery disease without LMCAD is discussed elsewhere. (See “Bypass surgery versus percutaneous intervention in the management of stable angina pectoris: Recommendations”.)

http://www.uptodate.com/contents/management-of-left-main-coronary-artery-disease

 

Management of significant left main coronary disease before and after trans-apical transcatheter aortic valve replacement in a patient with severe and complex arterial disease.

Source

Columbia University Medical Center, New York, New York; Cardiovascular Research Foundation, New York, New York.

Abstract

We report the case of an 81-year-old woman with symptomatic severe aortic stenosis, extremely significant peripheral arterial disease, and obstructive coronary artery disease who underwent percutaneous coronary intervention via a transaxillary conduit immediately before a trans-apical transcatheter aortic valve replacement performed with a transfemoral device. After deployment of the transcatheter heart valve, there was a left main coronary obstruction and the patient required an emergent PCI. This multifaceted case clearly underlines the importance of a well functioning heart team including the interventional cardiologist, the cardiovascular surgeon, and the echocardiographer. © 2013 Wiley Periodicals, Inc.

Copyright © 2013 Wiley Periodicals, Inc.

This is an interesting surgical case presented by the Columbia University Cardiovascular Surgery team, illustrating the importance of combined team skills in the most difficult of cases.  It is part of a series on cardiovascular surgery.

Management of significant left main coronary disease before and after trans-apical transcatheter aortic valve replacement in a patient with severe and complex arterial disease.

Paradis JM, George I, and Kodali S
Catheterization and Cardiovascular Interventions  (2013)

Introduction

Transcatheter aortic valve replacement (TAVR) with the Edwards SAPIEN transcatheter heart valve (THV) (Edwards Lifesciences, Irvin, CA) has been shown to reduce mortality when compared to medical therapy alone for patients with symptomatic severe aortic stenosis deemed unsuitable for surgical aortic valve replacement due to multiple co-morbidities. The Edwards SAPIEN THV, sizes 23 and 26 mm, and the RetroFlex 3 transfemoral delivery system, have been recently approved by the US Food and Drug Administration (FDA) for commercial use outside of the PARTNER clinical trial for patients considered inoperable.  However, an alternative site needs to be selected for patients with peripheral arteries inadequate for transfemoral TAVR.  Although not fully validated, the transapical approach or the transaortic route using a balloon expandable THV,  appears to be appropriate for this specific purpose.  Significant coronary artery disease (CAD) is often found in patients with severe aortic stenosis. in > 50% of patients with aortic stenosis over 70 years of age and in > 65% of patients who are  over 80 years of age. There is no established guideline for managing significant CAD in the context of TAVR, including the appropriate revascularization strategy as well as the timing of interventions.

Case Report

An 81-year-old woman  presented with symptomatic severe aortic stenosis, extremely significant peripheral arterial disease, and obstructive coronary artery disease. She had a six-month history prior to admission of progressive exertional shortness of breath and fatigue, and a long history fo hypertension, hyperlipidemia, obesity, and severe peripheral vascular disease.  In 2003, she underwent a coronary artery bypass graft (CABG) surgery, with grafting of the left internal mammary artery (LIMA) to the left anterior descending (LAD) artery, a saphenous vein graft (SVG) to the first obtuse marginal (OM) branch, and a SVG to the right coronary artery (RCA). Due to associated severe mitral regurgitation, a mitral valve ring annuloplasty was also performed. A transthoracic echocardiogram (TTE) revealed severe aortic stenosis with a peak gradient across the aortic valve of 63 mm Hg, a mean gradient of 39 mm Hg, and an aortic valve area of 0.8 cm2.  The left ventricular ejection fraction (LVEF) was 64% while the pulmonary artery systolic pressure was measured at 28 mm Hg.  Extreme calcification and tortuosity precluded the advancement of any wire, catheter, or sheath, contributing to two attempts at cardiac catheterization prior to transfer with a total occlusion of the distal abdominal aorta, at the level of the aorto-iliac bifurcation, and the left main, proximal LAD, proximal left circumflex, and the proximal RCA all had greater than 70% coronary lesions. In addition, ostial total occlusions were seen in both SVGs.
left main coronary artery
After transfer, a cardiac catheterization through the right radial artery was attempted without success due to calcification and tortuosity in the arterial bed.  An 80% distal left main lesion was clearly identified with a Judkins left 3.5 guiding catheter.  There was non-flow limiting coronary disease in the left circumflex and competitive retrograde flow seen in the LIMA graft, but they still were unable to cannulate the RCA and the SVGs. It was determined that the patient was inoperable, on grounds of her significant frailty, reoperative status and overall comorbid state (Society of Thoracic Surgeons (STS) risk score of 11%). Furthermore, due to the occlusion of the distal aorta, the patient was unsuitable for a TAVR via the transfemoral approach.
They chose to approach her PCI via a conduit on the right axillary artery and perform a concomitant TAVR from a trans-apical approach due to the serious limiting condition of the patient.  She underwent percutaneous coronary intervention via a transaxillary conduit immediately before a trans-apical transcatheter aortic valve replacement performed with a transfemoral device.  Excellent flow from the conduit was noted. A 7 French (Fr) sheath was connected to the end of the conduit, which was kept long to allow better maneuverability (Fig. 1). A Rosen wire was passed with some difficulty to the aortic root, and was switched to a stiff wire in an attempt to straighten the vessel.
PowerPoint Presentation
Fig. 1. Transaxillary conduit used during the procedure. A 7 French sheath was connected to an 8 mm dacron graft, which was previously sewn to the axillary artery.
After deployment of the transcatheter heart valve, there was a left main coronary obstruction and the patient required an emergent PCI.  This multifaceted case clearly underlines the importance of a well functioning heart team including the interventional cardiologist, the cardiovascular surgeon, and the echocardiographer. A Xience
V everolimus eluting stent 3.5 mm  18 mm was implanted starting 2 mm distal to the ostium of the left main, extending in the proximal portion of the left circumflex artery. After one post-dilatation with a non-compliant balloon, the final angiographic result was excellent.
They used a Retroflex 3 transfemoral delivery sheath to perform the trans-apical TAVR. They estimated the size and length of the ventricular cavity, and then placed markers on the delivery sheath (prior to insertion) indicating the appropriate length of sheath to remain outside the heart (Fig. 2).
PowerPoint Presentation
Fig. 2. Marker placed on the RetroFlex 3 transfemoral sheath to safely guide its insertion inside the left ventricular cavity during the trans-apical transcatheter aortic valve replacement.
A 23 mm Edwards SAPIEN valve was selected and deployed under fluoroscopic and transesophageal echocardiographic guidance. Immediately after deployment, turbulent flow was noted within the left main with the color Doppler on TEE, indicating a new obstruction of the left main, which a left coronary angiogram showed to be a severe proximal lesion.  Through the trans-axillary conduit, a  guiding catheter was laboriously brought in the ascending aorta and cannulated the left main artery which permitted a predilation and a stent insertion in the ostial portion of the left main.  She was discharged to a rehabilitation facility 7 days after the procedure.
On follow-up TTE, the LVEF was 55% without any significant wall motion abnormality. There was no aortic regurgitation, and the peak and mean gradients were 14.9 mm Hg and 8.0 mm Hg, respectively. The patient is still doing well more than 6 months after the procedure. She is now in NYHA class 2 and has not had any recurrent hospitalization for congestive heart failure.
Discussion
This report is a case of a complex percutaneous coronary intervention of the left main coronary artery via a right axillary conduit followed immediately by an off label commercial transapical TAVR using the Retro-Flex 3 trans-femoral introducer sheath, complicated finally by a new left main coronary obstruction mandating another PCI. It is the first description of a TAVR procedure preceded and followed by a left main trans-axillary PCI. The role of TEE (color Doppler) in the diagnosis of a very rare TAVR complication is also noteworthy. In a recent meta-analysis of 3,519 patients from 16 studies using the Valve Academic Research Consortium (VARC) definitions, the pooled estimate rate of coronary
obstruction following TAVR was only 0.7%. Obviously, the early recognition and treatment of this hazard is imperative.
The surgical management of this patient also warrants discussion. The hybrid surgical approach of accessing the axillary artery via a conduit provides numerous advantages:
(1) the ascending aorta, coronaries, and aortic valve are easily accessible;
(2) transition to cardiopulmonary bypass or extra-corporeal membrane oxygenation, if needed, is quick; and
(3) long-term morbidity is minimal for the patient when compared to aorto-iliac, aortic, or femoral conduits.
Finally, the heart team approach not only allowed the realization of a difficult coronary
stent implantation through an unusual transaxillary graft followed by a transapical TAVR in a patient with significant peripheral arterial disease, but also permitted the early  recognition and management of a potentially fatal left main obstruction. Considerations such as team-based care, close communication between the different specialties
involved and careful planning for outlining management of potential complications are therefore essential for the success of a TAVR program.

REFERENCES

 1. Leon MB, Smith CR, Mack M, Miller DC, Moses JW, Svensson LG, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med 2010;363:1597–1607.
2. Iung B. Interface between valve disease and ischaemic heart disease. Heart 2000;84:347–352.
3. Wenaweser P, Pilgrim T, Guerios E, Stortecky S, Huber C, Khattab AA, et al. Impact of coronary artery disease and percutaneous coronary intervention on outcomes in patients with severe aortic stenosis undergoing transcatheter aortic valve implantation.
EuroIntervention 2011;7:541–548.
4. Genereux P, Head SJ, Van Mieghem NM, Kodali S, Kirtane AJ, Xu K, et al. Clinical outcomes after transcatheter aortic valve replacement using valve academic research consortium definitions: A weighted meta-analysis of 3,519 patients from 16 studies.
J Am Coll Cardiol 2012;59:2317–2326.
Three coronary artery bypass grafts, a LIMA to...

Three coronary artery bypass grafts, a LIMA to LAD and two saphenous vein grafts – one to the right coronary artery (RCA) system and one to the obtuse marginal (OM) system. (Photo credit: Wikipedia)

heart with coronary arteries

heart with coronary arteries (Photo credit: Wikipedia)

Micrograph of an artery that supplies the hear...

Micrograph of an artery that supplies the heart with significant atherosclerosis and marked luminal narrowing. Tissue has been stained using Masson’s trichrome. (Photo credit: Wikipedia)

Other Related articles on this topic published on this Open Access Online Scientific Journal, include the following:

Investigational Devices: Edwards Sapien Transcatheter Aortic Valve Transapical Deployment

Aviva Lev-Ari, PhD, RN 6/6/2012

http://pharmaceuticalintelligence.com/2012/06/04/investigational-devices-edwards-sapien-transcatheter-heart-valve/

Lev-Ari, A. 2/12/2013 Clinical Trials on transcatheter aortic valve replacement (TAVR) to be conducted by American College of Cardiology and the Society of Thoracic Surgeons

http://pharmaceuticalintelligence.com/2013/02/12/american-college-of-cardiologys-and-the-society-of-thoracic-surgeons-entrance-into-clinical-trials-is-noteworthy-read-more-two-medical-societies-jump-into-clinical-trial-effort-for-tavr-tech-f/

Lev-Ari, A. 8/13/2012 Coronary Artery Disease – Medical Devices Solutions: From First-In-Man Stent Implantation, via Medical Ethical Dilemmas to Drug Eluting Stents http://pharmaceuticalintelligence.com/2012/08/13/coronary-artery-disease-medical-devices-solutions-from-first-in-man-stent-implantation-via-medical-ethical-dilemmas-to-drug-eluting-stents/

Lev-Ari, A. 7/18/2012 Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

http://pharmaceuticalintelligence.com/2012/07/18/percutaneous-endocardial-ablation-of-scar-related-ventricular-tachycardia/

Lev-Ari, A. 6/22/2012 Competition in the Ecosystem of Medical Devices in Cardiac and Vascular Repair: Heart Valves, Stents, Catheterization Tools and Kits for Open Heart and Minimally Invasive Surgery (MIS)

http://pharmaceuticalintelligence.com/2012/06/22/competition-in-the-ecosystem-of-medical-devices-in-cardiac-and-vascular-repair-heart-valves-stents-catheterization-tools-and-kits-for-open-heart-and-minimally-invasive-surgery-mis/

Lev-Ari, A. 6/19/2012 Executive Compensation and Comparator Group Definition in the Cardiac and Vascular Medical Devices Sector: A Bright Future for Edwards Lifesciences Corporation in the Transcatheter Heart Valve Replacement Market

http://pharmaceuticalintelligence.com/2012/06/19/executive-compensation-and-comparator-group-definition-in-the-cardiac-and-vascular-medical-devices-sector-a-bright-future-for-edwards-lifesciences-corporation-in-the-transcatheter-heart-valve-replace/

Lev-Ari, A. 6/22/2012 Global Supplier Strategy for Market Penetration & Partnership Options (Niche Suppliers vs. National Leaders) in the Massachusetts Cardiology & Vascular Surgery Tools and Devices Market for Cardiac Operating Rooms and Angioplasty Suites

http://pharmaceuticalintelligence.com/2012/06/22/global-supplier-strategy-for-market-penetration-partnership-options-niche-suppliers-vs-national-leaders-in-the-massachusetts-cardiology-vascular-surgery-tools-and-devices-market-for-car/

 We reported on the following Medical Devices News:

Lev-Ari A. 4/6/2012.  Investigational-devices-edwards-sapien-transcatheter-heart-valve. 

http://pharmaceuticalintelligence.com/2012/06/04/investigational-devices-edwards-sapien-transcatheter-heart-valve/

Cardiac Surgery Theatre in China vs. in the US: Cardiac Repair Procedures, Medical Devices in Use, Technology in Hospitals, Surgeons’ Training and Cardiac Disease Severity”    http://pharmaceuticalintelligence.com/2013/01/08/cardiac-surgery-theatre-in-china-vs-in-the-us-cardiac-repair-procedures-medical-devices-in-use-technology-in-hospitals-surgeons-training-and-cardiac-disease-severity/

Acute Chest Pain/ER Admission: Three Emerging Alternatives to Angiography and PCI    http://pharmaceuticalintelligence.com/2013/03/10/acute-chest-painer-admission-three-emerging-alternatives-to-angiography-and-pci/

FDA Pending 510(k) for The Latest Cardiovascular Imaging Technology
http://pharmaceuticalintelligence.com/2013/01/28/fda-pending-510k-for-the-latest-cardiovascular-imaging-technology/

PCI Outcomes, Increased Ischemic Risk associated with Elevated Plasma Fibrinogen not Platelet Reactivity
http://pharmaceuticalintelligence.com/2013/01/10/pci-outcomes-increased-ischemic-risk-associated-with-elevated-plasma-fibrinogen-not-platelet-reactivity/

The ACUITY-PCI score: Will it Replace Four Established Risk Scores — TIMI, GRACE, SYNTAX, and Clinical SYNTAX
http://pharmaceuticalintelligence.com/2013/01/03/the-acuity-pci-score-will-it-replace-four-established-risk-scores-timi-grace-syntax-and-clinical-syntax/

Coronary artery disease in symptomatic patients referred for coronary angiography: Predicted by Serum Protein Profiles
http://pharmaceuticalintelligence.com/2012/12/29/coronary-artery-disease-in-symptomatic-patients-referred-for-coronary-angiography-predicted-by-serum-protein-profiles/

Ablation Devices Market to 2016 – Global Market Forecast and Trends Analysis by Technology, Devices & Applications
http://pharmaceuticalintelligence.com/2012/12/23/ablation-devices-market-to-2016-global-market-forecast-and-trends-analysis-by-technology-devices-applications/

Heart Renewal by pre-existing Cardiomyocytes: Source of New Heart Cell Growth Discovered
http://pharmaceuticalintelligence.com/2012/12/23/heart-renewal-by-pre-existing-cardiomyocytes-source-of-new-heart-cell-growth-discovered/

To Stent or Not? A Critical Decision
http://pharmaceuticalintelligence.com/2012/10/23/to-stent-or-not-a-critical-decision/

Transcatheter Aortic-Valve Replacement for Inoperable Severe Aortic Stenosis

http://pharmaceuticalintelligence.com/2012/09/03/transcatheter-aortic-valve-replacement-for-inoperable-severe-aortic-stenosis/

New Definition of MI Unveiled, Fractional Flow Reserve (FFR)CT for Tagging Ischemia

http://pharmaceuticalintelligence.com/2012/08/27/new-definition-of-mi-unveiled-fractional-flow-reserve-ffrct-for-tagging-ischemia/

New Drug-Eluting Stent Works Well in STEMI
http://pharmaceuticalintelligence.com/2012/08/22/new-drug-eluting-stent-works-well-in-stemi/

Expected New Trends in Cardiology and Cardiovascular Medical Devices
http://pharmaceuticalintelligence.com/2012/08/17/expected-new-trends-in-cardiology-and-cardiovascular-medical-devices/

Read Full Post »

Curator: Aviva Lev-Ari, PhD, RN

We covered the Elevated Blood Pressure and High Adult Arterial Stiffness in the following articles on this Open Access Online Scientific Journal:

Pearlman, JD and A. Lev-Ari 5/24/2013 Imaging Biomarker for Arterial Stiffness: Pathways in Pharmacotherapy for Hypertension and Hypercholesterolemia Management

http://pharmaceuticalintelligence.com/2013/05/24/imaging-biomarker-for-arterial-stiffness-pathways-in-pharmacotherapy-for-hypertension-and-hypercholesterolemia-management/

Lev-Ari, A. 5/17/2013 Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

http://pharmaceuticalintelligence.com/2013/05/17/synthetic-biology-on-advanced-genome-interpretation-for-gene-variants-and-pathways-what-is-the-genetic-base-of-atherosclerosis-and-loss-of-arterial-elasticity-with-aging/

Bernstein, HL and A. Lev-Ari 5/15/2013 Diagnosis of Cardiovascular Disease, Treatment and Prevention: Current & Predicted Cost of Care and the Promise of Individualized Medicine Using Clinical Decision Support Systems

http://pharmaceuticalintelligence.com/2013/05/15/diagnosis-of-cardiovascular-disease-treatment-and-prevention-current-predicted-cost-of-care-and-the-promise-of-individualized-medicine-using-clinical-decision-support-systems-2/

Pearlman, JD and A. Lev-Ari 5/11/2013 Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus

http://pharmaceuticalintelligence.com/2013/05/11/arterial-elasticity-in-quest-for-a-drug-stabilizer-isolated-systolic-hypertension-caused-by-arterial-stiffening-ineffectively-treated-by-vasodilatation-antihypertensives/

Pearlman, JD and A. Lev-Ari 5/7/2013 On Devices and On Algorithms: Arrhythmia after Cardiac Surgery Prediction and ECG Prediction of Paroxysmal Atrial Fibrillation Onset

http://pharmaceuticalintelligence.com/2013/05/07/on-devices-and-on-algorithms-arrhythmia-after-cardiac-surgery-prediction-and-ecg-prediction-of-paroxysmal-atrial-fibrillation-onset/

Pearlman, JD and A. Lev-Ari 5/4/2013 Cardiovascular Diseases: Decision Support Systems for Disease Management Decision Making

http://pharmaceuticalintelligence.com/2013/05/04/cardiovascular-diseases-decision-support-systems-for-disease-management-decision-making/

Lev-Ari, A. 5/29/2012 Triple Antihypertensive Combination Therapy Significantly Lowers Blood Pressure in Hard-to-Treat Patients with Hypertension and Diabetes

http://pharmaceuticalintelligence.com/2012/05/29/445/

Lev-Ari, A. 12/31/2012 Renal Sympathetic Denervation: Updates on the State of Medicine

http://pharmaceuticalintelligence.com/2012/12/31/renal-sympathetic-denervation-updates-on-the-state-of-medicine/

Manuela Stoicescu, MD, PhD, 2/9/2013 An Important Marker of Hypertension in Young Adults

http://pharmaceuticalintelligence.com/2013/02/09/an-important-marker-of-hypertension-in-young-adults/

Manuela Stoicescu, MD, PhD, 2/9/2013 Arterial Hypertension in Young Adults: An Ignored Chronic Problem

http://pharmaceuticalintelligence.com/2013/02/09/arterial-hypertension-in-young-adults-an-ignored-chronic-problem/

We present below, a new study on whether elevated pediatric BP could predict high PWV in adulthood and if there is a difference in the predictive ability between the standard BP definition endorsed by the National High Blood Pressure Education Program and the recently proposed 2 simplified definitions.

Simplified Definitions of ElevatedPediatric Blood Pressure and High Adult Arterial Stiffness

  1. Heikki Aatola, MDa,
  2. Costan G. Magnussen, PhDb,c,
  3. Teemu Koivistoinen, MD, MSca,
  4. Nina Hutri-Kähönen, MD, PhDd,
  5. Markus Juonala, MD, PhDb,e,
  6. Jorma S.A. Viikari, MD, PhDe,
  7. Terho Lehtimäki, MD, PhDf,
  8. Olli T. Raitakari, MD, PhDb,g, and
  9. Mika Kähönen, MD, PhDa

+Author Affiliations


  1. aDepartments of Clinical Physiology,

  2. dPediatrics, and

  3. fClinical Chemistry, Fimlab Laboratories, University of Tampere and Tampere University Hospital, Tampere, Finland;

  4. eDepartments of Medicine, and

  5. gClinical Physiology and Nuclear Medicine, and

  6. bthe Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku and Turku University Hospital, Turku, Finland; and

  7. cMenzies Research Institute Tasmania, University of Tasmania, Tasmania, Australia

ABSTRACT

OBJECTIVE: The ability of childhood elevated blood pressure (BP) to predict high pulse wave velocity (PWV), a surrogate marker for cardiovascular disease, in adulthood has not been reported. We studied whether elevated pediatric BP could predict high PWV in adulthood and if there is a difference in the predictive ability between the standard BP definition endorsed by the National High Blood Pressure Education Program and the recently proposed 2 simplified definitions.

METHODS: The sample comprised 1241 subjects from the Cardiovascular Risk in Young Finns Study followed-up 27 years since baseline (1980, aged 6–15 years). Arterial PWV was measured in 2007 by whole-body impedance cardiography.

RESULTS: The relative risk for high PWV was 1.5 using the simple 1 (age-specific) definition, 1.6 using the simple 2 (age- and gender-specific) definition, and 1.7 using the complex (age-, gender-, and height-specific) definition (95% confidence interval: 1.1–2.0, P = .007; 1.2–2.2, P = .001; and 1.2–2.2, P = .001, respectively). Predictions of high PWV were equivalent for the simple 1 or simple 2 versus complex definition (P = .25 and P = .68 for area under the curve comparisons, P = .13 and P = .35 for net reclassification indexes, respectively).

CONCLUSIONS: Our results support the previous finding that elevated BP tracks from childhood to adulthood and accelerates the atherosclerotic process. The simplified BP tables could be used to identify pediatric patients at increased risk of high arterial stiffness in adulthood and hence to improve the primary prevention of cardiovascular diseases.

Key Words:

  • blood pressure
  • pediatrics
  • prehypertension
  • screening
  • stiffness
  • Abbreviations:
    AUC —
    area under receiver-operating characteristic curve
    BP —
    blood pressure
    CVD —
    cardiovascular diseases
    NHBPEP —
    National High Blood Pressure Education Program
    NPV —
    negative predictive value
    NRI —
    net reclassification improvement
    PPV —
    positive predictive value
    PWV —
    pulse wave velocity
  • Accepted March 12, 2013.

http://pediatrics.aappublications.org/content/early/2013/06/05/peds.2012-3426.abstract?sid=1755f2a0-4e03-4bc8-a563-23458d9dc988

Kids’ High BP Tied to Arterial Stiffness as Adults

By Todd Neale, Senior Staff Writer, MedPage Today

Published: June 10, 2013

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

High blood pressure in childhood defined in three different ways was associated with high pulse wave velocity — a surrogate marker for cardiovascular disease — 27 years later, researchers found.

The relationship remained significant whether high blood pressure was identified using a complex definition that incorporated age, sex, and height or one of two simplified definitions (relative risk 1.5 to 1.7), according to Mika Kähönen, MD, PhD, of Tampere University Hospital in Finland, and colleagues.

The predictive ability of the two simplified definitions was comparable to that of the more complex definition, the researchers reported online in Pediatrics.

In guidelines published in 2004, the National High Blood Pressure Education Program recommended screening blood pressure at all pediatric visits starting at age 3. The document provides definitions for normal, prehypertensive, and hypertensive blood pressure levels according to age, sex, and height. But including all three of those factors results in hundreds of blood pressure thresholds for patients up to age 17.

Recently, two simplified definitions have been proposed — one that relies only on age and sex and reduces the number of blood pressure thresholds to 64 and another that relies on age alone and reduces the number of thresholds to 10.

“Our results support the previous finding that elevated blood pressure tracks from childhood to adulthood and accelerates the atherosclerotic process,” they wrote. “The simplified blood pressure tables could be used to identify pediatric patients at increased risk of high arterial stiffness in adulthood and hence to improve the primary prevention of cardiovascular diseases.”

“This complex definition could at least partly explain the poor diagnosis of prehypertension and hypertension in children and adolescents reported previously,” Kähönen and colleagues wrote.

The researchers explored the relationship between high blood pressure in childhood and high pulse wave velocity, which is a measure of arterial stiffness, in adulthood, as well as whether the definition of high blood pressure mattered, using 1,241 participants from the Cardiovascular Risk in Young Finns Study.

The participants were 6- to 15-years-old (mean age 10.7) at baseline in 1980. The researchers followed them for 27 years, at which point arterial pulse wave velocity was measured using whole-body impedance cardiography.

At baseline, the percentage of participants who had high blood pressure was 53.9% according to the definition based on age, 57.8% according to the definition based on age and sex, and 43.2% according to the more complex definition recommended in the guidelines.

At the 27-year follow-up assessment, 20% of the participants had a high pulse wave velocity. Compared with those with a low pulse wave velocity, these individuals had significantly higher blood pressure values and higher rates of elevated blood pressure at baseline. The differences widened at the adult follow-up.

Elevated pediatric blood pressure was associated with a greater risk of having a high pulse wave velocity for all three definitions used in the study:

  • Age-based: RR 1.5, 95% CI 1.1-2.0
  • Age- and sex-based: RR 1.6, 95% CI 1.2-2.2
  • Age-, sex-, and height-based: RR 1.7, 95% CI 1.2-2.2

The predictive ability of the definitions were not different from one another, as illustrated by a lack of significant differences when comparing area under the receiving-operating characteristic curves and net reclassification indexes (P>0.1 for all comparisons).

“This finding is clinically meaningful because both these simplified tables could be more easily implemented as a screening tool in pediatric healthcare settings and outside of a physician’s office when the height percentile required for the complex definition may not be obtainable,” the authors wrote.

They acknowledged that their study was potentially limited in that the method for measuring pulse wave velocity is not commonly used in epidemiologic settings. In addition, there could have been bias stemming from participants dropping out during follow-up and generalizability of the findings may be limited to white European individuals.

The study was supported by the Academy of Finland, the Social Insurance Institution of Finland, the Turku University Foundation, the Medical Research Fund of Kuopio University Hospital, the Medical Research Fund of Tampere University Hospital, the Turku University Hospital Medical Fund, the Emil Aaltonen Foundation, the Juha Vainio Foundation, the Finnish Foundation of Cardiovascular Research, the Finnish Cultural Foundation, and The Tampere Tuberculosis Foundation.

The authors reported no conflicts of interest.

From the American Heart Association:

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guidelines for the management of arterial

hypertension: The task force for the management

of arterial hypertension of the

european society of hypertension (ESH)

and of the European society of cardiology

(ESC). Eur Heart J. 2007;28(12):1462–1536

 

17. Aatola H, Hutri-Kähönen N, Juonala M, et al.

Lifetime risk factors and arterial pulse

wave velocity in adulthood: the cardiovascular

risk in young Finns study. Hypertension.

2010;55(3):806–811

 

18. Aatola H, Koivistoinen T, Hutri-Kähönen N,

et al. Lifetime fruit and vegetable consumption

and arterial pulse wave velocity

in adulthood: the Cardiovascular Risk in

Young Finns Study. Circulation. 2010;122

(24):2521–2528

 

19. Li S, Chen W, Srinivasan SR, Berenson GS.

Childhood blood pressure as a predictor of

arterial stiffness in young adults: the

Bogalusa Heart Study. Hypertension. 2004;

43(3):541–546

 

20. Raitakari OT, Juonala M, Rönnemaa T, et al.

Cohort profile: the cardiovascular risk in

Young Finns Study. Int J Epidemiol. 2008;37

(6):1220–1226

 

21. Uhari M, Nuutinen M, Turtinen J, Pokka T.

Pulse sounds and measurement of diastolic

blood pressure in children. Lancet.

1991;338(8760):159–161

 

22. Tahvanainen A, Koskela J, Tikkakoski A,

et al. Analysis of cardiovascular responses

to passive head-up tilt using continuous

pulse wave analysis and impedance cardiography.

Scand J Clin Lab Invest. 2009;69

(1):128–137

 

23. Kööbi T, Kähönen M, Iivainen T, Turjanmaa V.

Simultaneous non-invasive assessment of

arterial stiffness and haemodynamics—

a validation study. Clin Physiol Funct Imaging.

2003;23(1):31–36

 

24. Koivistoinen T, Kööbi T, Jula A, et al. Pulse

wave velocity reference values in healthy

adults aged 26–75 years. Clin Physiol Funct

Imaging. 2007;27(3):191–196

 

25. Hlatky MA, Greenland P, Arnett DK, et al;

American Heart Association Expert Panel

on Subclinical Atherosclerotic Diseases

and Emerging Risk Factors and the Stroke

Council. Criteria for evaluation of novel

markers of cardiovascular risk: a scientific

statement from the American Heart Association

[published correction appears in

Circulation. 2009;119(25):e606]. Circulation.

2009;119(17):2408–2416

 

26. DeLong ER, DeLong DM, Clarke-Pearson DL.

Comparing the areas under two or more

correlated receiver operating characteristic

curves: a nonparametric approach.

Biometrics. 1988;44(3):837–845

 

27. Pencina MJ, D’Agostino RBS Sr, D’Agostino

RB Jr, Vasan RS. Evaluating the added

predictive ability of a new marker: from

area under the ROC curve to reclassification

and beyond. Stat Med. 2008;27(2):157–

172, discussion 207–212

 

28. Cook NR, Ridker PM. Advances in measuring

the effect of individual predictors of

cardiovascular risk: the role of reclassification

measures. Ann Intern Med. 2009;150

(11):795–802

 

29. Juonala M, Magnussen CG, Venn A, et al.

Influence of age on associations between

childhood risk factors and carotid intimamedia

thickness in adulthood: the Cardiovascular

Risk in Young Finns Study, the

Childhood Determinants of Adult Health

Study, the Bogalusa Heart Study, and the

Muscatine Study for the International Childhood

Cardiovascular Cohort (i3C) Consortium.

Circulation. 2010;122(24):2514–2520

 

30. Sun SS, Grave GD, Siervogel RM, Pickoff AA,

Arslanian SS, Daniels SR. Systolic blood

pressure in childhood predicts hypertension

and metabolic syndrome later in life.

Pediatrics. 2007;119(2):237–246

 

31. Juhola J, Oikonen M, Magnussen CG, et al.

Childhood physical, environmental, and

genetic predictors of adult hypertension:

the cardiovascular risk in young Finns

study. Circulation. 2012;126(4):402–409

 

32. Juonala M, Järvisalo MJ, Mäki-Torkko N,

Kähönen M, Viikari JS, Raitakari OT. Risk

factors identified in childhood and decreased

carotid artery elasticity in adulthood:

the Cardiovascular Risk in Young Finns

Study. Circulation. 2005;112(10):1486–1493

 

33. Zieman SJ, Melenovsky V, Kass DA. Mechanisms,

pathophysiology, and therapy of arterial

stiffness. Arterioscler Thromb Vasc

Biol. 2005;25(5):932–943

 

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arteries. J Pathol. 2007;211(2):157–172

FUNDING: Supported by the Academy of Finland (grants 77841, 117832, 201888, 121584, and 126925); the Social Insurance Institution of Finland; the Turku University Foundation; the Medical Research Fund of Kuopio University Hospital; the Medical Research Fund of Tampere University Hospital; the Turku University Hospital Medical Fund; the Emil Aaltonen Foundation (T. Lehtimäki); the Juha Vainio Foundation; the Finnish Foundation of Cardiovascular Research; the Finnish Cultural Foundation; and The Tampere Tuberculosis Foundation.

Aatola H, et al “Simplified definitions of elevated pediatric blood pressure and high adult arterial stiffness” Pediatrics2013; DOI: 10.1542/peds.2012-3426.

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Antioxidant micronutrients, such as vitamins and carotenoids, exist in abundance in fruit and vegetables and have been known to contribute to the body’s defence against reactive oxygen species. Numerous epidemiological studies have demonstrated that a high dietary consumption of fruit and vegetables rich in carotenoids or with high serum carotenoid concentrations results in lower risks of certain cancers, diabetes and cardiovascular disease. These epidemiological studies have suggested that antioxidant carotenoids may have a protective effect against diabetes or cardiovascular disease. However, the consumption of carotenoids in pharmaceutical forms for the treatment or prevention of these chronic diseases cannot be recommended, because some large randomized controlled trials did not reveal any reduction in cardiovascular events or type 2 diabetes with b-carotene. High doses of carotenoids used in the supplementation studies could have a pro-oxidant effect. Therefore, it is favourable to intake carotenoids from foods through the combination of other nutrients such as vitamins, minerals or phytochemicals, not by supplements.

The metabolic syndrome is a clustering of metabolic abnormalities that increase the risk for diabetes and cardiovascular disease. Typically, it includes excess weight, hyperglycaemia, evaluated blood pressure, low concentration of HDL-cholesterol, and hypertriacylglycerolaemia. This syndrome is emerging as one of the major medical and public health problems in Japan, and persons with this syndrome have an increased risk of morbidity and mortality due to cardiovascular disease and diabetes. Recently, many studies have examined the associations of dietary patterns with the metabolic syndrome and shown that diets rich in fruit and vegetables have been inversely associated with the metabolic syndrome. These previous reports suggest that a high intake of fruit and vegetables may reduce the risk of the metabolic syndrome through the beneficial combination of antioxidants, fibre, minerals, and other phytochemicals. Some recent cross-sectional and case–control studies have shown the associations of serum antioxidant status with the metabolic syndrome. Ford et al. reported that low intake and/or low serum concentrations of vitamins and carotenoids were associated with the risk of the metabolic syndrome. Although very few data are available about the associations of antioxidant carotenoids with the metabolic syndrome, people who have the metabolic syndrome are more likely to have increased oxidative stress than people who do not have this syndrome.

In some recent studies, it has been reported that oxidative stress, which is an imbalance between pro-oxidants and antioxidants, occurs more frequently in metabolic syndrome subjects than in non-metabolic syndrome subjects. Oxidative stress may play a key role in the pathophysiology of diabetes and cardiovascular disease. On the other hand, smoking is a potent oxidative stress in man. This increment of oxidative stress induced by smoking may develop insulin resistance, and increased insulin resistance may result in the clustering of the metabolic abnormality. Therefore, antioxidants could have a beneficial effect on reducing the risk of these conditions in smokers. However, there is limited information about the interaction of serum antioxidant carotenoids and the metabolic syndrome with smoking habit. This study was aimed to investigate the interaction of serum carotenoid concentrations and the metabolic syndrome with smoking. The association of the concentrations of six serum carotenoids, i.e. lutein, lycopene, a-carotene, b-carotene, b-cryptoxanthin and zeaxanthin, with metabolic syndrome status stratified by smoking status was evaluated crosssectionally.

In this study, the associations of the serum carotenoids with the metabolic syndrome stratified by smoking habit were evaluated cross-sectionally. A total of 1073 subjects (357 male and 716 female) who had received health examinations in the town of Mikkabi, Shizuoka Prefecture, Japan, participated in the study. Inverse associations of serum carotenoids with the metabolic syndrome were more evident among current smokers than non-smokers. These results support that antioxidant carotenoids may have a protective effect against development of the metabolic syndrome, especially in current smokers who are exposed to a potent oxidative stress.

Source References:

http://www.ncbi.nlm.nih.gov/pubmed/18445303

http://www.ncbi.nlm.nih.gov/pubmed/19450371

http://www.ncbi.nlm.nih.gov/pubmed/21216053

http://www.ncbi.nlm.nih.gov/pubmed/19631019

http://www.ncbi.nlm.nih.gov/pubmed/12324189

http://www.ncbi.nlm.nih.gov/pubmed/18689373

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The Implications of a Newly Discovered  CYP2J2 Gene Polymorphism  Associated with Coronary Vascular Disease in the Uygur Chinese Population

Author, Curator: Larry H Bernstein, MD, FCAP

This is an interesting genomic study of the relationship of genetic polymorphism in the Chinese Uygur population that highlights the difficulty in CVD genomics, and casts a promising light on difficulties over
1.  possibly no more than 8 genetic signatures to account for all of human CVD conditions
2.  genetic signatures may no be equally distributed over studied populations
3.  genetic signatures may be more pronounced in different populations
4.  there is little predictable validity in such studies over large assimilated populations (such as African-Americans
5.  the best genomic evidence for meaningful associations does appear to tie in with endothelial metabolism
6.  the greatest difficulty in all studies is the small dose of information provided by an such linkage
7.  there has been too little information provided in studies of the effect of dietary factors on the affected population, which would entail nutrigenomics.
8.  there is an association between certain distinct CVD’s and later development of coronary heart disease (CHD).
This study concepts, methods and difficulties were recently reviewed in the following articles:
Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging
Aviva Lev-Ari, PhD, RN
Genomics & Genetics of Cardiovascular Disease Diagnoses: A Literature Survey of AHA’s Circulation Cardiovascular Genetics, 3/2010 – 3/2013
Aviva Lev-Ari, PhD, RN and Larry H Bernstein, MD, FCAP
Diagnosis of Cardiovascular Disease, Treatment and Prevention: Current & Predicted Cost of Care and the Promise of Individualized Medicine Using Clinical Decision Support Systems
Aviva Lev-Ari, PhD, RN and Larry H Bernstein, MD, FCAP
Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus
Justin D. Pearlman, MD, PhD, and Aviva Lev-Ari, PhD, RN
Clinical Trials Results for Endothelin System: Pathophysiological role in Chronic Heart Failure, Acute Coronary Syndromes and MI – Marker of Disease Severity or Genetic Determination?
Aviva Lev-Ari, PhD, RN
Vascular Medicine and Biology: CLASSIFICATION OF FAST ACTING THERAPY FOR PATIENTS AT HIGH RISK FOR MACROVASCULAR EVENTS Macrovascular Disease – Therapeutic Potential of cEPCs
Aviva Lev-Ari, PhD, RN
Endothelial Function and Cardiovascular Disease
Larry H Bernstein, MD, FCAP
Reversal of Cardiac Mitochondrial Dysfunction
Larry H Bernstein, MD, FCAP
A Second Look at the Transthyretin Nutrition Inflammatory Conundrum
Larry H Bernstein, MD, FCAP

A Novel Polymorphism of the CYP2J2 Gene is Associated with Coronary Artery Disease in Uygur Population in China

Qing Zhu, Zhenyan Fu, Yitong Ma, Hong Yang, Ding Huang, Xiang Xie, Fen Liu, Yingying Zheng, Erdenbat Cha
PII: S0009-9120(13)00174-4    Available online 15 May 2013
Reference: CLB 8375
To appear in: Clinical Biochemistry
Received date: 17 February 2013
Revised date: 13 April 2013
Accepted date: 3 May 2013
Background: Cytochrome P450 (CYP) 2J2 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs).
  • The EETs are potent endogenous vasodilators and
  • inhibitors of vascular inflammation.
The aim of the present study was to assess the association between the human CYP2J2 gene polymorphism and coronary artery disease (CAD) in a Han and Uygur population of China.
We use two independent case-control studies:
  1. a Han population (206 CAD patients and 262 control subjects) and
  2. a Uygur population (336 CAD patients and 448 control subjects).
All CAD patients  and controls were genotyped for the same three single nucleotide polymorphisms (SNPs)
  1. rs890293
  2. rs11572223
  3. rs2280275
of CYP2J2 gene by a Real-time PCR instrument.
Results: In the Uygur population, for total, the distribution of SNP3 (rs2280275) genotypes showed a significant difference between CAD and control participants (P=0.048).
For total and men, the distribution of SNP3 (rs2280275) alleles and the dominant model (CC vs CT + TT)
  • showed a significant difference between CAD and control participants (for allele: P=0.014 and P=0.035, respectively; for dominant model: P=0.014 and P=0.034, respectively).
The significant difference in dominant model was retained after adjustment for covariates (OR: 0.279, 95% confidence interval [CI]: 0.176-0.440, P=0.001; OR: 0.240, 95% CI: 0.128-0.457, P=0.001, respectively).
Conclusions: The CC genotype of rs2280275 in CYP2J2 gene could be a protective genetic marker of CAD and T allele may be a risk genetic marker of CAD in men of Uygur population in China.
Highlights:
1. We used two independent case-control studies: one was in a Han population and the other was in a Uygur population.
2. The CC genotype of rs2280275 in CYP2J2 gene could be a protective genetic marker of CAD and T allele may be a risk genetic marker of CAD in men of Uygur population in China.
3. Polymorphism of the CYP2J2 gene can affect the synthesis of epoxyeicosatrienoic acids (EETs).
Reviewer Observations:
This article describes the association between CYP2J2 polymorphism(SNP1, SNP2 and SNP3) and coronary artery disease (CAD) in two populations of China (Han and Uygur).
Results show that
  1. the frequency of T allele of rs2280275 (SNP3 of the CYP2J2) is higher in CAD patients than in control subjects and
  2. that CC genotype of rs 2280275 is significantly lower in CAD patients than in control subjects.
  3. “T allele of rs2280275 was significantly higher in CAD patients than in control participants. CC genotype of rs2280275 was significantly lower in CAD patients than in control participants.”;
  4. It appears that CC is the homozygous and dominant state of this SNP3 sequence in a pairing-combination.
  5. The effect of decreased CHD is seen only in the CC double combination, in men and not women. The difference between men and women with CAD is in LDL.
For Uygur population,
(1) after adjusting major confounding factors such as Glu、LDL、EH、DM and smoking, the effect of decreased CAD is seen only in the CC double combination, in men and not women.
(2) for men, the LDL level is higher in CAD than in control, for women, there isn’t a difference of LDL level between CAD and control.
(3) for men, the distribution of T and C allele is different between CAD and control (p=0.035), and not in women (p=0.118).
The T allele of SNP3 is increased in CAD. So the C allele is important, and a CT pair is neutral. Neither SNP1 or SNP2, or presumably both have lower incidence.

I might conjecture that having(heterozygous rs2280275), a C & a T, and eating a lot of fish and/or flax seed would show a difference

  • because of the intimal enzymatic conversion of arachidonic acid to EETs.

Arachidonic acid is a derivative of linoleic acid,an n-6 PUFA, while linolenic acid is an omega-3 PUFA. Substantial documentation of the effect of EETs is given. The anti-inflammatory advantage of an n-3 PUFA is also known.
It appears that the intimal conversion results in an omega-3 product.  In addition, the EET activates eNOS, so that there is endothelial NO produced.

The studies of both Spiecker and Ping Yin Liu showed the polymorphism of CYP2J2 (rs890293, SNP1) has relation with CAD. However, in this study, the authors found there was no association between the polymorphism of CYP2J2 (rs890293, SNP1) and CAD in Han population and Uygur population. We found (rs 2280275, SNP3) has association with CAD.
  • “The CC genotype of rs2280275 in CYP2J2 gene could be a protective genetic marker of CAD and T allele may be a risk genetic marker of CAD in men of Uygur population in China”
All participants had a differential diagnosis for chest pain encountered in the Cardiac Catheterization Laboratory of First Affiliated Hospital of Xinjiang Medical University. We recruited randomly CAD group and control group, subjects with valvular disease were excluded, control subjects were not healthy individuals, some of them have hypertension, some of them have DM, some of them have hyperlipidemia, which means control group expose to the same risk factors of CAD while the results of coronary angiogram is normal. All control subjects underwent a coronary angiogram and have no coronary artery stenosis.
The analysis was a logistic regression analysis, we used the major variables of CAD to analysis and found the CC genotype was the dependent useful factor after adjusting for major confounding factors such as Glu、LDL、EH、DM and smoking.
Schematic of EET interactions with cardiovascularion channels.
A: In the cardiac myocyte, EETs activate sarcolemmal or mitochondrial KATP channels.
B: In the vasculature, EETs activate endothelial small-(SKCa) or intermediate (IKCa)–conductance calcium-activated channels to cause hyperpolarization, which can be transmitted to the vascular smooth muscle via myoendothelial gap junctions. EETs also activate TRPV4 channels to activate Ca2+influx. In the vascular smooth muscle, EETs activate large conductance, calcium-activated (BK-Ca) channels through a G protein-Coupled event.
C: In platelets, EETs activate BK-Ca channels.calcium-activated (BK-Ca) channels through a G-protein-coupled event. C, In platelets, EETs activate BK-Ca channels.

Association of the ADRA2A polymorphisms with the risk of type 2 diabetes: A meta-analysis

Xi Chen, Lei Liu, Wentao He, Yu Lu, Delin Ma, Tingting Du, Qian Liu, Cai Chen, Xuefeng Yu
Clinical Biochemistry 2013;  46 (9): 722–726   http://dx.doi.org/10.1016/j.clinbiochem.2013.02.004
Results from the published studies on the association of ADRA2A (adrenoceptor alpha 2A) variants with type 2 diabetes (T2D) are conflicting and call for further assessment. The aim of this meta-analysis was to quantitatively summarize the effects of the two recently reported ADRA2A single nucleotide polymorphisms (SNPs) rs553668 and rs10885122 on T2D risk.
Results
Twelve studies with 40,828 subjects from seven eligible papers were included in the meta-analysis. Overall, the present meta-analysis failed to support a positive association between ADRA2A SNPs (rs553668 and rs10885122) and susceptibility to T2D (OR = 1.05, p = 0.17, 95% CI: 0.98, 1.12; and OR = 1.06, p = 0.11, 95% CI: 0.99, 1.13; respectively).
However, in the subgroup analysis by ethnicity, the significant association between rs553668 and the risk of T2D was obtained in Europeans under the recessive genetic model (OR = 1.36, p = 0.02, 95% CI: 1.05, 1.76).
Conclusion
The results of the meta-analyses indicated that both SNPs were associated with CHD in Caucasians (P < 0.05) but not in Asians. The results from our case-control study and meta-analyses might be explained by genetic heterogeneity in the susceptibility of CHD and ethnic differences between Asians and Caucasians.

Association between PCSK9 and LDLR gene polymorphisms with coronary heart disease: Case-control study and meta-analysis

Lina Zhang, Fang Yuan, Panpan Liu, Lijuan Fei, Yi Huang, Limin Xu, et al.
Clinical Biochemistry 2013; 46 (9): 727–732
► Association of rs11206510 and rs1122608 with CHD in 813 Chinese participants.
► The first association test of rs1122608 with the risk of CHD in Han Chinese.
► Meta-analyses were performed for rs11206510 and rs1122608.
► The two SNPs were associated with CHD in Caucasians but not in Asians.
Objective
To explore the association of rs11206510 (PCSK9 gene) and rs1122608 (LDLR gene) polymorphisms with coronary heart disease (CHD) in Han Chinese.
Methods
A total of 813 participants (290 CHD cases, 193 non-CHD controls and 330 healthy controls) were recruited in the case-control study. DNA genotyping was performed on the SEQUENOM® Mass–ARRAY iPLEX® platform. χ2-test was used to compare the genotype distribution and allele frequencies. Two meta-analyses were performed to establish the association between the two polymorphisms with CHD.
Results
No significant associations between the two SNPs and the risk of CHD were observed in the present study. The meta-analysis of rs11206510 of PCSK9 gene comprises 11 case-control studies with a total of 69,054 participants. Significant heterogeneity was observed in Caucasian population in subgroup analysis of the association studies of rs11206510 with CHD (P = 0.003, I2 = 67.2%). The meta-analysis of LDLR gene rs1122608 polymorphism comprises 7 case-control studies with a total of 20,456 participants and the heterogeneity of seven studies was minimal (P = 0.148, I2 = 36.7%).
Conclusion
The results of the meta-analyses indicated that both SNPs were associated with CHD in Caucasians (P < 0.05) but not in Asians.

The effect of hyperhomocysteinemia on aortic distensibility in healthy individuals

I Eleftheriadou, P Grigoropoulou, I Moyssakis, A Kokkinos. et al.
Nutrition 18 Feb 2013; 29 (6): 876-880, PII: S0899-9007(13)00015-4
Elevated plasma homocysteine (HCY) levels have been associated with increased risk for cardiovascular disease. Aortic distensibility and aortic pulse wave velocity (PWV) are indices of aortic elasticity. The aim of the present study was to determine the effect of acute methionine-induced HHCY on aortic distensibility and PWV in healthy individuals and the effect of acute HHCY on myocardial performance of the left ventricle (Tei index).
Thirty healthy volunteers were included in this crossover study. Aortic distensibility and Tei index were determined non-invasively by ultrasonography at baseline and 3 h after methionine or water consumption, while PWV was measured by applanation tonometry at baseline and every 1 h for the same time interval.
Oral methionine induced an increase in total plasma HCY concentrations (P < 0.001), whereas HCY concentrations did not change after water consumption. Aortic distensibility decreased 3 h after methionine load (P < 0.001) and Tei index increased (P < 0.001), suggesting worsening compared with baseline values. Water consumption had no effect on aortic distensibility or Tei index values. PWV values did not change after either methionine or water consumption.
Acute methionine-induced HHCY reduces aortic distensibility and worsens myocardial performance in healthy individuals. Further research is warranted to examine in the long term the direct effects of HHCY on cardiovascular function and the indirect effects on structural remodeling.
Micrograph of an artery that supplies the hear...

Micrograph of an artery that supplies the heart with significant atherosclerosis and marked luminal narrowing. Tissue has been stained using Masson’s trichrome. (Photo credit: Wikipedia)

Estimated propability of death or non-fatal my...

Estimated propability of death or non-fatal myocardial-infarction over one year corresponding ti selectet values of the individual scores. Ordinate: individual score, abscissa: Propability of death or non-fatal myocardial infarction in 1 year (in %) (Photo credit: Wikipedia)

 

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Reporter: Aviva Lev-Ari, PhD, RN
  • Original Article

HYPERTENSIONAHA.113.01039 Published online before print May 20, 2013,doi: 10.1161/​HYPERTENSIONAHA.113.01039

Arterial Stiffness From Monitoring of Timing of Korotkoff Sounds Predicts the Occurrence of Cardiovascular Events Independently of Left Ventricular Mass in Hypertensive Patients

  1. Philippe Gosse,
  2. Antoine Cremer,
  3. Georgios Papaioannou,
  4. Sunthareth Yeim

+Author Affiliations


  1. From the Department of Cardiology and Hypertension, University Hospital of Bordeaux, Bordeaux, France.
  1. Correspondence to Philippe Gosse, Department of Cardiology and Hypertension, University Hospital of Bordeaux, Hopital Saint Andre, 1 Rue Jean Burguet, 33075 Bordeaux, France. E-mail philippe.gosse@chu-bordeaux.fr

Abstract

Several studies have established that the increase in arterial stiffness (AS) is a cardiovascular risk factor but to date no studies have evaluated in hypertensive patients its prognostic value in comparison with another powerful risk factor, left ventricular mass (LVM) as measured by echocardiography. We prospectively evaluated the prognostic value of AS and LVM in patients with essential hypertension. The population studied comprised 793 patients (56% men) aged 54±14 years. For 519 patients, baseline measurements were made before any antihypertensive treatment, for 274 patients, the measurement were obtained during the follow-up period under antihypertensive treatment. AS was assessed from ambulatory monitoring of blood pressure and timing of Korottkoff sounds. Left ventricular mass was measured in 523 patients. After a mean follow-up of 97 months, 122 cardiovascular events were recorded in the whole population and 74 in the group with LVM determination. AS as continuous or discontinuous variable was independently related to cardiovascular events. The existence or not of antihypertensive treatment at the time of its measurement did not affect its prognostic value. When LVM was forced in the model, AS remained significantly related to cardiovascular events. Thus, AS has an independent prognostic value in the hypertensive, whether measured before or after the administration of antihypertensive treatment. This prognostic value persists after taking LVM into account.

Key Words:

  • Received January 10, 2013.
  • Revision received March 25, 2013.
  • Accepted April 22, 2013.

http://hyper.ahajournals.org/content/early/2013/05/20/HYPERTENSIONAHA.113.01039.abstract.html?papetoc

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Treatment, Prevention and Cost of Cardiovascular Disease: Current & Predicted Cost of Care and the Potential for Improved Individualized Care Using Clinical Decision Support Systems

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC

Author and Curator: Larry H Bernstein, MD, FACP

and

Curator: Aviva Lev-Ari, PhD, RN

This article has the following FIVE parts:

1. Forecasting the Impact of Heart Failure in the United States : A Policy Statement From the American Heart Association

2. A Case Study from the GENETIC CONNECTIONS — In The Family: Heart Disease Seeking Clues to Heart Disease in DNA of an Unlucky Family

3. Arterial Stiffness and Cardiovascular Events : The Framingham Heart Study

4. Arterial Elasticity in Quest for a Drug Stabilizer: Isolated Systolic Hypertension
caused by Arterial Stiffening Ineffectively Treated by Vasodilatation Antihypertensives

5. Clinical Decision Support Systems: Realtime Clinical Expert Support — Biomarkers of Cardiovascular Disease : Molecular Basis and Practical Considerations

 

1. Forecasting the Impact of Heart Failure in the United States : A Policy Statement From the American Heart Association

PA Heidenreich, NM Albert, LA Allen, DA Bluemke, J Butler, et al. Circulation: Heart Failure 2013;6.
Print ISSN: 1941-3289, Online ISSN: 1941-3297.

Heart failure (HF) poses a major burden on productivity and cost of national healthcare expenditures

  • among older Americans, more are hospitalized for HF than for any other medical condition.

As the population ages, the prevalence of HF is expected to increase.

The purpose of this report is to

  • provide an in-depth look at how the changing demographics in the United States will impact the prevalence and cost of care for HF for different US populations.

 Projections of HF Prevalence

Prevalence estimates for HF were determined from

 Projections of the US Population With HF From 2010 to 2030 for Different Age Groups

Year

All ages

18-44 y

45-64 y

65-79 y

> 80

2012 5 813 262 396 578 1 907 141 2 192 233 1 317 310
2015 6 190 606 402 926 1 949 669 2 483 853 1 354 158
2020 6 859 623 417 600 1 974 585 3 004 002 1 463 436
2025 7 644 674 434 635 1 969 852 3 526 347 1 713 840
2030 8 489 428 450 275 2 000 896 3 857 729 2 180 528

Future Costs of HF

The future costs of HF were estimated by methods developed by the American Heart Association

  • project the prevalence and costs of HF from 2012 to 2030
  • factor out  the costs attributable to comorbid conditions.

The model does this by assuming that

(1) HF prevalence percentages will remain constant by age, sex, and race/ethnicity;

(2) the costs of technological innovation will rise at the current rate.

HF prevalence and costs (direct and indirect) were projected using the following steps:

1. HF prevalence and average cost per person were estimated by age group (18–44, 45–64, 65–79, ≥80 years), gender (male, female), and race/ethnicity (white non-Hispanic, white Hispanic, black, other) [32]. The initial HF cost per person and rate of increase in cost was determined for each demographic group, as a percentage of total healthcare expeditures.

2. Inflation is separately addressed by correcting dollar values from Medical Expenditure Panel Survey (MEPS) to 2010 dollars.

3. Nursing home spending triggered an adjustment. The estimates project the incremental cost of care attributable to heart failure (HF).

4. Total HF population prevalence and costs were projected by multiplying the US Census–projected population of each demographic group by the percentage prevalence and average cost

5. The total work loss and home productivity loss costs were generated by multiplying per capita work days lost attributable to HF by (1) prevalence of HF, (2) the probability of employment given HF (for work loss costs only), (3) mean per capita daily earnings, and (4) US Census population projection counts.

Projections of Indirect Costs

Indirect costs of lost productivity from morbidity and premature mortality were estimated as detailed below.
Morbidity costs represent the value of lost earnings attributable to HF and include loss of work among

  • currently employed individuals and those too sick to work, as well as
  • home productivity loss, which is the value of household services performed by household members who do not receive pay for the services.

Total Costs Attributable to Heart Failure (HF)

Projections of Total Cost of Care ($ Billions) for HF for Different Age Groups of the US Population

Year All 18–44 45–64 65–79 ≥ 80
2012
Medical 20.9 0.33 3.67 8.46 8.42
Indirect: Morbidity 5.42 0.52 1.92 2.05 0.93
Indirect: Mortality 4.35 0.66 2.53 0.98 0.18
Total 30.7 1.51 8.12 11.5 9.53
2020
Medical 31.1 0.43 4.58 14.2 11.8
Indirect: Morbidity 7.09 0.66 2.20 3.11 1.12
Indirect: Mortality 5.39 0.79 2.89 1.49 0.22
Total 43.6 1.88 9.67 18.8 13.2
2030
Medical 53.1 0.59 5.86 23.3 23.4
Indirect: Morbidity 9.80 0.91 2.54 4.48 1.87
Indirect: Mortality 6.84 0.98 3.32 2.16 0.37
Total 69.7 2.48 11.7 29.9 25.6

Excludes HF care costs that have been attributed to comorbid conditions.

Cost of Care

Total medical costs are projected to increase from $20.9 billion in 2012 to $53.1 billion in 2030, a 2.5-fold increase. Assuming continuation of current hospitalization practices, the majority (80%) of the costs stem from

  • hospitalization. Also, the majority of increase is from directs costs. Indirect costs are expected to rise as well, but at a lower rate, from $9.8 billion to $16.6 billion, an increase of 69%.

Direct costs (cost of medical care) are expected to increase at a faster rate than indirect costs because of premature deaths and lost productivity.

The total cost of HF (direct and indirect costs) is expected to increase in 2030 from the current $30.7 billion to at least $69.8 billion. This will amount to $244 for every US adult in 2030.

Thus the burden of HF for the US healthcare system will grow substantially during the next 18 years if current trends continue.

It is estimated that

  • by 2030, the prevalence of HF in the United States will increase by 25%, to 3.0%.
  • >8 million people in the US (1 in every 33) will have HF by 2030.
  • the projected total direct medical costs of HF between 2012 and 2030 (in 2010 dollars) will increase from $21 billion to $53 billion.
  • Total costs, including indirect costs for HF, are estimated to increase from $31 billion in 2012 to $70 billion in 2030.
  • If one assumes all costs of cardiac care for HF patients are attributable to HF
    (no cost attribution to comorbid conditions), the 2030 projected cost estimates of treating patients with HF will be 3-fold higher ($160 billion in direct costs).

Projections can be lowered if action is taken to reduce the health and economic burden of HF. Strategies, plans, and implementation to prevent HF and improve the efficiency of care are needed.

Causes and Stages of HF

If the projections for accelerating HF costs are to be avoided, attention to the different causes of HF and their risk factors is warranted.
HF is a clinical syndrome that results from a variety of cardiac disorders

  1. idiopathic dilated cardiomyopathy
  2. cardiac valvular disease
  3. pericarditis or pericardial effusion
  4. ischemic heart disease
  5. primary or secondary hypertension
  6. renovascular disease
  7. advanced liver disease with decreased venous return
  8. pulmonary hypertension
  9. prolonged hypoalbuminemia with generalized interstitial edema
  10. diabetic nephropathy
  11. heart muscle infiltration disease such as primary or secondary amyloidosis
  12. myocarditis
  13. rhythm disorders
  14. congenital diseases
  15. accidental trauma (war, chest trauma)
  16. toxicities (methamphetamine, cocaine, heavy metals, chemotherapy)

HF generally causes symptoms:

  • shortness of breath
  • fatigue
  • swelling (edema)
  • inability to lay flat (orthopnea, paroxysmal nocturnal dyspnea)
  • possibly cough, wheezing

In the Western world the predominant causes of HF are:

  • coronary artery disease
  • valvular disease
  • hypertension
  • viral, alcohol, methamphetamine or other drug  toxicity cardiomyopathy
  • stress (catechol toxicity, takotsubo “broken heart” cardiomyopathy)
  • atrial fibrillation/rapid heart rates
  • thyroid disease

In 2001, the American College of Cardiology and AHA practice guidelines for chronic HF promoted a classification system that encompasses 4 stages of HF.

  • Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder.
  • Stage B: a structural heart disorder but no symptoms.
  • Stage C: previous or current symptoms of heart failure, manageable with medical treatment.
  • Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

Stages A and B are considered precursors to the clinical HF and are meant

  1. to alert healthcare providers to known risk factors for HF and
  2. the available therapies aimed at mitigating disease progression.

Stage A patients have risk factors for HF hypertension, atherosclerotic heart disease, and/or diabetes mellitus.

Patients with stage B are asymptomatic patients who have  developed structural heart disease from a variety of potential insults to the heart muscle such as myocardial infarction or valvular heart disease.

Stages C and D represent the symptomatic phases of HF, with stage C manageable and stage D failing medical management, resulting in marked symptoms at rest or with minimal activity despite optimal medical therapy.

Therapeutic interventions include:

  • dietary salt restriction and diuretics
  • medications known to prolong survival (beta blockers, ACE inhibitors, aldosterone inhibitors)
  • implantable devices such as pacemakers and defibrillators
  • stoppage of tobacco, toxic drugs, excess alcohol

Classic demographic risk factors for the development of HF include

  • older age, male gender, ethnicity, and low socioeconomic status.
  • comorbid disease states contribute to the development of HF
    • Ischemic heart disease
    • Hypertension

Diabetes mellitus, insulin resistance, and obesity are also linked to HF development,

  • with diabetes mellitus increasing the risk of HF by ≈2-fold in men and up to 5-fold in women.

Smoking remains the single largest preventable cause of disease and premature death in the United States.

Translation of Scientific Evidence into Clinical Practice

In multiple studies, failures to apply evidence-based management strategies are blamed for avoidable hospitalizations and/or deaths from HF

Improved implementation of guidelines can delay, mitigate or prevent the onset of HF, and improve survival. Performance improvement programs have facilitated the implementation of evidence-based therapies in both hospital and ambulatory care settings.

Care transition programs by hospitals have become more widespread

  • in an effort to reduce avoidable readmissions.

The interventions used by these programs include

  • initiating discharge planning early in the course of hospital care,
  • actively involving patients and families or caregivers in the plan of care,
  • providing new processes and systems that ensure patient understanding of the plan of care before discharge from the hospital, and
  • improving quality of care by continually monitoring adherence to national evidence-based guidelines with appropriate adaptations for individual differences in needs and responses.

In multiple studies,adherence to the HF plan of care was associated with reduced all-cause mortality as well as HF hospitalization.

It is anticipated that care transition programs may increase appropriate admissions while decreasing inappropriate admissions

This would have a potentially benenficial impact on the 30-day all-cause readmission rate that has become

  • a focus of public reporting in pay for performance.

More than a quarter of Medicare spending occurs in the last year of life, and

  • the costs of care during the last 6 months for a patient with HF have been increasing (11% from 2000 to 2007).

Improving end-of-life care cost effectiveness for patients with stage D HF will require ongoing

  • improved prediction of outcomes
  • integration of multiple aspects of care
  • educated examination of alternatives and priorities
  • improved decision-making
  • unbiased allocation of resources and coverage for this process rather than unbalanced coverage favoring catastrophic care

Palliative care, including formal hospice care, is increasingly advocated for patients with advanced HF.
Offering palliative care to patients with HF may lead to

  • more conservative (and less expensive) treatment
  • consistent with many patients’ goals for care

The use of hospice services is growing among the HF population,

  • HF now the second most common reason for entering hospice
  • but hospice declaration may impose automated restrictions on care that can impose an impediment to election of hospice

A recent study of patients in hospice care found that

  • patients with HF were more likely than patients with cancer to use hospice services longer than 6 months or to be discharged from hospice care alive.

Highlights:

1. Increasing incidence and costs of care for heart failure projected from 2012 to 2030

2. Direct costs rising at greater rate than indirect costs

3. American Heart Association has defined 4 stages of HF, the last 2 of which are advanced

4. Stages C & D are clinically overt and contribute to rehospitalization

5. Stage D accounts for a significant use of end-of-life hospice care

6. There are evidence-based guidelines for the provision of coordinated care that are not widely applied at present

Basic questions raised:

1. If stages A & B are under the radar, then what measures can best trigger the use of evidence-based guidelines for care?
2. Why are evidence-based guidelines commonly not deployed?

  • Flaws in the “evidence” due to bias, design errors, limted ability to extrapolate to the patients it should address
  • Delays in education, convincing of caretakers, and deployment
  • Inadequate resources
  • Financial or other disincentives

The arguments for introducing coordinated care and for evidence-based guidelines is strong.

Arguments AGAINST slavish imposition of evidence based medicine include genetic individuality (what is best on average is not necessarily best for each genetically and behaviorly distinct individual). Strict adherence to evidence-based guidelines also stifles innovative explorations. None-the-less, deviations from evidence-based plans should be cautious, well-documented, and well-informed, not due to mal-aligned incentives, ignorance, carelessness or error.

The question of when and how to intervene most cost effectively is unanswered. If some patients are salt-sensitive as a contribution to the prevalence of hypertension and heart failure, should EVERYONE be salt restricted or should there be a more concerted effort to define who is salt sensitive? What if it proved more cost-effective to restrict salt intake for everyone, even though many might be fine with high sodium intake, and some might even benefit from or require high sodium intake? Is it reasonable to impose costs, hurdles, even possible harm on some as a cheaper way to achieve “greater good”?
These issues are highly relevant to the proposed emphasis on holistic solutions.

2. A Case Study from the GENETIC CONNECTIONS — In The Family: Heart Disease Seeking Clues to Heart Disease in DNA of an Unlucky Family

By GINA KOLATA   2013.05.13  New York Times

Scientists are studying the genetic makeup of the Del Sontro family for

  • telltale mutations or aberrations in the DNA.

Robin Ashwood, one of Mr. Del Sontro’s sisters, found out she had extensive heart disease even though her electrocardiograms was normal. Six of her seven siblings also have heart disease, despite not having any of the traditional risk factors. Then, after a sister, just 47 years old, found out she had advanced heart disease, Mr. Del Sontro, then 43, went to a cardiologist. An X-ray of his arteries revealed the truth. Like his grand-father, his mother, his four brothers and two sisters, he had heart disease.

Now he and his extended family have joined an extraordinary federal research project that is using genetic sequencing to find factors that increase the risk of heart disease beyond the usual suspects — high cholesterol, high blood pressure, smoking and diabetes.“We don’t know yet how many pathways there are to heart disease,” said Dr. Leslie Biesecker, who directs the study Mr. Del Sontro joined. “That’s the power of genetics. To try and dissect that.”

“I had bought the dream: if you just do the right things and eat the right things, you will be O.K.,” said Mr. Del Sontro, whose cholesterol and blood pressure are reassuringly low.

3. Arterial Stiffness and Cardiovascular Events : The Framingham Heart Study

GF Mitchell, Shih-Jen Hwang, RS Vasan, MG Larson.

Circulation. 2010;121:505-511.  http://circ.ahajournals.org/content/121/4/505
http://dx.doi.org/10.1161/CIRCULATIONAHA.109.886655

Various measures of arterial stiffness and wave reflection have been proposed as cardiovascular risk markers.
Prior studies have not assessed relations of a comprehensive panel of stiffness measures to prognosis.
First-onset major cardiovascular disease events in relation to arterial stiffness

  • pulse wave velocity [PWV]
  • wave reflection
    • augmentation index
    • carotid-brachial pressure amplification)
  • central pulse pressure

were analyzed  in 2232 participants (mean age, 63 years; 58% women) in the Framingham Heart Study by a proportional hazards model. During median follow-up of 7.8 (range, 0.2 to 8.9) years,

  • 151 of 2232 participants (6.8%) experienced an event.

In multivariable models adjusted for

  • age
  • sex
  • systolic blood pressure
  • use of antihypertensive therapy
  • total and high-density lipoprotein cholesterol concentrations
  • smoking
  • presence of diabetes mellitus

higher aortic PWV was associated with a 48% increase in cardiovascular disease risk (95% confidence interval, 1.16 to 1.91 per SD; P 0.002).

After PWV was added to a standard risk factor model, integrated discrimination improvement was 0.7% (95% confidence interval, 0.05% to 1.3%; P 0.05).

In contrast,

  • augmentation index,
  • central pulse pressure, and
  • pulse pressure amplification

were not related to cardiovascular disease outcomes in multivariable models.

Higher aortic stiffness assessed by PWV

  • is associated with increased risk for a first cardiovascular event.

Aortic PWV improves risk prediction when added to standard risk factors and may represent

  • a valuable biomarker of cardiovascular disease risk

We shall here visit a recent article by Justin D. Pearlman and Aviva Lev-Ari, PhD, RN, on

Pros and Cons of Drug Stabilizers for Arterial  Elasticity as an Alternative or Adjunct to Diuretics and Vasodilators in the Management of Hypertension, titled

4. Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus

http://pharmaceuticalintelligence.com/2013/05/11/arterial-elasticity-in-quest-for-a-drug-stabilizer-isolated-systolic-hypertension-caused-by-arterial-stiffening-ineffectively-treated-by-vasodilatation-antihypertensives/

Speaking at the 2013 International Conference on Prehypertension and Cardiometabolic Syndrome, meeting cochair Dr Reuven Zimlichman (Tel Aviv University, Israel) argued that there is a growing number of patients for whom the conventional methods are inappropriate for

  • the definitions of hypertension
  • the risk-factor tables used to guide treatment

Most antihypertensives today work by producing vasodilation or decreasing blood volume which may be

  • ineffective treatments for patients in whom average arterial diameter and circulating volume are not the causes of hypertension and as targets of therapy may promote decompensation

In the future, he predicts, “we will have to start looking for a totally different medication that will aim to

  • improve or at least to stabilize arterial elasticity: medication that might affect factors that determine the stiffness of the arteries, like collagen, like fibroblasts.

Those are not the aim of any group of antihypertensive medications today.”

Zimlichman believes existing databases could be used to develop algorithms that focus on

  • inelasticity as a mechanism of hypertensive disease

He also points out that

  • ambulatory blood-pressure-monitoring devices can measure elasticity

http://www.theheart.org/article/1502067.do

A related article was published on the relationship between arterial stiffening and primary hypertension.

Arterial stiffening provides sufficient explanation for primary hypertension.

KH Pettersen, SM Bugenhagen, J Nauman, DA Beard, SW Omholt.

By use of empirically well-constrained computer models describing the coupled function of the baroreceptor reflex and mechanics of the circulatory system, we demonstrate quantitatively that

  • arterial stiffening seems sufficient to explain age-related emergence of hypertension.

Specifically,

  • the empirically observed chronic changes in pulse pressure with age
  • the capacity of hypertensive individuals to regulate short-term changes in blood pressure becomes impaired

The results suggest that a major target for treating chronic hypertension in the elderly  may include

  • the reestablishment of a proper baroreflex response.

http://arxiv.org/abs/1305.0727v2?goback=%2Egde_4346921_member_240018699

5. Clinical Decision Support Systems: Realtime Clinical Expert Support: Biomarkers of Cardiovascular Disease — Molecular Basis and Practical Considerations

RS Vasan.  Circulation. 2006;113:2335-2362

http://dx.doi.org/10.1161/CIRCULATIONAHA.104.482570

http://circ.ahajournals.org/content/113/19/2335

Substantial data indicate that CVD is a life course disease that begins with the evolution of risk factors that contribute to

  • subclinical atherosclerosis.

Subclinical disease culminates in overt CVD. The onset of CVD itself portends an adverse prognosis with greater

  • risks of recurrent adverse cardiovascular events, morbidity, and mortality.

Clinical assessment alone has limitations. Clinicians have used additional tools to aid clinical assessment and to enhance their ability to identify the “vulnerable” patient at risk for CVD, as suggested by a recent National Institutes of Health (NIH) panel.

Biomarkers are one such tool to better identify high-risk individuals, to diagnose disease conditions promptly for diagnosis, prognosis, and treatment guidance.

Biological marker (biomarker): A laboratory test value that is objectively measured and evaluated as an indicator of

  1. normal biological processes,
  2. pathogenic processes, or
  3. pharmacological responses to a therapeutic intervention.

Type 0 biomarker: A marker of the natural history of a disease

  • Type 0 correlates longitudinally with known clinical indices/predicts outcomes.

Type I biomarker: A marker that captures the effects of a therapeutic intervention

  • Type I assesses an aspect of treatment mechanism of action.

Type 2 biomarker (surrogate end point):  A marker intended to predict outcomes on the basis of

  • epidemiologic
  • therapeutic
  • pathophysiologic or
  • other scientific evidence.

With biomarkers monitoring disease progression or response to therapy, the patient can serve as  his or her own control (follow-up values may be compared to baseline  values).

Costs may be less important for prognostic markers when they are largely restricted to people with disease (total cost=cost per person x number to be tested, plus down-stream costs). Some biomarkers (e.g., an exercise stress test) may be used for both diagnostic and prognostic purposes.

Generally there are cost differences in establishing a prognostic value versus diagnostic value of a biomarker:

  • prognostic utility typically requires a large sample and a prospective design, whereas
  • diagnostic value often can be determined with a smaller sample in a cross-sectional design

Regardless of the intended use, it is important to remember that biomarkers that do not change disease management

  • cannot affect patient outcome and therefore
  • are unlikely to be cost-effective (judged in terms of quality-adjusted life-years gained).

Typically, for a biomarker to change management, it is important to have evidence that risk reduction strategies should vary with biomarker levels, and/or biomarker-guided management achieves advantages over a management scheme that ignores the biomarker levels.

Typically it means that biomarker levels should be modifiable by therapy.

Gil David and Larry Bernstein have developed, in consultation with Prof. Ronald Coifman, in the Yale University Applied Mathematics Program, a software system that is the equivalent of an intelligent Electronic Health Records Dashboard that

  • provides empirical medical reference and
  • suggests quantitative diagnostics options.

The current design of the Electronic Medical Record (EMR) is a
linear presentation of portions of the record

  • by services
  • by diagnostic method, and
  • by date

to cite examples.

This allows perusal through a graphical user interface (GUI) that

  • partitions the information or necessary reports in a workstation entered by keying to icons.
  • presents decision support

Examples of data partitions include:

  • history
  • medications
  • laboratory reports
  • imaging
  • EKGs

The introduction of a DASHBOARD adds presentation of

  • drug reactions
  • allergies
  • primary and secondary diagnoses, and
  • critical information

about any patient the care giver needing access to the record.

A basic issue for such a tool is what information is presented and how it is displayed.

A determinant of the success of this endeavor is if it

  • facilitates workflow
  • facilitates decision-making process
  • reduces medical error.

Continuing work is in progress in extending the capabilities with model datasets, and sufficient data based on the assumption that computer extraction of data from disparate sources will, in the long run, further improve this process.

For instance, there is synergistic value in finding coincidence of:

  • ST shift on EKG
  • elevated cardiac biomarker (troponin)
  • in the absence of substantially reduced renal function.

Similarly, the conversion of hematology based data into useful clinical information requires the establishment of problem-solving constructs based on the measured data.

The most commonly ordered test used for managing patients worldwide is the hemogram that often incorporates

  • morphologic review of a peripheral smear
  • descriptive statistics

While the hemogram has undergone progressive modification of the measured features over time the subsequent expansion of the panel of tests has provided a window into the cellular changes in the

  • production
  • release
  • or suppression

of the formed elements from the blood-forming organ into the circulation. In the hemogram one can view data reflecting the characteristics of a broad spectrum of medical conditions.

Progressive modification of the measured features of the hemogram has delineated characteristics expressed as measurements of

  • size
  • density, and
  • concentration

resulting in many characteristic features of classification. In the diagnosis of hematological disorders

  • proliferation of marrow precursors
  • domination of a cell line
  • suppression of hematopoiesis

Other dimensions are created by considering

  • the maturity and size of the circulating cells.

The application of rules-based, automated problem solving should provide a valid approach to

  • the classification and interpretation of the data used to determine a knowledge-based clinical opinion.

The exponential growth of knowledge since the mapping of the human genome enabled by parallel advances in applied mathematics that have not been a part of traditional clinical problem solving.

As the complexity of statistical models has increased

  • the dependencies have become less clear to the individual.

Contemporary statistical modeling has a primary goal of finding an underlying structure in studied data sets.
The development of an evidence-based inference engine that can substantially interpret the data at hand and

  • convert it in real time to a “knowledge-based opinion”

could improve clinical decision-making by incorporating into the model

  • multiple complex clinical features as well as onset and duration .

An example of a difficult area for clinical problem solving is found in the diagnosis of Systemic Inflammatory Response Syndrome (SIRS) and associated sepsis. SIRS is a costly diagnosis in hospitalized patients.   Failure to diagnose it in a timely manner increases the financial and safety hazard.  The early diagnosis of SIRS/sepsis is made by the application of defined criteria by the clinician.

  • temperature
  • heartrate
  • respiratory rate and
  • WBC count

The application of those clinical criteria, however, defines the condition after it has developed, leaving unanswered the hope for

  • a reliable method for earlier diagnosis of SIRS.

The early diagnosis of SIRS may possibly be enhanced by the measurement of proteomic biomarkers, including

  • transthyretin
  • C-reactive protein
  • procalcitonin
  • mean arterial pressure

Immature granulocyte (IG) measurement has been proposed as a

  • readily available indicator of the presence of granulocyte precursors (left shift).

The use of such markers, obtained by automated systems in conjunction with innovative statistical modeling, provides

  • a promising support to early accurate decision making.

Such a system aims to reduce medical error by utilizing

  • the conjoined syndromic features of disparate data elements .

How we frame our expectations is important. It determines

  • the data we collect to examine the process.

In the absence of data to support an assumed benefit, there is no proof of validity at whatever cost.

Potential arenas of benefit include:

  • hospital operations
  • nonhospital laboratory studies
  • companies in the diagnostic business
  • planners of health systems

The problem stated by LL  WEED in “Idols of the Mind” (Dec 13, 2006):
“ a root cause of a major defect in the health care system is that, while we falsely admire and extol the intellectual powers of highly educated physicians, we do not search for the external aids their minds require.” Hospital information technology (HIT) use has been focused on information retrieval, leaving

  • the unaided mind burdened with information processing.

We deal with problems in the interpretation of data presented to the physician, and how the situation could be improved through better

  • design of the software that presents data .

The computer architecture that the physician uses to view the results is more often than not presented

  • as the designer would prefer, and not as the end-user would like.

In order to optimize the interface for physician, the system could have a “front-to-back” design, with the call up for any patient

  • A dashboard design that presents the crucial information that the physician would likely act on in an easily accessible manner
  • Each item used has to be closely related to a corresponding criterion needed for a decision.

Feature Extraction.

Eugene Rypka contributed greatly to clarifying the extraction of features in a series of articles, which

  • set the groundwork for the methods used today in clinical microbiology.

The method he describes is termed S-clustering, and

  • will have a significant bearing on how we can view laboratory data.

He describes S-clustering as extracting features from endogenous data that

  • amplify or maximize structural information to create distinctive classes.

The method classifies by taking the number of features with sufficient variety to generate maps.

The mapping is done by

  • a truth table NxN of messages and choices
  • each variable is scaled to assign values for each message choice.

For example, the message for an antibody titer would be converted from 0 + ++ +++ to 0 1 2 3.

Even though there may be a large number of measured values, the variety is reduced by this compression, even though it may represent less information.

The main issue is

  • how a combination of variables falls into a table to convey meaningful information.

We are concerned with

  • accurate assignment into uniquely variable groups by information in test relationships.

One determines the effectiveness of each variable by its contribution to information gain in the system. The reference or null set is the class having no information.  Uncertainty in assigning to a classification can be countered by providing sufficient information.

One determines the effectiveness of each variable by its contribution to information gain in the system. The possibility for realizing a good model for approximating the effects of factors supported by data used

  • for inference owes much to the discovery of Kullback-Liebler distance or “information”, and Akaike
  • found a simple relationship between K-L information and Fisher’s maximized log-likelihood function.

In the last 60 years the application of entropy comparable to

  • the entropy of physics, information, noise, and signal processing,
  • developed by Shannon, Kullback, and others
  • integrated with modern statistics,
  • as a result of the seminal work of Akaike, Leo Goodman, Magidson and Vermunt, and work by Coifman

Akaike pioneered recognition that the choice of model influence results in a measurable manner. In particular, a larger number of variables promotes further explanations of variance, such that a model selection criterion is important that penalizes for the number of variables when success is measured by explanation of variance.

Gil David et al. introduced an AUTOMATED processing of the data available to the ordering physician and

  • can anticipate an enormous impact in diagnosis and treatment of perhaps half of the top 20 most common
  • causes of hospital admission that carry a high cost and morbidity.

For example:

  1. anemias (iron deficiency, vitamin B12 and folate deficiency, and hemolytic anemia or myelodysplastic syndrome);
  2. pneumonia; systemic inflammatory response syndrome (SIRS) with or without bacteremia;
  3. multiple organ failure and hemodynamic shock;
  4. electrolyte/acid base balance disorders;
  5. acute and chronic liver disease;
  6. acute and chronic renal disease;
  7. diabetes mellitus;
  8. protein-energy malnutrition;
  9. acute respiratory distress of the newborn;
  10. acute coronary syndrome;
  11. congestive heart failure;
  12. hypertension
  13. disordered bone mineral metabolism;
  14. hemostatic disorders;
  15. leukemia and lymphoma;
  16. malabsorption syndromes; and
  17. cancer(s)[breast, prostate, colorectal, pancreas, stomach, liver, esophagus, thyroid, and parathyroid].
  18. endocrine disorders
  19. prenatal and perinatal diseases

Rudolph RA, Bernstein LH, Babb J: Information-Induction for the diagnosis of
myocardial infarction. Clin Chem 1988;34:2031-2038.

Bernstein LH (Chairman). Prealbumin in Nutritional Care Consensus Group.

Measurement of visceral protein status in assessing protein and energy
malnutrition: standard of care. Nutrition 1995; 11:169-171.

Bernstein LH, Qamar A, McPherson C, Zarich S, Rudolph R. Diagnosis of myocardial infarction:
integration of serum markers and clinical descriptors using information theory.
Yale J Biol Med 1999; 72: 5-13.

Kaplan L.A.; Chapman J.F.; Bock J.L.; Santa Maria E.; Clejan S.; Huddleston D.J.; Reed R.G.;
Bernstein L.H.; Gillen-Goldstein J. Prediction of Respiratory Distress Syndrome using the
Abbott FLM-II amniotic fluid assay. The National Academy of Clinical Biochemistry (NACB)
Fetal Lung Maturity Assessment Project.  Clin Chim Acta 2002; 326(8): 61-68.

Bernstein LH, Qamar A, McPherson C, Zarich S. Evaluating a new graphical ordinal logit method
(GOLDminer) in the diagnosis of myocardial infarction utilizing clinical features and laboratory
data. Yale J Biol Med 1999; 72:259-268.

Bernstein L, Bradley K, Zarich SA. GOLDmineR: Improving models for classifying patients with
chest pain. Yale J Biol Med 2002; 75, pp. 183-198.

Ronald Raphael Coifman and Mladen Victor Wickerhauser. Adapted Waveform Analysis as a Tool for Modeling, Feature Extraction, and Denoising. Optical Engineering, 33(7):2170–2174, July 1994.

R. Coifman and N. Saito. Constructions of local orthonormal bases for classification and regression.
C. R. Acad. Sci. Paris, 319 Série I:191-196, 1994.

Realtime Clinical Expert Support and validation System

We have developed a software system that is the equivalent of an intelligent Electronic Health Records Dashboard that provides empirical medical reference and suggests quantitative diagnostics options. The primary purpose is to gather medical information, generate metrics, analyze them in realtime and provide a differential diagnosis, meeting the highest standard of accuracy. The system builds its unique characterization and provides a list of other patients that share this unique profile, therefore

  • utilizing the vast aggregated knowledge (diagnosis, analysis, treatment, etc.) of the medical community.
  • The main mathematical breakthroughs are provided by accurate patient profiling and inference methodologies
  • in which anomalous subprofiles are extracted and compared to potentially relevant cases.

As the model grows and its knowledge database is extended, the diagnostic and the prognostic become more accurate and precise.
We anticipate that the effect of implementing this diagnostic amplifier would result in

  • higher physician productivity at a time of great human resource limitations,
  • safer prescribing practices,
  • rapid identification of unusual patients,
  • better assignment of patients to observation, inpatient beds,
    intensive care, or referral to clinic,
  • shortened length of patients ICU and bed days.

The main benefit is a

  1. real time assessment as well as
  2. diagnostic options based on comparable cases,
  3. flags for risk and potential problems

as illustrated in the following case acquired on 04/21/10. The patient was diagnosed by our system with severe SIRS at a grade of 0.61 .

Graphical presentation of patient status

The patient was treated for SIRS and the blood tests were repeated during the following week. The full combined record of our system’s assessment of the patient, as derived from the further hematology tests, is illustrated below. The yellow line shows the diagnosis that corresponds to the first blood test (as also shown in the image above). The red line shows the next diagnosis that was performed a week later.

Progression changes in patient ICU stay with SIRS

The MISSIVE(c) system, by Justin Pearlman, is an alternative approach that includes not only automated data retrieval and reformatting of data for decision support, but also an integrated set of tools to speed up analysis, structured for quality and error reduction, couplled to facilitated report generation, incorporation of just-in-time knowledge and group expertise, standards of care, evidence-based planning, and both physician and patient instruction.

See also in Pharmaceutical Intelligence:

The Cost Burden of Disease: U.S. and Michigan.CHRT Brief. January 2010. @www.chrt.org

The National Hospital Bill: The Most Expensive Conditions by Payer, 2006. HCUP Brief #59.

Rudolph RA, Bernstein LH, Babb J: Information-Induction for the diagnosis of myocardial infarction. Clin Chem 1988;34:2031-2038.

Bernstein LH, Qamar A, McPherson C, Zarich S, Rudolph R. Diagnosis of myocardial infarction:
integration of serum markers and clinical descriptors using information theory.
Yale J Biol Med 1999; 72: 5-13.

Kaplan L.A.; Chapman J.F.; Bock J.L.; Santa Maria E.; Clejan S.; Huddleston D.J.; Reed R.G.;
Bernstein L.H.; Gillen-Goldstein J. Prediction of Respiratory Distress Syndrome using the Abbott FLM-II amniotic fluid assay. The National Academy of Clinical Biochemistry (NACB) Fetal Lung Maturity Assessment Project.  Clin Chim Acta 2002; 326(8): 61-68.

Bernstein LH, Qamar A, McPherson C, Zarich S. Evaluating a new graphical ordinal logit method (GOLDminer) in the diagnosis of myocardial infarction utilizing clinical features and laboratory
data. Yale J Biol Med 1999; 72:259-268.

Bernstein L, Bradley K, Zarich SA. GOLDmineR: Improving models for classifying patients with chest pain. Yale J Biol Med 2002; 75, pp. 183-198.

Ronald Raphael Coifman and Mladen Victor Wickerhauser. Adapted Waveform Analysis as a Tool for Modeling, Feature Extraction, and Denoising.
Optical Engineering 1994; 33(7):2170–2174.

R. Coifman and N. Saito. Constructions of local orthonormal bases for classification and regression. C. R. Acad. Sci. Paris, 319 Série I:191-196, 1994.

W Ruts, S De Deyne, E Ameel, W Vanpaemel,T Verbeemen, And G Storms. Dutch norm data for 13 semantic categoriesand 338 exemplars. Behavior Research Methods, Instruments,
& Computers 2004; 36 (3): 506–515.

De Deyne, S Verheyen, E Ameel, W Vanpaemel, MJ Dry, WVoorspoels, and G Storms.  Exemplar by feature applicability matrices and other Dutch normative data for semantic
concepts.
  Behavior Research Methods 2008; 40 (4): 1030-1048

Landauer, T. K., Ross, B. H., & Didner, R. S. (1979). Processing visually presented single words: A reaction time analysis [Technical memorandum].  Murray Hill, NJ: Bell Laboratories.
Lewandowsky , S. (1991).

Weed L. Automation of the problem oriented medical record. NCHSR Research Digest Series DHEW. 1977;(HRA)77-3177.

Naegele TA. Letter to the Editor. Amer J Crit Care 1993;2(5):433.

Sheila Nirenberg/Cornell and Chethan Pandarinath/Stanford, “Retinal prosthetic strategy with the capacity to restore normal vision,” Proceedings of the National Academy of Sciences.

Other related articles published in this Open Access Online Scientific Journal include the following:

http://pharmaceuticalintelligence.com/2012/08/13/the-automated-second-opinion-generator/

http://pharmaceuticalintelligence.com/2012/09/21/the-electronic-health-record-how-far-we-
have-travelled-and-where-is-journeys-end/

http://pharmaceuticalintelligence.com/2013/02/18/the-potential-contribution-of-
informatics-to-healthcare-is-more-than-currently-estimated/

http://pharmaceuticalintelligence.com/2013/05/04/cardiovascular-diseases-decision-support-
systems-for-disease-management-decision-making/?goback=%2Egde_4346921_member_239739196

http://pharmaceuticalintelligence.com/2012/08/13/demonstration-of-a-diagnostic-clinical-
laboratory-neural-network-agent-applied-to-three-laboratory-data-conditioning-problems/

http://pharmaceuticalintelligence.com/2012/12/17/big-data-in-genomic-medicine/

http://pharmaceuticalintelligence.com/2013/02/13/cracking-the-code-of-human-life-
the-birth-of-bioinformatics-and-computational-genomics/

http://pharmaceuticalintelligence.com/2013/04/28/genetics-of-conduction-disease-
atrioventricular-av-conduction-disease-block-gene-mutations-transcription-excitability-
and-energy-homeostasis/

http://pharmaceuticalintelligence.com/2012/12/10/identification-of-biomarkers-that-
are-related–to-the-actin-cytoskeleton/

http://pharmaceuticalintelligence.com/2012/08/14/regression-a-richly-textured-method-
for-comparison-and-classification-of-predictor-variables/

http://pharmaceuticalintelligence.com/2012/08/02/diagnostic-evaluation-of-sirs-by-
immature-granulocytes/

http://pharmaceuticalintelligence.com/2012/08/01/automated-inferential-diagnosis-
of-sirs-sepsis-septic-shock/

http://pharmaceuticalintelligence.com/2012/08/12/1815/

http://pharmaceuticalintelligence.com/2012/08/15/1946/

http://pharmaceuticalintelligence.com/2013/05/13/vinod-khosla-20-doctor-included-speculations-
musings-of-a-technology-optimist-or-technology-will-replace-80-of-what-doctors-do/

http://pharmaceuticalintelligence.com/2013/05/05/bioengineering-of-vascular-and-tissue-models/

The Heart: Vasculature Protection – A Concept-based Pharmacological Therapy including THYMOSIN
Aviva Lev-Ari, PhD, RN 2/28/2013
http://pharmaceuticalintelligence.com/2013/02/28/the-heart-vasculature-protection-a-concept-
based-pharmacological-therapy-including-thymosin/

FDA Pending 510(k) for The Latest Cardiovascular Imaging Technology
Aviva Lev-Ari, PhD, RN 1/28/2013
http://pharmaceuticalintelligence.com/2013/01/28/fda-pending-510k-for-the-latest-
cardiovascular-imaging-technology/

PCI Outcomes, Increased Ischemic Risk associated with Elevated Plasma Fibrinogen not
Platelet Reactivity    Aviva Lev-Ari, PhD, RN 1/10/2013
http://pharmaceuticalintelligence.com/2013/01/10/pci-outcomes-increased-ischemic-risk-
associated-with-elevated-plasma-fibrinogen-not-platelet-reactivity/

The ACUITY-PCI score: Will it Replace Four Established Risk Scores — TIMI, GRACE, SYNTAX,
and Clinical SYNTAX   Aviva Lev-Ari, PhD, RN 1/3/2013
http://pharmaceuticalintelligence.com/2013/01/03/the-acuity-pci-score-will-it-replace-four-
established-risk-scores-timi-grace-syntax-and-clinical-syntax/

Coronary artery disease in symptomatic patients referred for coronary angiography: Predicted by
Serum Protein Profiles    Aviva Lev-Ari, PhD, RN 12/29/2012
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Aviva Lev-Ari, PhD, RN 8/27/2012
http://pharmaceuticalintelligence.com/2012/08/27/new-definition-of-mi-unveiled-
fractional-flow-reserve-ffrct-for-tagging-ischemia/

Herceptin Fab (antibody) - light and heavy chains

Herceptin Fab (antibody) – light and heavy chains (Photo credit: Wikipedia)

Personalized Medicine

Personalized Medicine (Photo credit: Wikipedia)

Diagnostic of pathogenic mutations. A diagnost...

Diagnostic of pathogenic mutations. A diagnostic complex is a dsDNA molecule resembling a short part of the gene of interest, in which one of the strands is intact (diagnostic signal) and the other bears the mutation to be detected (mutation signal). In case of a pathogenic mutation, the transcribed mRNA pairs to the mutation signal and triggers the release of the diagnostic signal (Photo credit: Wikipedia)

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Pros and Cons of Drug Stabilizers for Arterial  Elasticity as an Alternative or Adjunct to Diuretics and Vasodilators in the Management of Hypertension.

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC

and

Article Curator: Aviva Lev-Ari, PhD, RN

This article presents the 2013 Thought Frontier on Hypertension and Vascular Compliance.

Conceptual development of the subject is presented in the following nine parts:

1.        Physiology of Circulation and Role of Arterial Elasticity

2.      Isolated Systolic Hypertension caused by Arterial Stiffening may be inadequately treated by Diuretics or Vasodilatation Antihypertensive Medications

3.         Physiology of Circulation and Compensatory Mechanism of Arterial Elasticity

4.         Vascular Compliance – The Potential for Novel Therapies

  • Novel Mechanism for Disease Etiology: Modulation of Nuclear and Cytoskeletal Actin Polymerization.
  • Genetic Therapy targeting Vascular Conductivity 
  • Regenerative Medicine for Vasculature Function Protection

5.        In addition to curtailing high pressures, stabilizing BP variability is a potential target for management of hypertension

6.        Mathematical Modeling: Arterial stiffening  explains much of primary hypertension

7.         Classification of Blood Pressure and Hypertensive Treatment Best Practice of Care in the US

8.         Genetic Risk for High Blood Pressure

9.         Is it Hypertension or Physical Inactivity: Cardiovascular Risk and Mortality – New results in 3/2013.

Summary By Justin D. Pearlman MD ME PhD MA FACC

1.       Physiology of Circulation and Role of Arterial Elasticity

  • Simplistically, high blood pressure stems from too much volume (salt water) for the vascular space, or conversely, too little space for the volume. Biological signals, such as endothelin, hypoxia, acidosis, nitric oxide, can modify vascular volume by constricting muscles in blood vessel walls. Less simplistically the physics of circulation are governed by numerous factors, with essentials detailed below.
  • The vascular space has two major circuits: pulmonary (lungs) and systemic (body).
  • Compliance (C)  relates change in volume (ΔV) to change in pressure (ΔP) as a measure of the strength of elasticity, where elasticity summarizes the intrinsic forces that  return to original shape after deformation: C = ΔV/ΔP . Those values can be estimated by ultrasound imaging with Doppler blood velocity estimation, by MRI, or invasively. Related properties can also be measured, such as wave propagation time or fractional flow reserve.
  • The vascular system is dynamic, with frequency components and reactive elements. The fundamental frequency is governed by the heart rate delivering a stroke volume forward into the vasculature; a heart rate of 60/minute corresponds to the frequency of 1 Hertz (1 cycle/second). The pressure rise due to the ejection of stroke volume is called the pulse pressure.
  • Numerous factors affect blood flow, including blood composition (affected by anemia or blood dilution), leakiness of vessels, elasticity, wave propagation, streamlines, viscosity, osmotic pressure (affected by protein deficiency and other factors),
  • In a static system, the driving force relates linearly flow by way of resistance (R  in units of dyn·s·cm−5): V=IR (Ohm’s law).
    • Pulmonary:\frac {80 \cdot (mean\ pulmonary\ arterial\ pressure - mean \ pulmonary \ artery \ wedge \ pressure)} {cardiac\ output}
    • Systemic:\frac {80 \cdot (mean\ arterial\ pressure - mean \ right \ atrial \ pressure)} {cardiac\ output}
  • In a dynamic, reactive system, the relation between the driving potential (pressure gradient), and current (blood flow) is governed by a differential equation. However, use of complex numbers and exponentials recovers simplicity similar to Ohm’s law:
    • Variables take the form Ae^{st}, where t is time, s is a complex parameter, and A is a complex scalar. Complex values simply mean two dimensional, e.g., magnitude (as in resistance) plus phase shift (to account for reactive components).
    • Complex version of Ohm’s law: \boldsymbol{V} = \boldsymbol{I} \cdot \boldsymbol{Z} where V and I are the complex scalars in the voltage and current respectively and Z is the complex impedance.
    • Frequency dependent “resistance” is captured by the term impedance.
  • Breathing in increases the return of blood to the heart, adding to pulse variation.
  • Dynamic elastance  (Eadyn)  relates volume variation (VVS) to pressure variation (PPV): Eadyn=PPV/SVV
    • PPV(%) = 100% × (PPmax − PPmin)/[(PPmax + PPmin)/2)]
      • where PPmax and PPmin are the maximum and minimum pulse pressures determined during a single  respiratory cycle
    • SVV(%) = 100% × [(SVmax − SVmin)/SVmean]
      • where SVmax and SVmin  are the maximum and minimum standard deviation of arterial pressure about the mean arterial pressure during a single respiratory cycle
  • The nervous system provides both stimulants and inhibitors (sympathetic and vagal nerves) to regulate blood vessel wall muscle tone and also heart rate. Many medications, and anesthetic agents in particular, reduce those responses to stimuli, so the vessels dilate, vascular impedance lowers, pressures drop, and autoregulation is impaired.
  • Diuretics aim to decrease volume of circulating fluid, vasodilators aim to increase the vascular space, and elasticity treatments will aim to preserve or improve the ability to accommodate changes in volume of fluid.
    • Vessel dilation near the skin promotes heat loss.
  • Vascular elasticity is impaired by atherosclerosis, menopause, and endothelial dysfunction (impaired nitric oxide signals  response, impaired endothelin response).
  • Elastance in a cyclic pressure system of systole-diastole (contraction-dilation) presents impedance as a pulsatile load on the heart. Inotropy describes the generation of pressure by cardiac contraction, lusiotropy the compliance of the heart to accept filling with minimal back pressure to the lungs. Chronic exposure to elevated vascular impedance leads to impairment of lusiotropy (diastolic failure, stiff heart) and inotropy (systolic failure, weak heart).

2.      Isolated Systolic Hypertension caused by Arterial Stiffening may be inadequately treated by Diuretics or Vasodilatation Antihypertensive Medications

3. Physiology of Circulation and Compensatory Mechanism of Arterial Elasticity

Antihypertensive agents have focused on the following approaches:

  1. The most common prescriptions, a mild diuretic, hydrochlorothiazide (HCTZ), is known to improve blood vessel compliance by reducing cell turgor, which explains why its full onset of benefit as well as its slow offset when stopped can take more than one month.
  2. Chlorthalidone  – Some evidence suggests that chlorthalidone may be superior to hydrochlorothiazide for the treatment of hypertension. However, a recent study concluded: chlorthalidone in older adults was not associated with fewer adverse cardiovascular events or deaths than hydrochlorothiazide. However, it was associated with a greater incidence of electrolyte abnormalities, particularly hypokalemia.
  • Increased vascular space (vasodilation)

    • Alternatively, the pressure can be lowered by increasing the vascular space for a given vascular volume. Examples of mediators for arterial tone (degree of dilation) include nitric oxide, prostacyclin and endothelin.

 

Class

Description

Hyperpolarization mediated (Calcium channel blocker) Changes in the resting membrane potential of thecell affects the level of intracellular calciumthrough modulation of voltage sensitive calcium channelsin the plasma membrane.
cAMP mediated Adrenergic stimulation results in elevated levelsof cAMP and protein kinase A, which results inincreasing calcium removal from the cytoplasm.
cGMP mediated (Nitrovasodilator) Through stimulation of protein kinase G.Until 2002, the enzyme for this conversion wasdiscovered to be mitochondrial aldehyde dehydrogenase.Proc. Natl. Acad. Sci. USA 102 (34): 12159–12164. doi:10.1073/pnas.0503723102http://www.pnas.org/content/102/34/12159.long

Class

Example

Hyperpolarization mediated (Calcium channel blocker) adenosineamlodipine (Norvasc),diltiazem (Cardizem,Dilacor XR) andnifedipine (Adalat, Procardia).
cAMP mediated prostacyclin
cGMP mediated (Nitrovasodilator) nitric oxide
  • Reduced pulsatile force (beta blockers)

These work by blocking certain nerve and hormonal signals to the heart and blood vessels, thus lowering blood pressure. Frequently prescribed beta blockers include

  • metoprolol (Lopressor, Toprol XL)
  • carvedilol (Coreg)
  • nadolol (Corgard)
  • penbutolol (Levatol).
  • Metabolized nebivolol increases vascular NO production, involves endothelial ß2-adrenergic receptor ligation, with a subsequent rise in endothelial free [Ca2+]i and endothelial NO synthase–dependent NO production
  • Angiotensin-converting enzyme (ACE) inhibitors

These allow blood vessels to widen by preventing the hormone angiotensin from affecting blood vessels. Frequently prescribed ACE inhibitors include captopril (Capoten), lisinopril (Prinivil, Zestril) and ramipril (Altace).

  • Angiotensin II receptor blockers

These help blood vessels relax by blocking the action of angiotensin. Frequently prescribed angiotensin II receptor blockers include losartan (Cozaar), olmesartan (Benicar) and valsartan (Diovan).
Another very commonly prescribed drug class of medication counteracts hardening of arteries.

Atheroma lipids have enzyme systems that explicitly disassemble cholesterol esters and reconstruct them inside blood vessel walls,e.g.,  Anacetrapib, Genetic variants that improve cholesterol levels are stimulating development of additional medications.

We can propose that atheroma build up in arterial blood vessel walls constitutes a maladaptive defense against aneurysm and risk of vessel rupture from hypertension.

Arguably, HMG-CoA reductase inhibitors,  statin therapy is a second example of a medication that helps protect vascular elasticity, both by its lipid effects and its anti-inflammatory effects.

The best-selling statin is atorvastatin, marketed as Lipitor (manufactured by Pfizer) and Torvast. By 2003, atorvastatin became the best-selling pharmaceutical in history,[4] with Pfizer reporting sales of US$12.4 billion in 2008.[5] As of 2010, a number of statinsare on the market: atorvastatin (Lipitor and Torvast), fluvastatin (Lescol), lovastatin (Mevacor, Altocor, Altoprev), pitavastatin(Livalo, Pitava), pravastatin (Pravachol, Selektine, Lipostat), rosuvastatin (Crestor) and simvastatin (Zocor, Lipex).[6] Several combination preparations of a statin and another agent, such as ezetimibe/simvastatin, are also available.

References for Statins from:

http://en.wikipedia.org/wiki/Statin

Clinical Considerations of Statin Therapy’s manifold effects, in

http://pharmaceuticalintelligence.com/2012/10/08/statins-nonlipid-effects-on-vascular-endothelium-through-enos-activation/

Compensatory Effects in the Physiology of Circulation

Before declaring vessel elasticity a new and highly desirable treatment target, consider that it is not firmly established that hardening of arteries (loss of elasticity) is entirely maladaptive.

In parallel with any focus on increasing vascular elasticity or compliance, each of the issues discussed, below merits scrutiny and investigation.

Cardiac Circulation Dynamics

Endothelium morphology, rheological properties of intra vasculature fluid dynamics and blood viscosity provided explanation for shear stress of vessels under arterial pressure

http://pharmaceuticalintelligence.com/2012/11/28/special-considerations-in-blood-lipoproteins-viscosity-assessment-and-treatment/

and

http://pharmaceuticalintelligence.com/2012/11/28/what-is-the-role-of-plasma-viscosity-in-hemostasis-and-vascular-disease-risk/

Aging and Vasculature Diminished Elasticity

While among other reasons for Hypertension increasing prevalence with aging, arterial stiffening is one.

Yet, stiffer vessels are more efficient at transmitting pressure to distal targets. With aging, muscle mass diminishes markedly and the contribution to circulation from skeletal muscle tissue compressions combined with competent venous valves fades.

http://pharmaceuticalintelligence.com/2012/08/27/endothelial-dysfunction-diminished-availability-of-cepcs-increasing-cvd-risk-for-macrovascular-disease-therapeutic-potential-of-cepcs/

and

http://pharmaceuticalintelligence.com/2012/10/19/clinical-trials-results-for-endothelin-system-pathophysiological-role-in-chronic-heart-failure-acute-coronary-syndromes-and-mi-marker-of-disease-severity-or-genetic-determination/

and

http://pharmaceuticalintelligence.com/2012/11/13/peroxisome-proliferator-activated-receptor-ppar-gamma-receptors-activation-pparγ-transrepression-for-angiogenesis-in-cardiovascular-disease-and-pparγ-transactivation-for-treatment-of-dia/

Aging and Myocardial Diminished Contractility and Ejection Fraction

With aging heart contractility diminishes. These issues can cause under perfusion of tissues, inadequate nutrient blood delivery (ischemia), lactic acidosis, tissue dysfunction and multi-organ failure. Hardened arteries may compensate. Thus, pharmacotherapy to increase Arterial Elasticity may be counterindicated for patients with mild to progressive CHF.

http://pharmaceuticalintelligence.com/2013/05/05/bioengineering-of-vascular-and-tissue-models/

and

http://pharmaceuticalintelligence.com/2012/10/20/nitric-oxide-and-sepsis-hemodynamic-collapse-and-the-search-for-therapeutic-options/

and

http://pharmaceuticalintelligence.com/2012/10/17/chronic-heart-failure-personalized-medicine-two-gene-test-predicts-response-to-beta-blocker-bucindolol/
Our biosystems are highly interdependent, and we cannot leap to conclusions without careful thorough evidence. Increasing arterial elastance will lower vascular impedance and change the frequency components of our pulsatile perfusion system.

MOST comprehensive review of the Human Cardiac Conduction System presented to date:

http://pharmaceuticalintelligence.com/2013/04/28/genetics-of-conduction-disease-atrioventricular-av-conduction-disease-block-gene-mutations-transcription-excitability-and-energy-homeostasis/

Diminished contractility will increase the amount of energy needed to maintain circulation. It will change efficiency dramatically – consider the difference between periodically pushing someone sitting on a swing at the resonance frequency if the pendulum versus significantly off resonance.

http://pharmaceuticalintelligence.com/2013/04/14/mitochondrial-metabolism-and-cardiac-function/

and

http://pharmaceuticalintelligence.com/2012/10/28/mitochondrial-damage-and-repair-under-oxidative-stress/

Increased Arterial Elasticity – Potential Risk to Myocardium

The hypothesis that we should focus on cellular therapies to increase vascular compliance may decrease the circulation efficiency and result in worsening of cardiac right ventricular morphology and development of Dilated cardiomyopathy and hypertrophic cardiomyopathy (muscle thickening and diastolic failure), an undesirable outcome resulting from an attempt to treat the hypertension.

4. Vascular Compliance – The Potential of Noval Therapies

  • Novel Mechanism for Disease Etiology for the Cardiac Phenotype: Modulation of Nuclear and Cytoskeletal Actin Polymerization.

Lamin A/C and emerin regulate MKL1–SRF activity by modulating actin dynamics

Chin Yee Ho,

Diana E. Jaalouk,

Maria K. Vartiainen

& Jan Lammerding

Nature (2013) doi:10.1038/nature12105

Published online 05 May 2013

Affiliations

Cornell University, Weill Institute for Cell and Molecular Biology/Department of Biomedical Engineering, Ithaca, New York 14853, USA

Chin Yee Ho &

Jan Lammerding

Brigham and Women’s Hospital/Harvard Medical School, Department of Medicine, Boston 02115, Massachusetts, USA

Chin Yee Ho,

Diana E. Jaalouk &

Jan Lammerding

Institute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland

Maria K. Vartiainen

Present address: American University of Beirut, Department of Biology, Beirut 1107 2020, Lebanon.

Diana E. Jaalouk

Contributions

C.Y.H., D.E.J. and J.L. conceived and designed the overall project, with valuable help from M.K.V. C.Y.H. and D.E.J. performed the experiments. C.Y.H., D.E.J. and J.L. analysed data. C.Y.H. and J.L. wrote the paper.

Corresponding author Jan Lammerding

Laminopathies, caused by mutations in the LMNA gene encoding the nuclear envelope proteins lamins A and C, represent a diverse group of diseases that include Emery–Dreifuss muscular dystrophy (EDMD), dilated cardiomyopathy (DCM), limb-girdle muscular dystrophy, and Hutchison–Gilford progeria syndrome1. Most LMNA mutations affect skeletal and cardiac muscle by mechanisms that remain incompletely understood. Loss of structural function and altered interaction of mutant lamins with (tissue-specific) transcription factors have been proposed to explain the tissue-specific phenotypes1. Here we report in mice that lamin-A/C-deficient (Lmna−/−) and LmnaN195K/N195K mutant cells have impaired nuclear translocation and downstream signalling of the mechanosensitive transcription factor megakaryoblastic leukaemia 1 (MKL1), a myocardin family member that is pivotal in cardiac development and function2. Altered nucleo-cytoplasmic shuttling of MKL1 was caused by altered actin dynamics in Lmna−/− and LmnaN195K/N195K mutant cells. Ectopic expression of the nuclear envelope protein emerin, which is mislocalized in Lmnamutant cells and also linked to EDMD and DCM, restored MKL1 nuclear translocation and rescued actin dynamics in mutant cells. These findings present a novel mechanism that could provide insight into the disease aetiology for the cardiac phenotype in many laminopathies, whereby lamin A/C and emerin regulate gene expression through modulation of nuclear and cytoskeletal actin polymerization.

 http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12105.html

  • Genetic Therapy to Conductivity Disease

http://pharmaceuticalintelligence.com/2012/10/01/ngs-cardiovascular-diagnostics-long-qt-genes-sequenced-a-potential-replacement-for-molecular-pathology/

  • Regenerative Medicine for Vasculature Function Protection

http://pharmaceuticalintelligence.com/2012/08/29/positioning-a-therapeutic-concept-for-endogenous-augmentation-of-cepcs-therapeutic-indications-for-macrovascular-disease-coronary-cerebrovascular-and-peripheral/

and

http://pharmaceuticalintelligence.com/2012/08/28/cardiovascular-outcomes-function-of-circulating-endothelial-progenitor-cells-cepcs-exploring-pharmaco-therapy-targeted-at-endogenous-augmentation-of-cepcs/

and

http://pharmaceuticalintelligence.com/2013/02/28/the-heart-vasculature-protection-a-concept-based-pharmacological-therapy-including-thymosin/

5. Stabilizing BP Variability is the next Big Target in Hypertension Management

Hypertension caused by Arterial Stiffening is Ineffectively Treated by Diuretics and Vasodilatation Antihypertensives

Barcelona, Spain – An aging population grappling with rising rates of hypertension and other cardiometabolic risk factors should prompt an overhaul of how hypertension is diagnosed and monitored and should spur development of drugs with entirely new mechanisms of action, one expert says. Speaking here at the 2013 International Conference on Prehypertension and Cardiometabolic Syndrome, meeting cochair Dr Reuven Zimlichman (Tel Aviv University, Israel) argued that the definitions of hypertension, as well as the risk-factor tables used to guide treatment, are no longer appropriate for a growing number of patients.

Most antihypertensives today work by producing vasodilation or decreasing blood volume and so are ineffective treatments in ISH patients. In the future, he predicts, “we will have to start looking for a totally different medication that will aim to improve or at least to stabilize arterial elasticity: medication that might affect factors that determine the stiffness of the arteries, like collagen, like fibroblasts. Those are not the aim of any group of antihypertensive medications today.”

Zimlichman believes existing databases could be used to develop algorithms that take this progression of disease into account, in order to better guide hypertension management. He also points out that new ambulatory blood-pressure-monitoring devices also measure arterial elasticity. “Unquestionably, these will improve our ability to diagnose both the status of the arteries and the changes of the arteries with time as a result of our treatment. So if we treat the patient and we see no improvement in arterial elasticity, or the patient is worse, something is wrong, something is not working—either the patient is not taking the medication, or our choice of medication is not appropriate, or the dose is insufficient, etc.”

http://www.theheart.org/article/1502067.do

Oslo, Norway – New research that is only just starting to be digested by the hypertension community indicates that visit-to-visit variability in blood-pressure readings will likely become another way of looking for “at-risk” hypertensive patients and in fact is likely to be more reliable as an indicator of cardiovascular risk than the currently used mean BP.

The Goal of Stabilizing BP variability 

June 29, 2010  

Discussing the importance of this issue for guidelines and clinical practice, Dr Tony Heagerty (University of Manchester, UK) told the recent European Society of Hypertension (ESH) European Meeting on Hypertension 2010: “We are poking around in the dark, offering treatment blankly across a large community, and probably treating a lot of people who don’t need to be treated, while not necessarily treating the highest-risk patients. We should stop being reassured by ‘occasional’ normal BPs. The whole game now is, can we improve the identification of our ‘at-risk’ individuals?”

Heagerty was speaking at a special plenary session on late-breaking research discussing BP variability as a risk factor. This issue has emerged following new analyses reported at the ACC meeting and published in a number of papers in the Lancet and Lancet Neurology earlier this year, which showed that variability in blood pressure is a much stronger determinant of both stroke and coronary disease outcome than average blood pressure.

http://www.theheart.org/article/1093553.do

Three years later, 2/1/2013, Zimlichman also argued that definitions of essential and secondary hypertension have changed very little over the past few decades and have typically only been tweaked up or down related to other CV risk factors. Diastolic hypertension has been the primary goal of treatment, and treatment goals have not adequately taken patient age into account (in whom arterial stiffening plays a larger role), and they have typically relied too heavily on threshold cutoffs, rather than the “linear progression” of risk factors and their impact on organ damage.

6. Mathematical Modeling: Arterial stiffening provides sufficient explanation for primary hypertension

Klas H. Pettersen, Scott M. Bugenhagen, Javaid Nauman, Daniel A. Beard, Stig W. Omholt

(Submitted on 3 May 2013 (v1), last revised 6 May 2013 (this version, v2))

Hypertension is one of the most common age-related chronic diseases and by predisposing individuals for heart failure, stroke and kidney disease, it is a major source of morbidity and mortality. Its etiology remains enigmatic despite intense research efforts over many decades. By use of empirically well-constrained computer models describing the coupled function of the baroreceptor reflex and mechanics of the circulatory system, we demonstrate quantitatively that arterial stiffening seems sufficient to explain age-related emergence of hypertension. Specifically, the empirically observed chronic changes in pulse pressure with age, and the impaired capacity of hypertensive individuals to regulate short-term changes in blood pressure, arise as emergent properties of the integrated system. Results are consistent with available experimental data from chemical and surgical manipulation of the cardio-vascular system. In contrast to widely held opinions, the results suggest that primary hypertension can be attributed to a mechanogenic etiology without challenging current conceptions of renal and sympathetic nervous system function. The results support the view that a major target for treating chronic hypertension in the elderly is the reestablishment of a proper baroreflex response.

Klas H. Pettersen1, Scott M. Bugenhagen2, Javaid Nauman3, Daniel A. Beard2 & Stig W. Omholt3

1Department of Mathematical and Technological Sciences, Norwegian University of Life Science, Norway

2Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA

3NTNU Norwegian University of Science and Technology, Department of Circulation and Medical Imaging, Cardiac Exercise Research Group, Trondheim, Norway

Correspondence should be addressed to: KHP (klas.pettersen@gmail.com)

Keywords: hypertension, mechanogenic, baroreceptor signaling, cardiovascular model, arterial stiffening

Author contributions: K.H.P. and S.W.O. designed the study. K.H.P. constructed the

integrated model and performed the numerical experiments with contributions from

D.A.B. and S.M.B.. J.N. extracted and compiled empirical test data from the HUNT2

Survey. S.W.O, K.H.P. and D.A.B. wrote the paper.

http://arxiv.org/abs/1305.0727v2

http://arxiv.org/pdf/1305.0727v2.pdf

 

7. Classification of Blood Pressure and Hypertensive Treatment:

Best Practice of Care in the US

8. Genetic Risk for High Blood Pressure

Hypertension.2013; 61: 931doi: 10.1161/​HYP.0b013e31829399b2

Blood Pressure Single-Nucleotide Polymorphisms and Coronary Artery Sisease (page 995)

Blood pressure (BP) is considered a major cardiovascular risk factor that is influenced by multiple genetic and environmental factors. However, the precise genetic underpinning influencing interindividual BP variation is not well characterized; and it is unclear whether BP-associated genetic variants also predispose to clinically apparent cardiovascular disease. Such an association of BP-related variants with cardiovascular disease would strengthen the concept of BP as a causal risk factor for cardiovascular disease. In this issue of Hypertension, analyses within the Coronary ARtery DIsease Genome-Wide Replication And Meta-Analysis consortium indicate that common genetic variants associated with BP in the population, indeed, contribute to the susceptibility for coronary artery disease (CAD). Lieb et al tested 30 single-nucleotide polymorphisms—that based on prior studies were known to affect BP—for their association with CAD. In total, data from 22 233 CAD cases and 64 762 controls were analyzed. The vast majority (88%) of BP-related single-nucleotide polymorphisms were also shown to increase the risk of CAD (as defined by an odds ratio for CAD >1; Figure). On average, each of the multiple BP-raising alleles was associated with a 3% (95% confidence interval, 1.8%–4.3%) risk increase for CAD.

Masked Hypertension in Diabetes Mellitus (page 964)

The first important finding in the IDACO study of masked hypertension (MH) in the population with diabetes mellitus and non–diabetes mellitus was that antihypertensive treatment converted some sustained hypertensives into sustained normotensives; this resulted in an increased cardiovascular disease risk in the treated versus untreated normotensive comparator group (Figure). Not surprisingly, normalization of blood pressure (BP) with treatment did not eliminate the lifetime cardiovascular disease burden associated with prior elevated BP nor did it correct other cardiometabolic risk factors that clustered with the hypertensive state.

The second important IDACO finding was that treatment increased the prevalence of MH by decreasing conventional BP versus daytime ambulatory BP (ABP) by a ratio of ≈3 to 2. The clinical implication of increased prevalence of MH with therapy in the population of both diabetes mellitus and non–diabetes mellitus was that these subjects did not receive sufficient antihypertensive therapy to convert MH into normalized ABP (ie, treated, normalized ABP being the gold standard for minimizing cardiovascular disease risk). Indeed, there is a transformation-continuum from sustained hypertension to MH and finally to sustained normotension with increasing antihypertensive therapy. These IDACO findings strongly suggest that many physicians mistakenly have their primary focus on normalizing in-office rather than out-of-office home BP and/or 24-hour ABP values and this results in an increased prevalence of MH. However, what constitutes optimal normalized ABP will remain empirical until established in randomized controlled trials.

Genetic Risk Score for Blood Pressure (page 987)

Elevated blood pressure (BP) is a strong, independent, and modifiable risk factor for stroke and heart disease. BP is a heritable trait, and genome-wide association studies have identified several genetic loci that are associated with systolic BP, diastolic BP, or both. Although the variants have modest effects on BP, typically 0.5 to 1.0 mm Hg, their presence may act over the entire life course and, therefore, lead to substantial increase in risk of cardiovascular disease (CVD). However, the independent impact of these variants on CVD risk has not been established in a prospective setting. Havulinna et al genotyped 32 common single-nucleotide polymorphisms in several Finnish cohorts, with up to 32 669 individuals after exclusion of prevalent CVD cases. The median follow-up was 9.8 years, during which 2295 incident CVD events occurred. Genetic risk scores were created for systolic BP and diastolic BP by multiplying the risk allele count of each single-nucleotide polymorphism by the effect size estimated in published genome-wide association studies on BP traits. The GRSs were strongly associated with baseline systolic BP, diastolic BP, and hypertension (all P<10–62). Hazard ratios for incident CVD increased roughly linearly by quintile of systolic BP or diastolic BP GRS (Figure). GRSs remained significant predictors of CVD risk after adjustment for traditional risk factors, even including BP and use of antihypertensive medication. These findings are consistent with a lifelong effect of these variants on BP and CVD risk.

Related Articles on Genetics and Blood Pressure

Genetic Predisposition to Higher Blood Pressure Increases Coronary Artery Disease Risk

  • Wolfgang Lieb,
  • Henning Jansen,
  • Christina Loley,
  • Michael J. Pencina,
  • Christopher P. Nelson,
  • Christopher Newton-Cheh,
  • Sekar Kathiresan,
  • Muredach P. Reilly,
  • Themistocles L. Assimes,
  • Eric Boerwinkle,
  • Alistair S. Hall,
  • Christian Hengstenberg,
  • Reijo Laaksonen,
  • Ruth McPherson,
  • Unnur Thorsteinsdottir,
  • Andreas Ziegler,
  • Annette Peters,
  • John R. Thompson,
  • Inke R. König,
  • Jeanette Erdmann,
  • Nilesh J. Samani,
  • Ramachandran S. Vasan,
  • andHeribert Schunkert
  • , on behalf of CARDIoGRAM

Hypertension. 2013;61:995-1001, published online before print March 11 2013,doi:10.1161/HYPERTENSIONAHA.111.00275

Masked Hypertension in Diabetes Mellitus: Treatment Implications for Clinical Practice

  • Stanley S. Franklin,
  • Lutgarde Thijs,
  • Yan Li,
  • Tine W. Hansen,
  • José Boggia,
  • Yanping Liu,
  • Kei Asayama,
  • Kristina Björklund-Bodegård,
  • Takayoshi Ohkubo,
  • Jørgen Jeppesen,
  • Christian Torp-Pedersen,
  • Eamon Dolan,
  • Tatiana Kuznetsova,
  • Katarzyna Stolarz-Skrzypek,
  • Valérie Tikhonoff,
  • Sofia Malyutina,
  • Edoardo Casiglia,
  • Yuri Nikitin,
  • Lars Lind,
  • Edgardo Sandoya,
  • Kalina Kawecka-Jaszcz,
  • Jan Filipovský,
  • Yutaka Imai,
  • Jiguang Wang,
  • Hans Ibsen,
  • Eoin O’Brien,
  • and Jan A. Staessen
  • , on behalf of the International Database on Ambulatory blood pressure in relation to Cardiovascular Outcomes (IDACO) Investigators

Hypertension. 2013;61:964-971, published online before print March 11 2013,doi:10.1161/HYPERTENSIONAHA.111.00289

A Blood Pressure Genetic Risk Score Is a Significant Predictor of Incident Cardiovascular Events in 32 669 Individuals

  • Aki S. Havulinna,
  • Johannes Kettunen,
  • Olavi Ukkola,
  • Clive Osmond,
  • Johan G. Eriksson,
  • Y. Antero Kesäniemi,
  • Antti Jula,
  • Leena Peltonen,
  • Kimmo Kontula,
  • Veikko Salomaa,
  • and Christopher Newton-Cheh

Hypertension. 2013;61:987-994, published online before print March 18 2013,doi:10.1161/HYPERTENSIONAHA.111.00649

9. Is it Hypertension or Physical Inactivity: Cardiovascular Risk and Mortality – New results in 3/2013.

Heart doi:10.1136/heartjnl-2012-303461

  • Epidemiology
  • Original article

Estimating the effect of long-term physical activity on cardiovascular disease and mortality: evidence from the Framingham Heart Study

  1. Susan M Shortreed1,2,
  2. Anna Peeters1,3,
  3. Andrew B Forbes1

+Author Affiliations


  1. 1Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia

  2. 2Biostatistics Unit, Group Health Research Institute, Seattle, Washington, USA

  3. 3Obesity and Population Health Unit, Baker IDI Heart and Diabetes Institute, Melbourne, Australia

Correspondence toDr Susan M Shortreed, Biostatistics Unit, Group Health Research Institute, 1730 Minor Avenue, Suite 1600, Seattle, WA 98101, USA; shortreed.s@ghc.org

  • Published Online First 8 March 2013

Abstract

Objective In the majority of studies, the effect of physical activity (PA) on cardiovascular disease (CVD) and mortality is estimated at a single time point. The impact of long-term PA is likely to differ. Our study objective was to estimate the effect of long-term adult-life PA compared with long-term inactivity on the risk of incident CVD, all-cause mortality and CVD-attributable mortality.

Design Observational cohort study.

Setting Framingham, MA, USA.

Patients 4729 Framingham Heart Study participants who were alive and CVD-free in 1956.

Exposures PA was measured at three visits over 30 years along with a variety of risk factors for CVD. Cumulative PA was defined as long-term active versus long-term inactive.

Main outcome measures Incident CVD, all-cause mortality and CVD-attributable mortality.

Results During 40 years of follow-up there were 2594 cases of incident CVD, 1313 CVD-attributable deaths and 3521 deaths. Compared with long-term physical inactivity, the rate ratio of long-term PA was 0.95 (95% CI 0.84 to 1.07) for CVD, 0.81 (0.71 to 0.93) for all-cause mortality and 0.83 (0.72 to 0.97) for CVD-attributable mortality. Assessment of effect modification by sex suggests greater protective effect of long-term PA on CVD incidence (p value for interaction=0.004) in men (0.79 (0.66 to 0.93)) than in women (1.15 (0.97 to 1.37)).

Conclusions

  • Cumulative long-term PA has a protective effect on incidence of all-cause and CVD-attributable mortality compared with long-term physical inactivity.
  • In men, but not women, long-term PA also appears to have a protective effect on incidence of CVD.

Summary – PENDING

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41. Nakayama Y et al. (2001) Heart Rate-Independent Vagal Effect on End-Systolic Elastance of the Canine Left Ventricle Under Various Levels of Sympathetic Tone. Circulation 104:2277–2279.

42. Cohen A (1991) A Padé approximant to the inverse Langevin function. Rheologic Acta 30:270–273.

43. Brown AM, Saum WR, Tuley FH (1976) A comparison of aortic baroreceptor discharge in normotensive and spontaneously hypertensive rats. Circ Res 39:488–496.

44. Smith H (2011) in Texts in Applied Mathematics, Texts in Applied Mathematics. (Springer New York, New York, NY), pp 119–130.

Other related articles were published on this Open Access Online Scientific Journal including the following:

Pearlman, JD and A. Lev-Ari 5/24/2013 Imaging Biomarker for Arterial Stiffness: Pathways in Pharmacotherapy for Hypertension and Hypercholesterolemia Management

http://pharmaceuticalintelligence.com/2013/05/24/imaging-biomarker-for-arterial-stiffness-pathways-in-pharmacotherapy-for-hypertension-and-hypercholesterolemia-management/

Lev-Ari, A. 5/17/2013 Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

http://pharmaceuticalintelligence.com/2013/05/17/synthetic-biology-on-advanced-genome-interpretation-for-gene-variants-and-pathways-what-is-the-genetic-base-of-atherosclerosis-and-loss-of-arterial-elasticity-with-aging/

Bernstein, HL and A. Lev-Ari 5/15/2013 Diagnosis of Cardiovascular Disease, Treatment and Prevention: Current & Predicted Cost of Care and the Promise of Individualized Medicine Using Clinical Decision Support Systems

http://pharmaceuticalintelligence.com/2013/05/15/diagnosis-of-cardiovascular-disease-treatment-and-prevention-current-predicted-cost-of-care-and-the-promise-of-individualized-medicine-using-clinical-decision-support-systems-2/

Pearlman, JD and A. Lev-Ari 5/7/2013 On Devices and On Algorithms: Arrhythmia after Cardiac Surgery Prediction and ECG Prediction of Paroxysmal Atrial Fibrillation Onset

http://pharmaceuticalintelligence.com/2013/05/07/on-devices-and-on-algorithms-arrhythmia-after-cardiac-surgery-prediction-and-ecg-prediction-of-paroxysmal-atrial-fibrillation-onset/

Pearlman, JD and A. Lev-Ari 5/4/2013 Cardiovascular Diseases: Decision Support Systems for Disease Management Decision Making

http://pharmaceuticalintelligence.com/2013/05/04/cardiovascular-diseases-decision-support-systems-for-disease-management-decision-making/

Larry H Bernstein, MD, FACP, 12/10/2012

Genomics & Genetics of Cardiovascular DiseaseDiagnoses: A Literature Survey of AHA’s Circulation Cardiovascular Genetics, 3/2010 – 3/2013

Aviva Lev-Ari, PhD, RN and Larry H. Bernstein, MD, FACP, 3/7/2013

Mitochondrial Dysfunction and Cardiac Disorders

Curator: Larry H Bernstein, MD, FACP

Aviva Lev-Ari, PhD, RN, 4/7/2013

 

Read Full Post »

Vascular Repair: Stents and Biologically Active Implants

Author and Curator: Larry H Bernstein, MD, FACP
and
Curator: Aviva Lev-Ari, PhD, RN

This is the second article of a three part series recognizing the immense contribution of Elazer Edelman, MD, PhD, and his laboratory group at MIT to vascular biology, cardiovascular disease studies, and the bioengineering, development, and use of stenting technology for drug delivery, vascular repair, and limitation of vessel damage caused by stent placement.

The first article, published on this Open Access Online Scientific Journal
was concerned with vascular biology, and largely on both the impact of drug delivery design and placement on the endothelium of the vessel wall, and on the kinetics of drug delivery based on the location of stent placement versus intravascular injection as well as the metabolic events taking place in the arterial endothelium, intima, and muscularis.
This second article, is concerned with stents and drug delivery as it has evolved since the last decade of the 20th century based on biomaterials development and vascular biology principles to minimize inherent injury risk over this period.
The third. will be concerned with the lessons from biomaterials and stent mechanics going forward.
Heart care is in the midst of a transformation. Patients who once required heart surgery are treated with a stent, catheters for repair of valves, rhythm abnormalities, and a growing number of heart or vascular distrbances.
The catheters are threaded in through the femoral artery, and sometimes through the radial artery. The American College of Cardiology annual meeting highlights research on these devices.  The procedure allows patients to leave the hospital after a day or two post-implant, but the initial cost of the novel devices is high.  Not everyone qualifies for the treatment, and it will take a few years to compare the long term results with the benefits from surgery. But these procedures have allowed many patients treatment alternatives to surgery, and they offer an option for people who cannot be successfully managed by conservative medical therapy.

The effects of stent placement on vascular injury and the initiation of an inflammatory response

Leukocytes are recruited early and abundantly to experimentally injured vessels,

  • in direct proportion to cell proliferation and intimal growth.
Activated circulating leukocytes and Mac-1 (CD11 by CD18, aMb2) (monocytic) expression are
  • markers of restenosis risk in patients undergoing angioplasty.
Angioplastied vessels lack endothelium but have extensive fibrin(ogen) and platelet deposition.  Consequently, Mac-1-dependent adhesion to fibrin(ogen)  would be expected to
  • signal leukocyte recruitment and function, thereby
  • promote intimal growth
In this study
  • M1/70, an anti-CD11b blocking mAb, was  administered to rabbits before, and every 48 hr for 3, 6, or 14 days after iliac artery balloon denudation.
  • M1/70 was bound to isolated rabbit monocytes.

The result was

  • Mac-1-mediated dose-dependent
  • inhibition of fibrinogen binding in vitro, thereby,
  • reducing by half leukocyte recruitment at 3, 6, and 14 days after injury.
Neointimal growth 14 days after injury was markedly attenuated by treatment with M1/70 –
intimal area after balloon injury, 0.12+0.09 mm2, compared with
  •  0.32+0.08 mm2 in vehicle treated controls, P<0.01, and
  •  0.38+0.08mm2 in IgG-treated controls, P<0.005;
intimal area after stent injury, 0.56+0.16 mm2, compared with
  •  0.84+ 0.13 mm2 in vehicle-treated controls, P <0.05, and
  •  0.90+0.15 mm2 in IgG-treated controls, P <0.02).
Mac-1 blockade reduces experimental neointimal thickening. These findings suggest that
  • leukocyte recruitment to and
  • infiltration of injured arteries

may be a valid target for preventing intimal hyperplasia. (1) Emerging data indicate that the inflammatory response after mechanical arterial injury

  • correlates with the severity of neointimal hyperplasia in animal models
  • and post angioplasty restenosis in humans.
The present study was designed to examine whether a nonspecific
  • stimulation of the innate immune system,
  • induced in close temporal proximity to the vascular injury,
  • would modulate the results of the procedure.
A LPS dose was chosen to be sufficient to induce systemic inflammation but not septic shock. Key markers of inflammation increased after LPS administration were:
  • serum interleukin-1 levels, and
  • monocytic stimulation (CD14 levels on monocytes)
Arterial macrophage infiltration at 7 days after injury was
  • 1.7+1.2% of total cells in controls and
  • 4.2+1.8% in LPS-treated rabbits (n=4, P<0.05).
The injured arteries 4 weeks after injury had significantly increased
  • luminal stenosis:   38+4.2% versus 23+2.6%, mean+SEM; n=8, P<0.05; and
  • neointima-to-media ratio:  1.26+0.21 versus 0.66+0.09, P<0.05 in LPS-treated animals compared with controls.
This effect was abolished by anti-CD14 Ab administration. Serum Il-1 levels and monocyte CD14 expression were significantly increased
  • in correlation with the severity of intimal hyperplasia.
  • LPS treatment increased neointimal area after stenting
    • from 0.57+0.07 to 0.77+0.1 mm2, and
  • stenosis from 9+1% to 13+1.7% (n=5, P<0.05).
Nonspecific systemic stimulation of the innate immune system
  • concurrently with arterial vascular injury
  • facilitates neointimal formation, and conditions associated with
  • increased inflammation may increase restenosis.(2)
Millions of patients worldwide have received drug-eluting stents
  • to reduce their risk for in-stent restenosis.
The efficacy and toxicity of these local therapeutics depend upon
  • arterial drug deposition,
  • distribution, and
  • retention.
To examine how administered dose and drug release kinetics control arterial drug uptake, a model was created using principles of
  • computational fluid dynamics and
  • transient drug diffusion–convection.
The modeling predictions for drug elution were validated using
  • empiric data from stented porcine coronary arteries.
Inefficient, minimal arterial drug deposition was predicted when a bolus of drug was released and depleted within seconds.
Month-long stent-based drug release
  • efficiently delivered nearly continuous drug levels, but
  • the slow rate of drug presentation limited arterial drug uptake.
Uptake was only maximized when
  • the rates of drug release and absorption matched,
  • which occurred for hour-long drug release.
Of the two possible means for increasing the amount of drug on the stent,
  • modulation of drug concentration potently impacts
  • the magnitude of arterial drug deposition,
  • while changes in coating drug mass affect duration of release.
We demonstrate the importance of drug release kinetics and administered drug dose
  • in governing arterial drug uptake and suggest
  • novel drug delivery strategies for controlling spatio-temporal arterial drug distribution.(3)
Arterial drug concentrations determine local toxicity. Therefore, the emergent safety concerns surrounding drug-eluting stents mandate an investigation of the factors contributing to fluctuations in arterial drug uptake.
  • Drug-eluting stents were implanted into porcine coronary arteries, arterial drug uptake was followed and modeled using 2-dimensional computational drug transport.
Arterial drug uptake in vivo occurred faster than predicted by free drug diffusion, thus
  • an alternate, mechanism for rapid transport has been proposed involving carrier-mediated transport.
Though there was minimal variation in vivo in release kinetics from stent to stent,
  • arterial drug deposition varied by up to 114% two weeks after stent implantation.
  • extent of adherent mural thrombus fluctuated by 113% within 3 days.
The computational drug transport model predicted that focal and diffuse thrombi
  • elevate arterial drug deposition in proportion to the thrombus size
  • by reducing drug washout subsequently increasing local drug availability.
Variable peristrut thrombus can explain fluctuations in arterial drug uptake even in the face of a narrow range of drug release from the stent. The mural thrombus effects on arterial drug deposition may be circumvented by forcing slow rate limiting arterial transport, that cannot be further hindered by mural thrombus. (4)
1.  A mAb to the b2-leukocyte integrin Mac-1 (CD11byCD18) Reduces Intimal Thickening after Angioplasty or Stent Implantation in Rabbits. C Rogers, ER Edelman, and DI Simon. PNAS Aug 1998; 95: 10134–10139.
2.  Formation After Balloon and Stent Injury in Rabbits Systemic Inflammation Induced by Lipopolysaccharide increases Neointimal Formation After Balloon and Stent Injury in Rabbits. HD Danenberg, FGP Welt, M Walker, III, P Seifert, et al. Circulation 2002;105;2917-2922; http://dx.doi.org/10.1161/01.CIR.0000018168.15904.BB
3.  Intravascular drug release kinetics dictate arterial drug deposition, retention, and distribution.
B Balakrishnan, JF Dooley, G Kopia, ER Edelman. J Controlled Release  2007;123:100–108.
http://dx. doi.org/10.1016/j.jconrel.2007.06.025.
4.  Thrombus causes fluctuations in arterial drug delivery from intravascular stents. B Balakrishnan, J Dooley, G Kopia, ER Edelman. J Control Release 2008. http://dx.doi.org/10.1016/j.jconrel.2008.07.027

Perivascular Graft Repair

Heparin remains the gold-standard inhibitor of the processes involved in the vascular response to injury. Though this compound has profound and wide-reaching effects on vascular cells, its clinical utility is unclear. It is clear that the mode of heparin delivery is critical to its potential and it may well be that
  • routine forms of administration are insufficient
  • to observe benefit given the heparin’s short half-life and complex pharmacokinetics.
When ingested orally, heparin is degraded to inactive oligomer fragments while systemic administration
  • is complicated by the need for continuous infusion
  • and the potential for uncontrolled hemorrhage.
Thus alternative heparin delivery systems have been proposed to maximize regional effects while limiting systemic toxicity. Yet, as heparin is such a potent antithrombotic compound and since existing local delivery systems lack the ability to
  • precisely regulate release kinetics,
  • even site-specific therapy is prone to bleeding.
Authors now describe the design and development of a novel biodegradable system for the perivascular delivery of heparin to the blood vessel wall with well-defined release kinetics.
This system consists of heparin-encapsulated
  • poly(DL lactide-co-glycolide) (pLGA) microspheres sequestered in an alginate gel.
Controlled release of heparin from this heterogeneous system is obtained for a period of 25 days.
The experimental variables affecting heparin release from these matrices were investigated by
  • gel permeation chromatography (GPC) and scanning electron microscopy (SEM)
  • to monitor the degradation process and correlated well with the release kinetics.
Heparin-releasing gels inhibited growth in tissue culture of
  • bovine vascular smooth muscle cells in a dose-dependent manner.
  • and also controlled vascular injury in denuding and
  • interposition vascular graft animal models of disease even when uncontrolled bleeding was evident with standard matrix-type release.
This system provided an effective means of examining
  • the effects of various compounds in
  • the control of smooth muscle cell proliferation in accelerated arteriopathies and also
  • shed light on the biologic nature of these processes.(1)
Soft tissue adhesives are employed to repair and seal many different organs that range in both
  • tissue surface chemistry and
  • mechanical effects during organ function.
This complexity motivates the development of tunable adhesive materials with
  • high resistance to uniaxial or multiaxial loads
  • dictated by a specific organ environment.
Co-polymeric hydrogels comprising
  • aminated star polyethylene glycol and
  • dextran aldehyde (PEG:dextran)
are materials exhibiting physico-chemical properties that can be modified
Here we report that resistance to failure
  • under specific loading conditions, as well as
  • tissue response at the adhesive material–tissue interface, can be modulated through regulation of
  • the number and density of adhesive aldehyde groups.
Author found that atomic force microscopy (AFM) can
  • characterize the material aldehyde density available for tissue interaction,
  • facilitating rapid, informed material choice.

Further, the correlation between AFM quantification of nanoscale unbinding forces

  • with macroscale measurements of adhesion strength
  • by uniaxial tension or multiaxial burst pressure allows the design of materials with specific cohesion and adhesion strengths.
However, failure strength alone does not predict optimal in vivo reactivity. The development of adhesive materials is significantly enabled when
  • experiments are integrated along length scales to consider
  • organ chemistry and mechanical loading states concurrently
  • with adhesive material properties and tissue response. (2)
Cell culture and animal data support the role of endothelial cells and endothelial-based compounds in regulating vascular repair after injury.
Authors describe a long-term study in pigs in which the biological and immunological
  • responses to endothelial cell implants were investigated 3 months after angioplasty,
  • approximately 2 months after the implants have degraded.
Confluent porcine or bovine endothelial cells grown in polymer matrices were implanted adjacent to 28 injured porcine carotid arteries.
Porcine and bovine endothelial cell implants significantly
  • reduced experimental restenosis compared to control by 56 and 31%, respectively.
Host humoral responses were investigated by detection of an increase in serum antibodies that bind to the bovine or porcine cell strains used for implantation.
A significant increase in titer of circulating antibodies to the bovine cells was observed
  • after 4 days in all animals implanted with xenogeneic cells.
Detected antibodies returned to presurgery levels after Day 40.
No significant increase in titer of antibodies to the porcine cells was observed during the experiment in animals implanted with porcine endothelial cells.
No implanted cells, Gelfoam, or focal inflammatory reaction could be detected
  • histologically at any of the implant sites at 90 days.

Suggesting that tissue engineered endothelial cell implants

  • may provide long term control of vascular repair after injury,
  • rather than simply delaying lesion formation and that
  • allogeneic implants are able to provide a greater benefit than xenogeneic implants. (3)
Vascular access complications are a major problem in hemodialysis patients. Native arteriovenous fistulae, historically the preferred mode of access, have a patency rate of only 60% at 1 year.
The most common mode of failure is due to progressive stenosis at the anastomotic site.
Authors have previously demonstrated that perivascular endothelial cell implants
  • inhibit intimal thickening following acute balloon injury in pigs, and now seek to determine if these
  • implants provide a similar benefit in the chronic and more complex injury model of arteriovenous anastomoses.
Side-to-side femoral artery-femoral vein anastomoses were created in 24 domestic swine.
  • toxicological,
  • biological and
  • immunological responses

were investigated 3 days and 1 and 2 months postoperatively to allogeneic endothelial cell implants . The anastomoses were wrapped with polymer matrices containing

  • confluent porcine aortic endothelial cells (PAE; n = 14) or
  • control matrices without cells (n = 10).
PAE implants significantly reduced intimal hyperplasia at the anastomotic sites
  • compared to controls by 68% (p ! 0.05) at 2 months.
The beneficial effects of the PAE implants were not due to
  • differences in the rates of reendothelialization between the groups.
No significant immunological response to the allogeneic endothelial cells that impacted on efficacy was detected in any of the pigs.
No apparent toxicity was observed in any of the animals treated with endothelial implants.
These data suggest that perivascular endothelial cell implants
  • are safe and reduce early intimal hyperplasia in a porcine model of arteriovenous anastomoses. (4)
1.  Perivascular graft heparin delivery using biodegradable polymer wraps. ER Edelman, A Nathan,
M Katada, J Gates, MJ Karnovsky. Biomaterials 2000; 21:2279 -2286.
onlinelibrary.wiley.com/doi/10.1002/anie.200461360/full
2.  Tuning adhesion failure strength for tissue-specific applications. N Artzi, A Zeiger, F Boehning,
A bon Ramos, K Van Vliet, ER Edelman.  Acta Biomateriala 2010.
http://dx.doi.org/10.1016/j.actbio.2010.07.008.
3. Endothelial Implants Provide Long-Term Control of Vascular Repair in a Porcine Model of Arterial Injury. HM Nugent, ER Edelman. J Surg Res 2001; 99:228–234.  http://dx.doi.org/10.1006/jsre.2001.6198
4.  Perivascular Endothelial Implants Inhibit Intimal Hyperplasia in a Model of Arteriovenous Fistulae: A Safety and Efficacy Study in the Pig. HM Nugent, A Groothuis, P Seifert, et al. J Vasc Res 2002;39:524–533.

Luminal Flow and Arterial Drug Delivery

Endovascular stents reside in a dynamic flow environment and yet the impact of flow
  • on arterial drug deposition after stent-based delivery is only now emerging.
Authors employed computational fluid dynamic modeling tools to investigate
  • the influence of luminal flow patterns on arterial drug deposition and distribution.
Flow imposes recirculation zones distal and proximal to the stent strut that extend
  • the coverage of tissue absorption of eluted drug and
  • induce asymmetry in tissue drug distribution.
Our analysis now explains how the disparity in
  • sizes of the two recirculation zones and
  • the asymmetry in drug distribution are determined by a complex interplay of local flow and strut geometry.
When temporal periodicity was introduced as a model of
  • pulsatile flow,
  • the net luminal flow served as an index of flow-mediated spatiotemporal tissue drug uptake.
Dynamically changing luminal flow patterns are intrinsic to the coronary arterial tree. Coronary drug-eluting stents should be appropriately considered where
  • luminal flow,
  • strut design and
  • pulsatility
have direct effects on tissue drug uptake after local delivery.(1)
The efficacy of drug-eluting stents (DES) requires delivery of potent compounds directly to the underlying arterial tissue.
The commercially available DES drugs rapamycin and paclitaxel bind specifically to
  • their respective therapeutic targets, FKBP12 and polymerized microtubules,
  • while also associating in a more general manner with other tissue elements.
As it is binding that provides biological effect, the question arises as to whether other
  • locally released or systemically circulating drugs can
  • displace DES drugs from their tissue binding domains.
Specific and general binding sites for both drugs are distributed across the media and adventitia with higher specific binding associated with the binding site densities in the media.
The ability of rapamycin and paclitaxel to compete for specific protein binding and general tissue deposition
  • was assessed for both compounds simultaneously and
  • in the presence of other commonly administered cardiac drugs.
Drugs classically used to treat standard cardiovascular diseases, such as hypertension and hypercoaguability,
  • displace rapamycin and paclitaxel from general binding sites, possibly
  • decreasing tissue reserve capacity for locally delivered drugs.
Paclitaxel and rapamycin do not affect the other’s binding
  • to their biologically relevant specific protein targets, but
  • can  displace each other from tissue at three log order molar excess,
  • decreasing arterial loads by greater than 50%.
Local competitive binding therefore should not limit the placement of rapamycin and paclitaxel eluting stents in close proximity.(2)
Stent thrombosis is a lethal complication of endovascular intervention. There is concern about the inherent risk associated with specific stent designs and drug-eluting coatings
Authored examined whether drug-eluting coatings are inherently thrombogenic and whether the response to these materials was determined to any degree
  • by stent design and
  • stent deployment with custom-built stents.
Drug/polymer coatings uniformly reduce rather than increase thrombogenicity relative to matched bare metal counterparts (0.65-fold; P 0.011).
Thick-strutted (162 m) stents were 1.5-fold more thrombogenic than otherwise
  • identical thin-strutted (81 m) devices in ex vivo flow loops (P< 0.001),
commensurate with 1.6-fold greater thrombus coverage
  • 3 days after implantation in porcine coronary arteries (P 0.004).
When bare metal stents were deployed in
  • malapposed or overlapping configurations, thrombogenicity increased compared with apposed, length-matched controls (1.58-fold, P < 0.001; and 2.32-fold, P <0.001).
The thrombogenicity of polymer-coated stents with thin struts was
  • lowest in all configurations and remained insensitive to incomplete deployment.
Computational modeling– based
  • predictions of stent-induced flow derangements
  • correlated with spatial distribution of formed clots.
Drug/polymer coatings do not inherently increase acute stent clotting;
  • they reduce thrombosis.
However, strut dimensions and positioning relative to the vessel wall
  • are critical factors in modulating stent thrombogenicity.
Optimal stent geometries and surfaces, as demonstrated with thin stent struts,
  • help reduce the potential for thrombosis
  • despite complex stent configurations and variability in deployment. (Circulation. 2011;123:1400-1409.) (3)
1. Luminal flow patterns dictate arterial drug deposition in stent-based delivery.
VB Kolachalama, AR Tzafriri, DY Arifin, ER Edelman. J Control Release 2009; 133:24–30.
2. Local and systemic drug competition in drug-eluting stent tissue deposition properties.
AD Levin, M Jonas, Chao-Wei Hwang, ER Edelman.  J Control Release 2005; 109:236-243.
3. Stent Thrombogenicity Early in High-Risk Interventional Settings Is Driven by
Stent Design and Deployment and Protected by Polymer-Drug Coatings
Kumaran Kolandaivelu, Rajesh Swaminathan, William J. Gibson,.. ER Edelman

Management of Obstructive Coronary Artery Disease

Multiple studies have shown that diabetes mellitus (DM) can affect the
  • efficacy of revascularization therapies and subsequent clinical outcomes.
Selecting the appropriate myocardial revascularization strategy is critically important
  • in the setting of multivessel coronary disease.
Optimal medical therapy is an appropriate first-line strategy in patients with DM and mild symptoms. When medical therapy does not adequately control symptoms,
  • revascularization with either PCI or CABG may be used.
In patients with treated DM, moderate to severe symptoms and complex multivessel coronary disease,
  • coronary artery bypass graft surgery provides better survival,
  • fewer recurrent infarctions and
  • greater freedom from re-intervention.
Decisions regarding revascularization in patients with DM must take into account multiple factors and as such require a multidisciplinary team approach (‘heart team’). (1)
An incomplete understanding of the transport forces and local tissue structures
  • that modulate drug distribution has hampered
  • local pharmacotherapies in many organ systems.
These issues are especially relevant to arteries, where stent-based delivery allows fine control of locally directed drug release.
Local delivery produces tremendous drug concentration gradients
  • these are in part derived from transport forces,
  • differences in deposition from tissue to tissue

This suggests that tissue ultrastructure also plays an important role.

Authors measured the equilibrium drug uptake and the penetration and diffusivity of
  • dextrans (a model hydrophilic drug similar to heparin) and albumin
  • in orthogonal planes in arteries explanted from different vascular beds.
Authors found significant variations in drug distribution with
  • geometric orientation and
  • arterial connective tissue content.
Drug diffusivities parallel to the connective tissue sheaths were
  • one to two orders of magnitude greater than across these sheaths.
This diffusivity difference remained relatively constant for drugs up to 70 kDa
  • before decreasing for larger drugs.
Drugs also distributed better into elastic arteries, especially at lower molecular weights,
  • with almost 66% greater transfer into the thoracic aorta
  • than into the carotid artery.
Arterial drug transport is thus highly anisotropic and
  • dependent on arterial tissue content.
The role of the local composition and geometric organization of arterial tissue
  • in influencing vascular pharmacokinetics
is likely to become a critical consideration for local vascular drug delivery (2)
Radiolabeled drug-eluting stents have been proposed
  • to potentially reduce restenosis in coronary arteries.
A P-32 labeled oligonucleotide (ODN) loaded on a polymer coated stent
  • is slowly released in the arterial wall to deliver a therapeutic dose to the target tissue.
A relatively low proportion of drugs is transferred to the arterial wall (< 2%– 5% typically). This raises questions about the degree to which radiolabeled drugs eluted from the stent
  • can contribute to the total radiation dose delivered to tissues.
A three-dimensional diffusion-convection transport model is used
  • to model the transport of a hydrophilic drug released
  • from the surface of a stent to the arterial media.
Large drug concentration gradients are observed
  • near the stent struts giving rise to a
  • non-uniform radiation activity distribution for the drug
  • in the tissues as a function of time.
A voxel-based kernel convolution method is used to calculate the radiation dose rate
  • resulting from this activity build-up in the arterial wall
  • based on the medical internal radiation dose formalism.
Measured residence time for the P-32 ODN in the arterial wall and
  • at the stent surface obtained from animal studies
  • are used to normalize the results in terms of absolute dose to tissue.
The results indicate radiation due to drug eluted from the stent
  • contributes only a small fraction of the total radiation delivered to the arterial wall,
  • the main contribution comes from the activity embedded in the stent coating.
For hydrophilic compounds with rapid transit times in arterial tissue and minimal binding interactions,
  • the activity build-up in the arterial wall contributes only a small fraction
  • to the total dose delivered by the P-32 ODN stent.
For these compounds, it is concluded that radiolabeled drug-eluting stent
  • would not improve the performance of radioactive stents in treating restenosis.
Also, variability in the efficacy of drug delivery devices
  • makes accurate dosimetry difficult and
  • the drug washout in the systemic circulatory system
may yield an unnecessary activity build-up and dose to healthy organs. (3)
The first compounds considered for stent-based delivery,
  • such as heparin have failed to stop restenosis clinically.
More recent compounds, such as paclitaxel, are of a different sort.
They are hydrophobic, and their effects after local release seem far more profound.
This dichotomy raises the question of whether drugs that have an effect when released from a stent do so because of
  • differences in biology or differences in physicochemical properties and targeting.
Authored applied continuum pharmacokinetics to examine the effects of
  • transport forces and device geometry on
the distribution of stent-delivered hydrophilic and hydrophobic drugs.
Stent-based delivery leads to large concentration gradients.
Drug concentrations range from nil to several times the
  • mean tissue concentration over a few micrometers.
Concentration variations were a function of the Peclet number (Pe),
  • the ratio of convective to diffusive forces.
Although hydrophobic drugs exhibit greater variability than hydrophilic drugs,
  • they achieve higher mean concentrations and
  • they remain closer to the intima.
Inhomogeneous strut placement influences hydrophilic drugs
  • more negatively than hydrophobic drugs, and notably
  • affect local concentrations without changing mean concentrations.
Local concentrations and gradients are inextricably linked to biological effect. Therefore,
  • these results provide a potential explanation for the variable success of stent-based delivery.
Authors conclude that mere proximity of delivery devices to tissues
  • does not ensure adequate targeting,
  • because physiological transport forces cause
  • local concentrations to deviate significantly from mean concentrations. (4)
1.  Role of CABG in the management of obstructive coronary arterial disease in patients with diabetes mellitus. D Aronson, ER Edelman.  Curr Opin Pharmacol 2012, 12:134–141. Issue on Cardiovascular and renal. [Eds: JY Jeremy, K Zacharowski, N Shukla, S Wan].  http://dx.doi.org/10.1016/j.coph.2012.01.011
2.  Arterial Ultrastructure Influences Transport of Locally Delivered Drugs. Chao-Wei Hwang, ER Edelman. Circ Res. 2002; 90:826-832. http://www.circresaha.org/dx.doi.org/10.1161/01.RES.0000016672.26000.9E
3.  Dose model for stent-based delivery of a radioactive compound for the treatment of restenosis in coronary arteries. C Janickia, Chao-Wei Hwang, ER Edelman.  Med Phys 2003; 30(10), 2622-7.    http://dx.doi.org/10.1118/1.1607506
4.  Physiological Transport Forces Govern Drug Distribution for Stent-Based Delivery. Chao-Wei Hwang, D Wu, ER Edelman. Circulation. 2001;104(5) :600-605; e14 – e9010.     http://dx.doi.org/10.1161/hc3101.09221
Stent-Versus-Stent Equivalency Trials. Are Some Stents More Equal Than Others? Elazer R. Edelman, Campbell Rogers Circulation. 1999; 100(9): 896-898; e47 – e47.  http://dx.doi.org/10.1161/01.CIR.100.9.896
New endovascular stent designs are displacing tried and-true devices for use in an ever-broader array of lesions. There is disagreement as to which device is most advantageous and whether design determines outcome. Preclinical research says that this should be the case. Clinical trials have failed to validate design dependence. Can the divergent results be reconciled? More than 50 different stent configurations are available. The processes of industrial development and federal regulatory evaluation support the importance of design.
Stents are made from
  • a spectrum of materials
  • a range of manufacturing techniques, and have
    • variable surfaces,
    • dimensions,
    • surface coverage, and
    • strut configurations.
The number of parameters involved may doom the number of subsets to approach the number of designs. Moreover, each device seems to have a unique optimal mode of placement.  Differences have been reported in
  • flexibility,
  • tracking ability,
  • expansion,
  • radiovisibility,
  • side-branch access, and
  • resistance to compression and recoil for different devices.
Regulatory approval includes standards for safety:
  • toxicity,
  • biocompatibility,
  • structural and material analysis, and
  • fatigue testing
It has been suggested that
  • hoop strength,
  • surface cracking,
  • uniformity of expansion, and
  • other features become standardized as well.
Four different direct comparisons of first-generation Palmaz-Schatz slotted-tube stents and
second-generation stents have been made. In several studies there were no significant differences
in restenosis at follow-up, including
  • minimal luminal diameter (MLD),
  • percent diameter stenosis,
  • late loss, or
  •  binary restenosis rate.
In the fourth study, restenosis was far greater for the Gianturco-Roubin II (GR-II) stent (Cook) than
  • the Palmaz-Schatz stent (Cordis-Johnson & Johnson).
The data for all stents bunch across trials: with the exception of the GR-II stent,
variability between the test stent groups was no greater than
  • the variability between the Palmaz-Schatz stent groups in the different trials.
Three distinct possibilities exist to explain the absence of clinical evidence that different designs behave differently:
(1) no differences in clinical outcomes exist between devices;
(2) differences exist but are so slight as to be clinically meaningless; and
(3) differences exist that may be clinically meaningful, but trials performed to date were not designed to detect them.
Schematic representation of device performance plotting outcome against indication indicates that
  • complication rates rise as lesion complexity increases.
When 2 devices are clinically different, their curves are displaced, and when they are indistinguishable, their curves overlap.
Clinical trials that restrict the test population to lesions low on the complexity scale
  • ensure safety for all patients but are not the ideal venues in which to detect differences between devices.
Thus, although stents 1 and 2 may have different clinical outcomes, in a restricted-criteria equivalency trial with low complexity, they appear identical. It is only when the test device performs worse than the standard, that differences can be appreciated.
In contrast, an open registry will not only show when a test stent is worse than the standard stent but also when it is better.

Equivalency Trials

Stent-versus-stent trials are equivalency trials, designed to show that a test device performs “as well as” a standard, currently acceptable device.  This is a valid regulatory threshold but
  • not the means to evaluate the full potential of a device.
Equivalency trials must by definition commence with a patient population for whom the standard device is safe. Trials with currently approved devices as the standard necessitate that
  • patient entry and lesion selection be determined by
  • limitations of the standard, not the device.
to observe a difference in such a trial
  •  the test device performs worse
For the test device to perform better, both the test and the standard must be challenged.
This was not the case for the trials in which
  • the average reference vessel size was 3.0+0.05 mm and
  • American College of Cardiology type B2 and C lesions accounted for only ~65% of lesions.
These lesions are those for which the Palmaz-Schatz stent is approved and technically suited, but
  • they represent only a minority of those lesions now receiving stents

Complexity, Equivalence, and Better

In truth, it may be most appropriate to think about parameters of device success and safety as a continuum, describing a correlation between events such as
  • thrombosis or restenosis and
  • a continuous measure of indication,
  • vessel dimension, or lesion complexity (Figure).
A given device may be represented by a characteristic response over a range of indications.
When there is a lateral offset to the curves,
  • differences in potential performance are anticipated.
Curves might even cross, rather than run parallel, indicating that devices might be matched
to lesions and indications. Open trials would consider the entire range of the curves.
  • equivalency trials are limited to a small region of the curve.
The first-generation stents were a major innovation in interventional cardiology, and their place in medical history and biotechnology is unassailable.
Demonstration that new stents are better than old will require that evaluations be
  • performed in lesions for which current devices have marginal or limited application.
Complex or acutely unstable lesions, small arteries, and diseased bypass grafts are
  • the next great challenges of interventional cardiology.
Perhaps in these settings, future stent trials will provide firm evidence that
  • the manner in which blood vessels are manipulated dictates biological sequelae.
Proof that stent design can alter clinical outcomes may then unleash the potential
  • to change the way in which we consider design, approval, and use of new devices.
REFERENCES

Menichelli, M. (2006). Sirolimus Stent vs. Bare Stent in Acute Myocardial Infarction Trial. Presented at The European Paris Course on Revascularization (EuroPCR), May 16-19, 2006, Paris, France Paris, France.http://www.medscape.com/viewprogram/5505?rss

Pfisterer, P.E. (2006). Basel Stent Cost-effectiveness Trial-Late Thrombotic events (BASKET LATE) Trial. Presented at American College of Cardiology 55th Annual Scientific Session, March 11 – 14, 2006, Atlanta, Georgia.http://www.medscape.com/viewprogram/5185 

Rogers, C. Edelman E.R. (2006). Pushing drug-eluting stents into uncharted territory, Simpler then you think – more complex than you imagine. Circulation,113, 2262-2265.

Shirota, T., Yasui, H., Shimokawa, H. & Matsuda, T. (2003). Fabrication of endothelial progenitor cell (EPC)-seeded intravascular stent devices and in vitro endothelialization on hybrid vascular tissue. Biomaterials 24(13), 2295–2302.

Simonton, C. (2006). The STENT Registry: A real-world look at Sirolimus- and Pacitaxel-Eluting Stents. Cath Lab Digest, 14 (1), 1-10.

Turco, M. (2006). TAXUS ATLAS Trial – 9-Month results: Evaluation of TAXUS Liberte vs. TAXUS Express. Presented at The European Paris Course on Revascularization (EuroPCR), May 16-19, 2006, Paris, France Paris, France.http://www.medscape.com/viewprogram/5505?rss

Verma, S. and Marsden, P.A. (2005). Nitric Oxide-Eluting Polyurethanes – Vascular Grafts of the Future? New England Journal Medicine, 353 (7), 730-731.

Wood, S. (2006). Guidant suspends release of Xience V everolimus-eluting stent due to manufacturing standards http://www.theheart.org/article/679851.do 

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http://pharmaceuticalintelligence.com/2013/04/03/fight-against-atherosclerotic-cardiovascular-disease-a-biologics-not-a-small-molecule-recombinant-human-lecithin-cholesterol-acyltransferase-rhlcat-attracted-astrazeneca-to-acquire-alphacore/

High-Density Lipoprotein (HDL): An Independent Predictor of Endothelial Function & Atherosclerosis, A Modulator, An Agonist, A Biomarker for Cardiovascular Risk

Aviva Lev-Ari, PhD, RN 3/31/2013

http://pharmaceuticalintelligence.com/2013/03/31/high-density-lipoprotein-hdl-an-independent-predictor-of-endothelial-function-artherosclerosis-a-modulator-an-agonist-a-biomarker-for-cardiovascular-risk/

Acute Chest Pain/ER Admission: Three Emerging Alternatives to Angiography and PCI

Aviva Lev-Ari, PhD, RN 3/10/2013

http://pharmaceuticalintelligence.com/2013/03/10/acute-chest-painer-admission-three-emerging-alternatives-to-angiography-and-pci/

Genomics & Genetics of Cardiovascular Disease Diagnoses: A Literature Survey of AHA’s Circulation Cardiovascular Genetics, 3/2010 – 3/2013

Lev-Ari, A. and L H Bernstein 3/7/2013

http://pharmaceuticalintelligence.com/2013/03/07/genomics-genetics-of-cardiovascular-disease-diagnoses-a-literature-survey-of-ahas-circulation-cardiovascular-genetics-32010-32013/

The Heart: Vasculature Protection – A Concept-based Pharmacological Therapy including THYMOSIN

Aviva Lev-Ari, PhD, RN 2/28/2013

http://pharmaceuticalintelligence.com/2013/02/28/the-heart-vasculature-protection-a-concept-based-pharmacological-therapy-including-thymosin/

Arteriogenesis and Cardiac Repair: Two Biomaterials – Injectable Thymosin beta4 and Myocardial Matrix Hydrogel

Aviva Lev-Ari, PhD, RN 2/27/2013

http://pharmaceuticalintelligence.com/2013/02/27/arteriogenesis-and-cardiac-repair-two-biomaterials-injectable-thymosin-beta4-and-myocardial-matrix-hydrogel/

Coronary artery disease in symptomatic patients referred for coronary angiography: Predicted by Serum Protein Profiles

Aviva Lev-Ari, PhD, RN 12/29/2012

http://pharmaceuticalintelligence.com/2012/12/29/coronary-artery-disease-in-symptomatic-patients-referred-for-coronary-angiography-predicted-by-serum-protein-profiles/

Special Considerations in Blood Lipoproteins, Viscosity, Assessment and Treatment

Bernstein, HL and Lev-Ari, A. 11/28/2012

http://pharmaceuticalintelligence.com/2012/11/28/special-considerations-in-blood-lipoproteins-viscosity-assessment-and-treatment/

Peroxisome proliferator-activated receptor (PPAR-gamma) Receptors Activation: PPARγ transrepression for Angiogenesis in Cardiovascular Disease and PPARγ transactivation for Treatment of Diabetes

Aviva Lev-Ari, PhD, RN 11/13/2012

http://pharmaceuticalintelligence.com/2012/11/13/peroxisome-proliferator-activated-receptor-ppar-gamma-receptors-activation-pparγ-transrepression-for-angiogenesis-in-cardiovascular-disease-and-pparγ-transactivation-for-treatment-of-dia/

Clinical Trials Results for Endothelin System: Pathophysiological role in Chronic Heart Failure, Acute Coronary Syndromes and MI – Marker of Disease Severity or Genetic Determination?

Aviva Lev-Ari, PhD, RN 10/19/2012

http://pharmaceuticalintelligence.com/2012/10/19/clinical-trials-results-for-endothelin-system-pathophysiological-role-in-chronic-heart-failure-acute-coronary-syndromes-and-mi-marker-of-disease-severity-or-genetic-determination/

Endothelin Receptors in Cardiovascular Diseases: The Role of eNOS Stimulation

Aviva Lev-Ari, PhD, RN 10/4/2012

http://pharmaceuticalintelligence.com/2012/10/04/endothelin-receptors-in-cardiovascular-diseases-the-role-of-enos-stimulation/

Inhibition of ET-1, ETA and ETA-ETB, Induction of NO production, stimulation of eNOS and Treatment Regime with PPAR-gamma agonists (TZD): cEPCs Endogenous Augmentation for Cardiovascular Risk Reduction – A Bibliography

Aviva Lev-Ari, PhD, RN 10/4/2012

http://pharmaceuticalintelligence.com/2012/10/04/inhibition-of-et-1-eta-and-eta-etb-induction-of-no-production-and-stimulation-of-enos-and-treatment-regime-with-ppar-gamma-agonists-tzd-cepcs-endogenous-augmentation-for-cardiovascular-risk-reduc/

Positioning a Therapeutic Concept for Endogenous Augmentation of cEPCs — Therapeutic Indications for Macrovascular Disease: Coronary, Cerebrovascular and Peripheral

Aviva Lev-Ari, PhD, RN 8/29/2012

http://pharmaceuticalintelligence.com/2012/08/29/positioning-a-therapeutic-concept-for-endogenous-augmentation-of-cepcs-therapeutic-indications-for-macrovascular-disease-coronary-cerebrovascular-and-peripheral/

Cardiovascular Outcomes: Function of circulating Endothelial Progenitor Cells (cEPCs): Exploring Pharmaco-therapy targeted at Endogenous Augmentation of cEPCs

Aviva Lev-Ari, PhD, RN 8/28/2012

http://pharmaceuticalintelligence.com/2012/08/28/cardiovascular-outcomes-function-of-circulating-endothelial-progenitor-cells-cepcs-exploring-pharmaco-therapy-targeted-at-endogenous-augmentation-of-cepcs/

Endothelial Dysfunction, Diminished Availability of cEPCs, Increasing CVD Risk for Macrovascular Disease – Therapeutic Potential of cEPCs

Aviva Lev-Ari, PhD, R N 8/27/2012

http://pharmaceuticalintelligence.com/2012/08/27/endothelial-dysfunction-diminished-availability-of-cepcs-increasing-cvd-risk-for-macrovascular-disease-therapeutic-potential-of-cepcs/

Vascular Medicine and Biology: CLASSIFICATION OF FAST ACTING THERAPY FOR PATIENTS AT HIGH RISK FOR MACROVASCULAR EVENTS Macrovascular Disease – Therapeutic Potential of cEPCs

Aviva Lev-Ari, PhD, RN 8/24/2012

http://pharmaceuticalintelligence.com/2012/08/24/vascular-medicine-and-biology-classification-of-fast-acting-therapy-for-patients-at-high-risk-for-macrovascular-events-macrovascular-disease-therapeutic-potential-of-cepcs/

Cardiovascular Disease (CVD) and the Role of agent alternatives in endothelial Nitric Oxide Synthase (eNOS) Activation and Nitric Oxide Production

Aviva Lev-Ari, PhD, RN 7/19/2012

http://pharmaceuticalintelligence.com/2012/07/19/cardiovascular-disease-cvd-and-the-role-of-agent-alternatives-in-endothelial-nitric-oxide-synthase-enos-activation-and-nitric-oxide-production/

Resident-cell-based Therapy in Human Ischaemic Heart Disease: Evolution in the PROMISE of Thymosin beta4 for Cardiac Repair

Aviva Lev-Ari, PhD, RN 4/30/2012

http://pharmaceuticalintelligence.com/2012/04/30/93/

Triple Antihypertensive Combination Therapy Significantly Lowers Blood Pressure in Hard-to-Treat Patients with Hypertension and Diabetes

Aviva Lev-Ari, PhD, RN 5/29/2012

http://pharmaceuticalintelligence.com/2012/05/29/445/

Macrovascular Disease – Therapeutic Potential of cEPCs: Reduction Methods for CV Risk

Aviva Lev-Ari, PhD, RN 7/2/2012

http://pharmaceuticalintelligence.com/2012/07/02/macrovascular-disease-therapeutic-potential-of-cepcs-reduction-methods-for-cv-risk/

Mitochondria Dysfunction and Cardiovascular Disease – Mitochondria: More than just the “powerhouse of the cell”

Aviva Lev-Ari, PhD, RN 7/9/2012

http://pharmaceuticalintelligence.com/2012/07/09/mitochondria-more-than-just-the-powerhouse-of-the-cell/

Bystolic’s generic Nebivolol – positive effect on circulating Endothelial Proginetor Cells endogenous augmentation

Aviva Lev-Ari, PhD, RN 7/16/2012

http://pharmaceuticalintelligence.com/2012/07/16/bystolics-generic-nebivolol-positive-effect-on-circulating-endothilial-progrnetor-cells-endogenous-augmentation/

Arteriogenesis and Cardiac Repair: Two Biomaterials – Injectable Thymosin beta4 and Myocardial Matrix Hydrogel

Aviva Lev-Ari, PhD, RN 2/27/2013

http://pharmaceuticalintelligence.com/2013/02/27/arteriogenesis-and-cardiac-repair-two-biomaterials-injectable-thymosin-beta4-and-myocardial-matrix-hydrogel/

Cardiac Surgery Theatre in China vs. in the US: Cardiac Repair Procedures, Medical Devices in Use, Technology in Hospitals, Surgeons’ Training and Cardiac Disease Severity”

Aviva Lev-Ari, PhD, RN 1/8/2013

http://pharmaceuticalintelligence.com/2013/01/08/cardiac-surgery-theatre-in-china-vs-in-the-us-cardiac-repair-procedures-medical-devices-in-use-technology-in-hospitals-surgeons-training-and-cardiac-disease-severity/

Heart Remodeling by Design – Implantable Synchronized Cardiac Assist Device: Abiomed’s Symphony

Aviva Lev-Ari, PhD, RN 7/23/2012

http://pharmaceuticalintelligence.com/2012/07/23/heart-remodeling-by-design-implantable-synchronized-cardiac-assist-device-abiomeds-symphony/

Acute Chest Pain/ER Admission: Three Emerging Alternatives to Angiography and PCI

Aviva Lev-Ari, PhD, RN 3/10/2013

http://pharmaceuticalintelligence.com/2013/03/10/acute-chest-painer-admission-three-emerging-alternatives-to-angiography-and-pci/

Dilated Cardiomyopathy: Decisions on implantable cardioverter-defibrillators (ICDs) using left ventricular ejection fraction (LVEF) and Midwall Fibrosis: Decisions on Replacement using late gadolinium enhancement cardiovascular MR (LGE-CMR)

Aviva Lev-Ari, PhD, RN 3/10/2013
http://pharmaceuticalintelligence.com/2013/03/10/dilated-cardiomyopathy-decisions-on-implantable-cardioverter-defibrillators-icds-using-left-ventricular-ejection-fraction-lvef-and-midwall-fibrosis-decisions-on-replacement-using-late-gadolinium/

The Heart: Vasculature Protection – A Concept-based Pharmacological Therapy including THYMOSIN

Aviva Lev-Ari, PhD, RN 2/28/2013
http://pharmaceuticalintelligence.com/2013/02/28/the-heart-vasculature-protection-a-concept-based-pharmacological-therapy-including-thymosin/

FDA Pending 510(k) for The Latest Cardiovascular Imaging Technology

Aviva Lev-Ari, PhD, RN 1/28/2013
http://pharmaceuticalintelligence.com/2013/01/28/fda-pending-510k-for-the-latest-cardiovascular-imaging-technology/

PCI Outcomes, Increased Ischemic Risk associated with Elevated Plasma Fibrinogen not Platelet Reactivity

Aviva Lev-Ari, PhD, RN 1/10/2013
http://pharmaceuticalintelligence.com/2013/01/10/pci-outcomes-increased-ischemic-risk-associated-with-elevated-plasma-fibrinogen-not-platelet-reactivity/

The ACUITY-PCI score: Will it Replace Four Established Risk Scores — TIMI, GRACE, SYNTAX, and Clinical SYNTAX

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2013/01/03/the-acuity-pci-score-will-it-replace-four-established-risk-scores-timi-grace-syntax-and-clinical-syntax/

Coronary artery disease in symptomatic patients referred for coronary angiography: Predicted by Serum Protein Profiles

Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2012/12/29/coronary-artery-disease-in-symptomatic-patients-referred-for-coronary-angiography-predicted-by-serum-protein-profiles/

Heart Renewal by pre-existing Cardiomyocytes: Source of New Heart Cell Growth Discovered

Aviva Lev-Ari, PhD, RN 12/23/2012
http://pharmaceuticalintelligence.com/2012/12/23/heart-renewal-by-pre-existing-cardiomyocytes-source-of-new-heart-cell-growth-discovered/

Cardiovascular Risk Inflammatory Marker: Risk Assessment for Coronary Heart Disease and Ischemic Stroke – Atherosclerosis.

Aviva Lev-Ari, PhD, RN 10/30/2012
http://pharmaceuticalintelligence.com/2012/10/30/cardiovascular-risk-inflammatory-marker-risk-assessment-for-coronary-heart-disease-and-ischemic-stroke-atherosclerosis/

To Stent or Not? A Critical Decision

Aviva Lev-Ari, PhD, RN 10/23/2012
http://pharmaceuticalintelligence.com/2012/10/23/to-stent-or-not-a-critical-decision/

New Definition of MI Unveiled, Fractional Flow Reserve (FFR)CT for Tagging Ischemia

Aviva Lev-Ari, PhD, RN 8/27/2012
http://pharmaceuticalintelligence.com/2012/08/27/new-definition-of-mi-unveiled-fractional-flow-reserve-ffrct-for-tagging-ischemia/

Ethical Considerations in Studying Drug Safety — The Institute of Medicine Report

Aviva Lev-Ari, PhD, RN 8/23/2012
http://pharmaceuticalintelligence.com/2012/08/23/ethical-considerations-in-studying-drug-safety-the-institute-of-medicine-report/

New Drug-Eluting Stent Works Well in STEMI

Aviva Lev-Ari, PhD, RN 8/22/2012
http://pharmaceuticalintelligence.com/2012/08/22/new-drug-eluting-stent-works-well-in-stemi/

Expected New Trends in Cardiology and Cardiovascular Medical Devices

Aviva Lev-Ari, PhD, RN 8/17/2012
http://pharmaceuticalintelligence.com/2012/08/17/expected-new-trends-in-cardiology-and-cardiovascular-medical-devices/

Coronary Artery Disease – Medical Devices Solutions: From First-In-Man Stent Implantation, via Medical Ethical Dilemmas to Drug Eluting Stents

Aviva Lev-Ari, PhD, RN 8/13/2012

http://pharmaceuticalintelligence.com/2012/08/13/coronary-artery-disease-medical-devices-solutions-from-first-in-man-stent-implantation-via-medical-ethical-dilemmas-to-drug-eluting-stents/

Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

Aviva Lev-Ari, PhD, RN 7/18/2012

http://pharmaceuticalintelligence.com/2012/07/18/percutaneous-endocardial-ablation-of-scar-related-ventricular-tachycardia/

Competition in the Ecosystem of Medical Devices in Cardiac and Vascular Repair: Heart Valves, Stents, Catheterization Tools and Kits for Open Heart and Minimally Invasive Surgery (MIS)

Aviva Lev-Ari, PhD, RN 6/22/2012

http://pharmaceuticalintelligence.com/2012/06/22/competition-in-the-ecosystem-of-medical-devices-in-cardiac-and-vascular-repair-heart-valves-stents-catheterization-tools-and-kits-for-open-heart-and-minimally-invasive-surgery-mis/

Global Supplier Strategy for Market Penetration & Partnership Options (Niche Suppliers vs. National Leaders) in the Massachusetts Cardiology & Vascular Surgery Tools and Devices Market for Cardiac Operating Rooms and Angioplasty Suites

Aviva Lev-Ari, PhD, RN 6/22/2012

http://pharmaceuticalintelligence.com/2012/06/22/global-supplier-strategy-for-market-penetration-partnership-options-niche-suppliers-vs-national-leaders-in-the-massachusetts-cardiology-vascular-surgery-tools-and-devices-market-for-car/

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Texas Heart Institute: 50 Years of Accomplishments

Reporter: Aviva Lev-Ari, PhD, RN

 

Texas Heart Institute’s Overachieving President and Medical Director Dr. James T Willerson Profiles THI’s 50 Years Of Accomplishments


Posted Thursday , April 25,2013

The Texas Heart Institute is a not-for-profit cardiology and heart surgery center located at the Texas Medical Center in Houston. Founded in 1962 by Dr. Denton A. Cooley, the mission of the Texas Heart Institute has been to reduce the devastating toll of cardiovascular disease through innovative programs in research, education and improved patient care. Over the past 51 years the Institute has been involved in training cardiologists, heart surgeons, imaging specialists in cardiovascular medicine and cardiac electrophysiology, and pathologists, and educated hundreds of cardiovascular specialists.

texasheart

A nonprofit organization in the truest sense, and unlike most institutions that have a source of operating revenue, the Texas Heart Institute relies solely on government grants, research contracts and, above all, philanthropy, with donations from grateful patients, foundations, corporations, physicians, and the general public account for more than half of the Institute’s annual operating budget. The Institute’s location in and affiliations with St. Luke’s Episcopal Hospital and Texas Children’s Hospital have assured that all age groups will be treated, and has freed the Institute of the burden of financing a health care facility.

The Texas Heart Institute (THI) and its clinical partner, St. Luke’s Episcopal Hospital, have become one of America’s largest cardiovascular centers, whose 160-member professional staff have reportedly performed more than 100,000 open heart operations, 200,000 cardiac catheterizations, and 1,000 heart transplants.

In its 2010 annual survey of “America’s Best Hospitals,” U.S. News & World Report ranked the Texas Heart Institute at St. Luke’s Episcopal Hospital number four in the United States for heart care, marking this its 20th consecutive year of inclusion as one of the top 10 heart centers in the country.

willersonIn an interview with the European science news journal Research Media, THI President and Medical Director, Dr. James T Willerson, says that when he originally came to the Institute in 2004, then still President Dr Cooley wanted him to be Medical Director of Cardiovascular Research, and upon Dr. Cooley’s resignation in 2008, he asked Dr. Willerston to succeed him in that position.

In the interview, Dr. Willerston, a native Texan, profiles the THI’s achievements and shares his thoughts on reducing the heavy burdens of Cardiovascular disease, which is estimated to cost the economy $449 billion annually.

Accounting for over a quarter of all deaths in the U.S. each year, cardiovascular disease is obviously a major health concern, but mortality from coronary heart disease (CHD) has substantially decreased in recent decades. Dr. Willerston attributes the decrease to research discoveries that have provided insights into mechanisms responsible for thrombosis in injured coronary and cerebral arteries, and led to improved treatment.

He cites as an example that increased understanding of ‘bad’ low-density lipoprotein (LDL) cholesterol in patients to values well below 100 mg/dl has been a very important contribution, as has the development of statins to lower LDL has also been crucial, the use of low-dose aspirin and other medications to control blood pressure, avoidance of smoking and use of recreational drugs, control of blood sugar in patients who are diabetic, emphasis on diet and exercise, and improved imaging techniques for blood vessels and the cardiovascular system, as factors that have played a role in protecting CHD patients and decreasing mortality risk.

However, he notes that the greatest GHD risk factor is a genetic one, and a remaining priority must be to identify genes that contribute to this risk; ultimately silencing the most dangerous ones using microRNA methodology. Dr. Willerston says numerous clinical studies in patients with cardiovascular disease using a variety of stem cell types, including mesenchymal stem cells taken from the bone marrow or adipose tissue have been conducted, and that through the pioneering work of Dr Doris Taylor, scientists are now able to deplete human hearts of their cellular structure and then restore that same heart to normal function by the infusion of stem cells. With continued success, these efforts could fill a great unmet need and pave the way to a new area of transplant medicine.

Dr. Willerston maintains that prevention would be the single most effective means of reducing healthcare costs, and should be the main concern initiated at very young ages and continue throughout adulthood.

Dr. James T. Willerson, born in Lampasas, Texas, is President of The University of Texas Health Science Center at Houston where he is the Alkek-Williams Distinguished Professor and holds the Edward Randall III Chair in Internal Medicine. In October 2004, Dr. Willerson was named President-Elect of the Texas Heart Institute in Houston, Texas. He holds the Dunn Chair in Cardiology Research and the John O’Quinn Chair named the “James T. Willerson Distinguished Chair in Cardiovascular Research,” both at the Texas Heart Institute, Houston, Texas. From 1989 through 2000, he was the Chairman of the Department of Internal Medicine at The University of Texas Medical School at Houston where an Annual Lectureship has been established in his name. During this same period, he served as the Chief of Medical Services at Memorial Hermann Hospital. He is also the Medical Director, Director of Cardiovascular Research, and Co-Director of the Cullen Cardiovascular Research Laboratories at the Texas Heart Institute. He is an Adjunct Professor of Medicine at Baylor College of Medicine and at The University of Texas M.D. Anderson Cancer Center in Houston.

Dr. Willerson also founded TexGen Research, a collaboration which brings together all of the institutions in the Texas Medical Center to collect blood samples necessary for the discovery of those genes and proteins that play a key role in causing major diseases. With TexGen, each Texas Medical Center institution obtains blood samples from patients who have a personal or family history of cardiovascular disease, stroke, dementia, or selected cancers and who are admitted to their hospitals. Great progress is being made by this collaborative biomedical research effort.

A graduate of the Texas Military Institute in San Antonio, Texas, where he was the Battalion Commander, President of the Senior Class, Editor of the school newspaper, and a state swimming champion, Dr. Willerston attended The University of Texas at Austin, graduating as a Phi Beta Kappa, member of the Texas Cowboys, and where he lettered for three years in varsity swimming. Upon graduating as a member of Alpha Omega Alpha from Baylor College of Medicine in Houston, Texas, he completed his medical and cardiology training as an intern, resident, and research and clinical fellow at the Massachusetts General Hospital in Boston, Massachusetts, and as a Clinical Associate at the National Institutes of Health in Bethesda, Maryland.

He is the former Chairman of the National American Heart Association Research Committee and of the Cardiovascular and Renal Study Section of the National Institutes of Health. He has received the Award of Merit from the American Heart Association and has served as a member of the Board of Directors and Steering Committee of the National American Heart Association. Before coming to The University of Texas Medical School at Houston, Dr. Willerson was Professor of Medicine and Director of the Cardiology Division at The University of Texas Southwestern Medical School in Dallas, Texas, and Director and Principal Investigator of the National Heart, Lung, and Blood Institute’s Specialized Center of Research under a major grant from the NIH. Upon his departure, the “James T. Willerson, M.D. Distinguished Chair in Cardiovascular Diseases” was established at The University of Texas Southwestern Medical School.

Dr. Willerson has served as visiting professor and invited lecturer at more than 220 institutions worldwide, and has received numerous national and international awards, as well as having served on editorial boards for many professional publications including: The New England Journal of Medicine, Journal of Clinical Investigation, Circulation, Circulation Research, Arteriosclerosis and Thrombosis, American Journal of Medicine, Journal of the American College of Cardiology, American Journal of Cardiology, American Heart Journal, and Cardiovascular Medicine. From 1993 to 2004, he was the longest-serving Editor of Circulation, the major publication of the American Heart Association. In 1998, the monthly journal was converted to a weekly publication and attained the highest Impact Factor of any cardiology journal in the world. He has edited or co-edited twenty-four textbooks, including the Third Edition of Cardiovascular Medicine which was released in February of 2007. Additionally, he has published more than 850 scientific articles.

Dr. Willerson has been elected to membership in numerous professional societies, including the American Society of Clinical Investigation, the Association of American Physicians, the Association of Professors of Medicine, and the Institute of Medicine of the National Academy of Sciences. He was named a Distinguished Alumnus by the Baylor College of Medicine in 1998 and a Distinguished Alumnus of The University of Texas at Austin in 1999.

SOURCE:

http://bionews-tx.com/news/2013/04/25/texas-heart-institutes-overachieving-president-and-medical-director-dr-james-t-willerson-profiles-this-50-years-of-accomplishments/

Comment of Note

Dr. Lev-Ari, was a visitor at Texas Heart Institute, Perfusion Program, and shadowed Open Heart Surgery in 8/2005.

The museum on the First floor of the building represents a Historical exhibit of Images of Cardiac Procedures. On display is a complete array of surgical tools used in Cardiac Repair during the last 50 years of unprecedented development in Cardiac Medical Devices and Procedures. A duplicate of the exhibit is available at the Smithsonian Museum at WashDC.

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