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Archive for the ‘Myocardial metabolism, Myocardial ischemia, myocardial perfusion, Myocardial adenine nucleotide metabolism’ Category

 

High Concordance Between Mental Stress-Induced and Adenosine-Induced Myocardial Ischemia Assessed Using SPECT in Heart Failure Patients: Hemodynami… – PubMed – NCBI

Reporter: Aviva Lev-Ari, PhD, RN

 

J Nucl Med. 2015 Jul 23. pii: jnumed.115.157990. [Epub ahead of print]

Sourced through Scoop.it from: www.ncbi.nlm.nih.gov

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High Concordance Between Mental Stress-Induced and Adenosine-Induced Myocardial Ischemia Assessed Using SPECT in Heart Failure Patients: Hemodynamic and Biomarker Correlates

Affiliations 

Free PMC article

Abstract

Mental stress can trigger myocardial ischemia, but the prevalence of mental stress-induced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stress-induced and adenosine-induced changes in myocardial perfusion and neurohormonal activation in CHF patients with reduced left-ventricular function using SPECT to precisely quantify segment-level myocardial perfusion.

Methods: Thirty-four coronary artery disease patients (mean age±SD, 62±10 y) with CHF longer than 3 mo and ejection fraction less than 40% underwent both adenosine and mental stress myocardial perfusion SPECT on consecutive days. Mental stress consisted of anger recall (anger-provoking speech) followed by subtraction of serial sevens. The presence and extent of myocardial ischemia was quantified using the conventional 17-segment model.

Results: Sixty-eight percent of patients had 1 ischemic segment or more during mental stress and 81% during adenosine. On segment-by-segment analysis, perfusion with mental stress and adenosine were highly correlated. No significant differences were found between any 2 time points for B-type natriuretic peptide, tumor necrosis factor-α, IL-1b, troponin, vascular endothelin growth factor, IL-17a, matrix metallopeptidase-9, or C-reactive protein. However, endothelin-1 and IL-6 increased, and IL-10 decreased, between the stressor and 30 min after stress. Left-ventricular end diastolic dimension was 179±65 mL at rest and increased to 217±71 after mental stress and 229±86 after adenosine (P<0.01 for both). Resting end systolic volume was 129±60 mL at rest and increased to 158±66 after mental stress (P<0.05) and 171±87 after adenosine (P<0.07), with no significant differences between adenosine and mental stress. Ejection fraction was 30±12 at baseline, 29±11 with mental stress, and 28±10 with adenosine (P=not significant).

Conclusion: There was high concordance between ischemic perfusion defects induced by adenosine and mental stress, suggesting that mental stress is equivalent to pharmacologic stress in eliciting clinically significant myocardial perfusion defects in CHF patients. Cardiac dilatation suggests clinically important changes with both conditions. Psychosocial stressors during daily life may contribute to the ischemic burden of CHF patients with coronary artery disease.

Keywords: adenosine; heart failure; ischemia; mental stress; myocardial perfusion; single-photon emission computed tomography.

SOURCE

https://pubmed.ncbi.nlm.nih.gov/26205303/

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Critical role of microRNAs after global myocardial ischemia and reperfusuion

Reporter: Aviva Lev-Ari, PhD, RN

Myocardial ischemia reperfusion injury

Sourced through Scoop.it from: ajbm.net

Critical role of microRNAs after global myocardial ischemia and reperfusuion

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American Journal of BioMedicine Volume 3, Issue 7, pages 451-467

Published: July 29, 2015


Renzo Grupper,  Ross Edward, Christian Walter, Eva Varnous

Abstract

Myocardial ischemia reperfusion injury is a major problem in heart transplantation and its mechanism is still not fully known. MicroRNAs (miRNAs) are small, single-stranded RNA molecules which play an important role in posttranscriptional regulation of gene expression by inhibiting translation of target mRNAs. The objective of this study is to investigate the mechanistic role of miRNAs on global myocardial ischemia-reperfusion injury in mice. The mice heart was mounted in a Langendorff-type isolated heart perfusion system. The coronary effluent volume was measured at the various time intervals for a total of 120 min. Coronary flow rate (CFR, in ml · min−1 · g−1) was defined as the total volume collected during the reperfusion interval divided by the time, normalized by the heart wet weight (g), which was measured at the beginning of the experiment. The volume fraction of interstitial space (VFITS) in myocardial tissue was determined from H-E-stained sections by using the equation VFITS = (100% × area of interstitial space)/total tissue area. The mitochondrial cross-sectional area was measured. The number of fragmented mitochondria, the number of mitochondria with amorphous matrix densities or granular densities, and the total number of mitochondria studied in each group were counted. Further, The average LV dP/dt during 0–30, 30–60, 60–90, and 90–120 min of reperfusion was calculated from data continuously recorded during the corresponding reperfusion period. In conclusion the present data show that the miRNAs have a great potential as biomarker, therapeutic target, and led to significant new insights into the pathophysiology of global myocardial I/R, graft rejection.

Keywords: Myocardial ischemia reperfusion injury; Heart transplantation; MicroRNAs; Coronary flow rate

SOURCE

https://ajbm.net/critical-role-of-micrornas-after-global-myocardial-ischemia-and-reperfusuion/

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Premature Ventricular Contraction percentage predicts new Systolic Dysfunction and clinically diagnosed CHF and overall Mortality

Reporter: Aviva Lev-Ari, PhD, RN

 

Cardiovascular Health Study (CHS)

This study has been completed. ClinicalTrials.gov processed this record on July 13, 2015
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00005133
First received: May 25, 2000
Last updated: May 1, 2009
Last verified: May 2009
  Purpose

To determine the extent to which known risk factors predict coronary heart disease and stroke in the elderly, to assess the precipitants of coronary heart disease and stroke in the elderly, and to identify the predictors of mortality and functional impairments in clinical coronary disease or stroke.

SOURCE

https://clinicaltrials.gov/ct2/show/NCT00005133?term=Cardiovascular+Health+Study&rank=2

Although links between frequent PVCs and ongoing heart failure have been observed, the current analysis, based on a cohort from the Cardiovascular Health Study (CHS), provides “the first evidence that PVC percentage predicts new systolic dysfunction, as well as clinically diagnosed CHF and overall mortality,” say the authors in their report, published in the July 14, 2015 issue of the Journal of the American College of Cardiology. It also raises the issue of whether PVCs might sometimes be an appropriate target for treatments aimed at preventing heart failure.

The observational study can’t demonstrate causality, note the authors, led by Dr Jonathan W Dukes (University of California, San Francisco). But overall, the findings “suggest that PVCs might be an important cause of occult or ‘idiopathic’ cardiomyopathy and might be an important determinant of incident CHF among those with other established CHF risk factors.”

Ablate PVCs in HF, LVEF Can Improve

“There’s this general notion that PVCs are very benign, which is certainly what I was taught, even in my general cardiology fellowship, before the more recent data that came out of the electrophysiology labs,” senior author Dr Gregory M Marcus (UCSF) said in an interview with heartwire from Medscape.

In recent years, he said, it’s been appreciated that ablation of PVCs in patients with lots of them can improve quality of life by alleviating symptoms such as syncope. And there are series of patients with PVCs and primarily nonischemic cardiomyopathy in the EP literature suggesting that “if you ablate those PVCs, their heart failure improves and often their reduced ejection fraction normalizes,” according to Marcus. “Many of us have seen that and witnessed it firsthand in many of our own patients.”

Although the analysis tried to control for such factors, she said, the question remains “whether PVCs are causing deterioration in EF and HF or if they are simply a marker of underlying disease. If the former is true, then treating PVCs would help. But if the latter is true, then treating PVCs may not make a difference.”

Marcus acknowledges that PVCs may be simply a risk marker in people with sick hearts. “But even if that’s the case, I think it’s potentially a very useful marker.” He said he hopes the report will help “motivate future research in potentially two different directions. One, might ablation be an effective therapy to prevent heart failure in the right patients? Alternatively, could this be used to help predict heart failure and implement other strategies, such as beta-blockers, to prevent heart failure in those patients?”

CASTing a New Light on Treatment of PVCs

The Cardiac Arrhythmia Suppression Trial (CAST), Marcus noted, “taught us a lot of important lessons. More generally, it was a great example of the need to look at hard outcomes rather than secondary or surrogate outcomes.”

As cardiology textbooks have since noted, CAST randomized about 2300 patients who had asymptomatic or only mildly symptomatic PVCs after acute MI to receive one of three antiarrhythmic agents or placebo. The drugs, which included the class Ic agents encainide and flecainide, were mostly effective at suppressing PVCs. But over a mean 10 months of follow-up, patients who had received those drugs showed steep rise in rate of arrhythmic death (the primary end point) as well as nonfatal cardiac arrest, almost certainly due to proarrhythmic effects.

The widely learned lesson: post-MI suppression of PVCs, a surrogate for the pathology behind sudden cardiac death in ischemic heart disease, doesn’t lower its risk; in fact, treatment of surrogate markers can make things a lot worse. (Importantly, CAST was conducted in the early days of arrhythmia ablation and implantable defibrillators, which were not options for its patients.)

As a result, according to Marcus, class Ic agents are generally avoided in patients with structural heart disease. “I think that while the proarrhythmic effects of those drugs were known, they weren’t fully appreciated, and CAST taught us to be wary of them.”

 

The CHS is sponsored by the National Heart, Lung, and Blood Institute. Dukes and Marcus report that they have no relevant financial relationships; disclosures for the other authors are in the report. Santangeli and Marchlinski report that they have no relevant financial relationships. Al-Khatib says she has no relevant financial relationships with industry.

 

SOURCE

http://www.medscape.com/viewarticle/847859?nlid=84244_2562&src=wnl_edit_medp_card&uac=93761AJ&spon=2&impID=760872&faf=1

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Continuing Education: ECG Clues to Identify the Site of Occlusion in Acute Myocardial Ischemia/Infar

Reporter: Aviva Lev-Ari, PhD, RN

Watch Video

https://www.youtube.com/v/2Fqs2PbJX50?fs=1&hl=fr_FR

ST depression and ST elevation in helping to better localize the acutely ischemic/infracted region.

Source: www.youtube.com

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Selenide protects heart muscle in the wake of cardiac arrest – Science Daily

Reporter: Aviva Lev-Ari, PhD, RN

 

 

 

 

 

 

 

 

Damage to heart muscle from insufficient blood supply during cardiac arrest and reperfusion injury after blood flow is restored can be reduced by nearly 90 percent if selenide, a form of the essential nutrient selenium, is administered…

Source: www.sciencedaily.com

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Fractional Flow Reserve vs. Angiography in Non-ST-segment Elevation Myocardial Infarction

Reporter: Aviva Lev-Ari, PhD, RN

 

Jamie Layland, Keith G. Oldroyd, Nick Curzen, Arvind Sood, Kanarath Balachandran, Raj Das, Shahid Junejo, Nadeem Ahmed, Matthew M.Y. Lee, Aadil Shaukat, Anna O’Donnell, Julian Nam, Andrew Briggs, Robert Henderson, Alex McConnachie, Colin Berry

Disclosures

Eur Heart J. 2015;36(2):100-111. 

Aim

We assessed the management and outcomes of non-ST segment elevation myocardial infarction (NSTEMI) patients randomly assigned to fractional flow reserve (FFR)-guided management or angiography-guided standard care.

Methods and results

We conducted a prospective, multicentre, parallel group, 1 : 1 randomized, controlled trial in 350 NSTEMI patients with ≥1 coronary stenosis ≥30% of the lumen diameter assessed visually (threshold for FFR measurement) (NCT01764334).

Enrolment took place in six UK hospitals from October 2011 to May 2013. Fractional flow reserve was disclosed to the operator in the FFR-guided group (n 1/4 176). Fractional flowreserve was measured but not disclosed in the angiography guided group (n 1/4 174). Fractional flowreserve ≤0.80was an indication for revascularization by percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG). The median (IQR) time from the index episode of myocardial ischaemia to angiographywas 3 (2, 5) days. For the primary outcome, the proportion of patients treated initially by medical therapy was higher in the FFR-guided group than in the angiography-guided group [40 (22.7%) vs. 23 (13.2%), difference 95% (95% CI: 1.4%, 17.7%), P 1/4 0.022]. Fractional flow reserve disclosure resulted in a change in treatment between medical therapy, PCI or CABG in 38 (21.6%) patients. At 12 months, revascularization remained lower in the FFR-guided group [79.0 vs. 86.8%, difference 7.8% (20.2%, 15.8%), P 1/4 0.054]. There were no statistically significant differences in health outcomes and quality of life between the groups.

Conclusion

In NSTEMI patients, angiography-guided management was associated with higher rates of coronary revascularization compared with FFR-guided management. A larger trial is necessary to assess health outcomes and cost-effectiveness.

SOURCE

 

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Chinese Medicine Forum: Silent myocardial ischemia and its’ Chinese medicine treatment

Reporter: Aviva Lev-Ari, PhD, RN

 

 

 

 

 

 

http://t.co/K0a4S97cJy myocardial ischemia#chinesemedecine#acupuncturehour#acupuncture#agopuntura#ischemia#myocardial http://t.co/YvUl0ek2cW

Tiejun Tang
Silent myocardial ischemia (SMI), also called asymptomatic myocardial ischemia, is the most common manifestation of coronary heart disease. SMI patients do not seek medical attention as often as angina pectoris patients because SMI does not necessarily cause severe chest pains. Hence the necessary diagnostic procedures such as blood tests, ECG and heart scan are left undone. This places SMI patients under a higher risk of experiencing a sudden and possibly fatal cardiac event. Some cases have been diagnosed as myocardial infarction after been sent to hospital, some cause sudden death. If the myocardial ischemic is emerged in the heart, no matter patient felt pain or not, the potential risk is the same. I would like to remind people, SMI is a silent killer!
Asymptomatic mean no symptom literally. But it does not mean patients didn’t have any symptoms at all. Actually it only means no chest pain. Some SMI patients might experience chest tightness, palpitation and short of breath sometimes, especially after exercise. A person experiencing any of the above symptoms should contact their GP.
SOURCE

Source: chinesemedicinesalon.blogspot.it

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Dynamic myocardial CT perfusion imaging for evaluation of myocardial ischemia as determined by MR imaging | DSCT.com – Your Dual-source CT experts

Reporter: Aviva Lev-Ari, PhD, RN

 

 

 

The aim of this study was to determine the feasibility of CT-based dynamic myocardial perfusion imaging for the assessment of myocardial ischemia and infarction compared with cardiac magnetic resonance (CMR).

Source: www.dsct.com

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Myocardial ischemia common in young women with CHD under mental stress | Cardiology

Reporter: Aviva Lev-Ari, PhD, RN

 

 

 

Cardiology | CHICAGO — Women aged 55 years and younger with stable CHD under mental stress are more likely to develop myocardial ischemia than men of the same age.

Source: www.healio.com

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YM758 Monophosphate, A Novel If Channel Inhibitor

Reporter: Larry H. Bernstein, MD, FCAP

YM758 is a novel If channel inhibitor for the treatment of stable angina and atrial fibrillation. A novel cardiovascular agent.
YM758 monophosphate (R)-1·H3PO4 has an inhibitory action for If current and shows a strong and specific activity selectively lowering a heart beat and decreasing oxygen consumption of heart muscle in a selective manner, whereby it is useful as a preventive and/or treating agent for diseases of circulatory system such as ischemic heart diseases (e.g., angina pectoris and myocardial infarction), congestive heart failure, arrhythmia, etc.
U.S. Patent No. 6,573,279, incorporated herein by reference, describes isoquinoline compounds with 1 channel blocker activity and their use in treating a variety of cardiovascular diseases. U.S. Patent Application Publication Nos. 20060084807 and

20070129357, each of which is incorporated herein by reference, describe methods for making those isoquinoline compounds as well as crystals of certain fluorobenzamide derivatives of them. U.S. Patent Publication No. 20090247572, incorporated herein by reference, relates to the use of one of these isoquinoline fluorobenzamide derivatives, (-)-N- {2-[(i?)-3-(6,7-dimethoxy-l ,2,3,4-tetrahydroisoquinoline-2-carbonyl)piperidino]ethyl}-4- fluorobenzamide monophosphate (referred to in that patent publication as “compound A” and “chemical formulation I” and referred to herein as “YM758″), for treating atrial fibrillation.

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