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Posts Tagged ‘Angina pectoris’


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

https://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

https://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 https://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

https://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)

https://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

https://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

https://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. 

https://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”    https://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    https://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
https://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
https://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
https://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
https://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
https://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
https://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
https://pharmaceuticalintelligence.com/2012/10/23/to-stent-or-not-a-critical-decision/

Transcatheter Aortic-Valve Replacement for Inoperable Severe Aortic Stenosis

https://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

https://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
https://pharmaceuticalintelligence.com/2012/08/22/new-drug-eluting-stent-works-well-in-stemi/

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

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Revascularization: PCI, Prior History of PCI vs CABG

Curator: Aviva Lev-Ari, PhD, RN

 

UPDATED 9/25/2013

Table. Comparison of Surgical Therapy and Coronary Angioplasty (Open Table in a new window)

Endpoint Pocock et al* Pocock et al BARI Study
CABG(N=358) PTCA(N=374) CABG(N=1303) PTCA(N=1336) CABG(N=914) PTCA(N=915)
Death (%) 0.3 1.9 2.8 3.1 10.7 13.7
Death or MI 4.5 7.2 8.5 8.1 11.7 10.9
Repeat CABG 1.4 16.0§ 0.8 18.3§ 0.7 20.5§
Repeat CABG or PTCA 3.6 30.5§ 3.2 34.5§ 8.0 54.0§
More than mild angina 6.5 14.6§ 12.1 17.8§
*Meta-analysis of results of 3 trials at 1 year. Patients with single-vessel disease were studied.[22] †Meta-analysis of results of 3 trials at 1 year. Patients with multivessel disease were studied.[22] 

‡Reported results are for 5-year follow-up. Patients with multivessel disease were studied.[21] 

§ P < .05.

BARI = Bypass Angioplasty Revascularization Investigation; CABG = coronary artery bypass grafting; MI = myocardial infarction; PTCA = percutaneous transluminal coronary angioplasty.

SOURCE

http://emedicine.medscape.com/article/161446-overview#aw2aab6b2b5

Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating multiple conditions, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD).

Essential update: Cangrelor decreases periprocedural complications of PCI

According to a pooled analysis of 3 CHAMPION trials—CHAMPION-PCI , CHAMPION-PLATFORM , and CHAMPION-PHOENIX—cangrelor can reduce the risk of periprocedural thrombotic complications of PCI.[1, 2, 3] The 3 trials included patients with ST-elevation MI (STEMI), non-STEMI, and stable CAD who were randomly assigned to receive either cangrelor or control therapy consisting of either clopidogrel or placebo.

The primary outcome in this analysis was a composite of death, MI, ischemia-driven revascularization, or stent thrombosis at 48 hours.[2] The frequency of this outcome was significantly lower in cangrelor-treated patients than in control subjects (absolute difference, 1.9%; relative risk reduction [RRR], 19%). Stent thrombosis was also reduced in the cangrelor-treated group (absolute difference, 0.3%; RRR, 41%). Primary safety outcomes were comparable in the 2 groups, but cangrelor-treated patients had a higher rate of mild bleeding.

Indications and contraindications

Clinical indications for PCI include the following:

In an asymptomatic or mildly symptomatic patient, objective evidence of a moderate-sized to large area of viable myocardium or moderate to severe ischemia on noninvasive testing is an indication for PCI. Angiographic indications include hemodynamically significant lesions in vessels serving viable myocardium (vessel diameter >1.5 mm).

Clinical contraindications for PCI include the presence of any significant comorbid conditions (this is a relative contraindication). Angiographic contraindications include the following:

  • Left main stenosis in a patient who is a surgical candidate (except in carefully selected patients[4] )
  • Diffusely diseased small-caliber artery or vein graft
  • Other coronary anatomy not amenable to PCI

In patients with stable angina, medical therapy is recommended as first-line therapy unless one or more of the following indications for cardiac catheterization and PCI or CABG are present:

  • A change in symptom severity
  • Failed medical therapy
  • High-risk coronary anatomy
  • Worsening left ventricular (LV) dysfunction

American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines on the management of unstable angina/non-STEMI recommend that an early invasive approach (angiography and revascularization within 24 hours) should be used to treat patients presenting with the following high-risk features[5] :

  • Recurrent angina at rest or low level of activity
  • Elevated cardiac biomarkers
  • PCI in the past 6 months or prior CABG
  • New ST-segment depression
  • Elevated cardiac biomarkers
  • High-risk findings on noninvasive testing
  • Signs or symptoms of heart failure or new or worsening mitral regurgitation
  • Hemodynamic instability
  • Sustained ventricular tachycardia
  • LV systolic function < 40%
  • High risk score (eg, Thrombolysis in Myocardial Infarction [TIMI] score >2) (see the TIMI Score for Unstable Angina Non ST Elevation Myocardial Infarction calculator)

See Overview for more detail.

Equipment

Balloon catheters for PCI have the following features:

  • A steerable guide wire precedes the balloon into the artery and permits navigation through the coronary tree
  • Inflation of the balloon compresses and axially redistributes atheromatous plaque and stretches the vessel wall
  • The balloon catheter also serves as an adjunctive device for many other interventional therapies

Atherectomy devices have the following features:

  • These devices are designed to physically remove coronary atheroma, calcium, and excess cellular material
  • Rotational atherectomy, which relies on plaque abrasion and pulverization, is used mostly for fibrotic or heavily calcified lesions that can be wired but not crossed or dilated by a balloon catheter
  • Atherectomy devices may be used to facilitate stent delivery in complex lesions
  • Directional coronary atherectomy (DCA) has been used to debulk coronary plaques
  • Laser atherectomy is not widely used at present
  • Atherectomy is typically followed by balloon dilation and stenting

Intracoronary stents have the following features:

  • Stents differ with respect to composition (eg, stainless steel, cobalt chromium, or nickel chromium), architectural design, and delivery system
  • Drug-eluting stents have demonstrated significant reductions in restenosis and target-lesion revascularization rates
  • In the United States, stents are available that elute the following drugs: sirolimus (Cypher), paclitaxel (Taxus), zotarolimus (Endeavor), and everolimus (Xience V)
  • Stents are conventionally placed after balloon predilation, but in selected coronary lesions, direct stenting may lead to better outcomes

Other devices used for PCI include the following:

  • Thrombus aspiration limits the adverse effects that prolonged time to treatment has on myocardial reperfusion[6]
  • Distal embolic protection during saphenous vein graft intervention has become the standard of care

See Periprocedural Care and Devices for more detail.

Technique

Intravascular ultrasonography (IVUS) is used in PCI as follows:

  • Provide information about the plaque, the vessel wall, and the degree of luminal narrowing
  • Assessment of indeterminate lesions
  • Evaluation of adequate stent deployment

Intracoronary Doppler pressure wires are used in PCI as follows:

  • To characterize coronary lesion physiology and estimate lesion severity
  • Comparison of pressure distal to a lesion with aortic pressure enables determination of fractional flow reserve (FFR)
  • An FFR measurement below 0.75-0.80 during maximal hyperemia (induced via administration of adenosine) is consistent with a hemodynamically significant lesion

Antithrombotic therapy

  • Aspirin and heparin have been the traditional adjunctive medical therapies
  • Direct thrombin inhibitors (ie, hirudin, bivalirudin) are slightly better than heparin in preventing ischemic complications during balloon angioplasty but do not affect restenosis rates
  • Low-molecular-weight heparins (LMWHs) are substituted for standard heparin at some centers

Antiplatelet therapy

Patients receiving stents are treated with a combination of aspirin and clopidogrel. Duration of therapy is as follows:

  • Bare-metal stents: A minimum of 4 weeks
  • Drug-eluting stents: A minimum of 12 months

Use of proton pump inhibitors is appropriate in patients with multiple risk factors for GI bleeding who require antiplatelet therapy.

Glycoprotein inhibitor therapy

  • Abciximab, tirofiban, and eptifibatide have all been shown to reduce ischemic complications in patients undergoing balloon angioplasty and coronary stenting
  • In primary PCI, GPIIb/IIIa receptor inhibitors have also been shown to improve flow and perfusion and to reduce adverse events
  • Abciximab may improve outcomes in patients when given before arrival in the catheterization lab for primary PCI[7]

See Technique and Medication for more detail.

SOURCE & References for the UPDATE, in

http://emedicine.medscape.com/article/161446-overview#aw2aab6b2b5

Outcomes comparison between PCI and CABG was explored in the past by authors on this Open Access Online Scientific Journal, in the following articles:

CABG or PCI: Patients with Diabetes – CABG Rein Supreme

https://pharmaceuticalintelligence.com/2012/11/05/cabg-or-pci-patients-with-diabetes-cabg-rein-supreme/

To Stent or Not? A Critical Decision

https://pharmaceuticalintelligence.com/2012/10/23/to-stent-or-not-a-critical-decision/

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

https://pharmaceuticalintelligence.com/2013/01/10/pci-outcomes-increased-ischemic-risk-associated-with-elevated-plasma-fibrinogen-not-platelet-reactivity/

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

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

Age-Dependent Depression in Circulating Endothelial Progenitor Cells in Coronary Artery Bypass Grafting Patients

https://pharmaceuticalintelligence.com/2012/08/17/age-dependent-depression-in-circulating-endothelial-progenitor-cells-in-coronary-artery-bypass-grafting-patients/

Now we are reporting  an Original Contribution on this subject which includes also Prior History of PCI, a factor NOT included in the other studies. The major conclusions are the following three:

  1. In a contemporary cohort of STEMI patients undergoing primary PCI, a history of prior CABG was found to be an independent predictor of in-hospital mortality.
  2. In contrast, despite more comorbidities at the time of STEMI, patients with prior PCI had no significant difference in the rates of death, stroke, or periprocedural MI when compared to a STEMI population without prior coronary revascularization.
  3. Thus, only prior surgical — and not percutaneousrevascularization should be considered a significant risk factor in the setting of primary PCI.

Number 1, above is related to patient medical history of cardiovascular disease SEVERITY prior to CABG

Number 2, above indicates that patients can tolerate and benefit several cycles of PCI and stent implantation rather than PCI being a determinant predictor of future prognosis

Number 3, above is as well related to patient medical history of cardiovascular disease SEVERITY prior to CABG

The Original Contribution on this subject is present, below.

The Impact of Previous Revascularization on Clinical Outcomes in Patients Undergoing Primary Percutaneous Coronary Intervention

Travis J. Bench, MD1, Puja B. Parikh, MD1, Allen Jeremias, MD1, Sorin J. Brener, MD2, Srihari S. Naidu, MD3,

Richard A. Shlofmitz, MD4, Thomas Pappas, MD4, Kevin P. Marzo, MD3, Luis Gruberg, MD1

Authors Affiliations:

1Division of Cardiovascular Medicine, Stony Brook University Medical Center, Stony Brook, New York,

2Department of Cardiology, Methodist Hospital, Brooklyn, New York,

3Division of Cardiology, Winthrop University Hospital, Mineola,

New York, and

4The Heart Center, St Francis Hospital, Roslyn, New York.

The authors report no conflicts of interest regarding the content herein.

Manuscript submitted October 10, 2012, provisional acceptance given October 20, 2012, final version accepted November 28, 2012.

Address for correspondence: 

Luis Gruberg, MD, FACC, Department of Medicine, Division of Cardiology, Health Sciences Center, T16-080, Stony Brook, NY 11794- 8160. Email: luis.gruberg@stonybrook.edu

 

Abstract : While the impact of prior coronary artery bypass graft surgery (CABG) on in-hospital outcomes in patients with STelevation myocardial infarction (STEMI) has been described, data are limited on patients with prior percutaneous coronary intervention (PCI) undergoing primary PCI in the setting of an STEMI. The aim of the present study was to assess the effect of previous revascularization on in-hospital outcomes in STEMI patients undergoing primary PCI. Between January 2004 and December 2007, a total of 1649 patients underwent primary PCI for STEMI at four New York State hospitals. Baseline clinical and angiographic characteristics and in-hospital outcomes were prospectively collected as part of the New York State PCI Reporting System (PCIRS). Patients with prior surgical or percutaneous coronary revascularization were compared to those without prior coronary revascularization. Of the 1649 patients presenting with STEMI, a total of 93 (5.6%) had prior CABG, 258 (15.7%) had prior PCI, and 1298 (78.7%) had no history of prior coronary revascularization. Patients with prior CABG were significantly older and had higher rates of peripheral vascular disease, diabetes mellitus, congestive heart failure, and prior stroke. Additionally, compared with those patients with a history of prior PCI as well as those without prior coronary revascularization, patients with previous CABG had more left main interventions (24% vs 2% and 2%; P<.001), but were less often treated with drug-eluting stents (47% vs 61% and 72%; P<.001).

Despite a low incidence of adverse in-hospital events, prior CABG was associated with higher all-cause in-hospital mortality (6.5% vs 2.2%; P=.012), and as a result, higher overall MACE (6.5% vs 2.7%; P=.039). By multivariate analysis, prior CABG (odds ratio, 3.40; 95% confidence interval, 1.15-10.00) was independently associated with in-hospital mortality. In contrast, patients with prior PCI had similar rates of MACE (4.3% vs 2.7%; P=.18) and inhospital mortality (3.1% vs 2.2%; P=.4) when compared to the de novo population. Patients with a prior history of CABG, but not prior PCI, undergoing primary PCI in the setting of STEMI have significantly worse in-hospital outcomes when compared with patients who had no prior history of coronary artery revascularization. Thus, only prior surgical — and not percutaneous — revascularization should be considered a significant risk factor in the setting of primary PCI.

J INVASIVE CARDIOL 2013;25(4):166-169

Key words: PCI risk factor, CABG

Demographics and Angiographic Characteristics

Between 2004 and 2007, a total of 25,025 patients underwent PCI at these medical institutions, and their data were prospectively collected and submitted as required by the New York State Department of Health. Of these patients, a total of 1649 underwent primary PCI in the setting of an STEMI and constituted our study population. In this group, a total

No Prior Revascularization (n = 1298)

Prior PCI (n = 258)

Prior CABG (n = 93)

Demographics

Age (years) 61 ± 13 62 ± 12 67 ± 12 <.001

Male gender 956 (73.6%) 194 (75.2%) 76 (81.7%) .21

White 1165 (89.8%) 231 (89.5%) 87 (93.5%) .51

African-American 78 (6%) 18 (7%) 1 (1.1%) .51

Hispanic 91 (7%) 11 (4.3%) 4 (4.3%) .51

Medical history

Ejection fraction (%) 43 ± 12 44 ± 13 45 ± 11 .079

Diabetes mellitus 196 (15.1%) 69 (26.7%) 27 (29%) <.001

Peripheral vascular disease 53 (4.1%) 25 (9.7%) 12 (12.9%) <.001

Chronic lung disease 47 (3.6%) 17 (6.6%) 4 (4.3%) .09

Congestive heart failure 74 (5.7%) 25 (9.7%) 10 (10.8%) .02

Prior myocardial infarction 3 (0.2%) 1 (0.4%) 1 (1.1%) .35

Prior cerebrovascular event 56 (4.3%) 9 (3.5%) 10 (11%) .01

Chronic dialysis 6 (0.5%) 6 (2.3%) 0 (0%) .004

Creatinine (mg/dL) 1.1 ± 0.8 1.3 ± 1.4 1.3 ± 1.1 .002

Glomerular filtration rate (mL/min/1.73 m2) 79 ± 26 75 ± 28 71 ± 27 .002

Angiographic characteristics

Left main 19 (1.5%) 5 (1.9%) 22 (23.7%) <.001

Left anterior descending 942 (72.6%) 178 (69%) 69 (74.2%) .45

Left circumflex 579 (44.6%) 122 (47.3%) 70 (75.3%) <.001

Right coronary 806 (62.1%) 187 (72.5%) 67 (72%) .002

Graft (arterial or venous) n/a n/a 20 (21.5%)

Stent type

Bare-metal stent 241 (18.6%) 52 (20.2%) 23 (24.7%) .31

Drug-eluting stent 928 (71.5%) 158 (61.2%) 44 (47.3%) <.001

of 1298 patients (78.7%) had no prior history of revascularization,

while 93 patients (5.6%) had a history of previous

CABG and 258 (15.7%) had a history of previous PCI. Considerable

differences in baseline clinical and procedural characteristics were noted among these groups (Table 1).

Discussion

While STEMI patients with prior CABG are well known to have worse clinical outcomes than those without prior revascularization, a direct comparison between patients who underwent primary PCI in the setting of prior CABG or prior PCI has not yet been reported. The principal findings from the present analysis suggest that in a contemporary, unrestricted patient population presenting with STEMI and undergoing primary PCI, patients with a prior history of CABG are:

(1) usually older and have multiple comorbidities, including peripheral vascular disease, diabetes, and chronic obstructive lung disease;

(2) are more likely to undergo intervention on a native vessel and not a bypass graft;

(3) are more likely to be treated with bare-metal stents; and (4) have higher rates of in-hospital mortality without a significant increase in stroke or MI rates, when compared with patients with a prior history of PCI or patients with no previous history of coronary artery revascularization. Interestingly, these outcomes did not apply to patients with a history of prior PCI in this analysis. Instead, this cohort of patients had no significant difference in the rate of death, stroke, or periprocedural infarction when compared to a STEMI population without prior coronary revascularization, despite a significantly higher burden of comorbidities than those with no prior revascularization.

Our findings concur with previous studies that have shown higher mortality rates among patients with prior surgical bypass presenting with acute MI.7,9,14 Despite changes in revascularization strategies over the past 30 years, invasive therapies to treat acute coronary syndromes in patients with prior bypass surgery appear to have yielded less robust results than in other populations. In fact, Stone and colleagues already described in the Primary Angioplasty in Myocardial Infarction (PAMI-2) study that patients with a previous CABG undergoing primary PCI in the setting of an acute MI had significantly greater in-hospital mortality than patients without previous CABG, especially if the infarct-related vessel was a bypass conduit. However, by logistic regression analysis, only advanced age (P=.004), triple-vessel disease (P=.004), and Killip class ≥2 (P=.02) were independent predictors of in-hospital mortality in that study.13 In a more contemporary study of 128 STEMI patients with prior CABG, who were enrolled in the Assessment of PEXelizumab in Acute

Figure 1. In-hospital major adverse cardiac and cerebrovascular events (MACCE), mortality, and stroke rates for patients without prior history of coronary revascularization (light grey bars), prior percutaneous coronary revascularization (PCI) (dark grey bars), and prior coronary artery bypass graft (CABG) (black bars). Vol. 25, No. 4, April 2013 169

STEMI and Prior Revascularization Myocardial Infarction (APEX-AMI) trial, Welsh and colleagues reported that post-CABG patients are less likely to undergo acute reperfusion (only 79% underwent primary PCI), have worse angiographic outcomes following primary PCI, and have higher 90-day mortality rates (19.0% vs 5.7%; P=.05). This difference was even more apparent when the infarct-related artery was a bypass graft that was not successfully reperfused (23.1% vs 8.5%; P=.03).3 These results are similar to our current analysis, where in-hospital mortality rates for patients who underwent primary PCI of a graft were numerically roughly 4 times as high as those undergoing PCI of a native vessel. Likewise, Gurfinkel et al reported a significant reduction in hard endpoints, such as all-cause death and MI at 6 months in patients treated with an invasive approach in the Global Registry of Acute Coronary Events (GRACE).15 In this large, multinational, observational study of 3853 patients with prior bypass surgery presenting with an acute coronary syndrome, only 497 (12.9%) were managed invasively and the rest were treated medically.

Despite significant differences in baseline characteristics, including a higher rate of STEMI in patients treated invasively (14% vs 27%; P<.001), in-hospital mortality was similar in both groups (3.4% vs 3.2%; P=.86). However, at 6-month follow-up, mortality was significantly higher in those patients treated medically (6.5% vs 3.4%; P<.02) as was the combined endpoint of death or MI (11% vs 5.8%; P<.01).

Whether these results apply to patients with a prior history of PCI has not been well defined. By the nature of vascular disease, patients with prior PCI are more likely to have more comorbidities than those without prior revascularization, a finding confirmed in our study. Despite considerable differences in baseline characteristics, however, these differences did not translate into a differential risk after STEMI. In fact, the cohort of patients presenting with STEMI who had a history of prior PCI had no statistically significant difference in in-hospital mortality or overall MACCE when compared to a population of patients presenting with STEMI in the absence of any prior revascularization.

Study limitations. The database utilized was derived from four New York State teaching hospitals and was designed to track quality of care and clinical outcomes. As all studies involving multicenter databases and registries, there is potential error in data entry and availability. Potential confounding comorbidities, including smoking status and family history of coronary artery disease, were not collected in this database, and information regarding long-term follow-up is not available, all of which are important limitations of this analysis. As such, deficiencies such as these limit the conclusions that can be drawn from our multivariate analysis. Additionally, there is no audit of data quality, and the low overall event rates limit effective statistical comparison.

Conclusions

In a contemporary cohort of STEMI patients undergoing primary PCI, a history of prior CABG was found to be an independent predictor of in-hospital mortality. In contrast, despite more comorbidities at the time of STEMI, patients with prior PCI had no significant difference in the rates of death, stroke, or periprocedural MI when compared to a STEMI population without prior coronary revascularization. Thus, only prior surgical — and not percutaneous — revascularization should be considered a significant risk factor in the setting of primary PCI.

REFERENCES

1. Kushner FG, Hand M, Smith SC Jr, et al. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Catheter Cardiovasc Interv. 2009;74(7):E25-E68.

2. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361(9351):13-20.

3. Welsh RC, Granger CB, Westerhout CM, et al. Prior coronary artery bypass graft patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. JACC Cardiovasc Interv. 2010;3(3):343-351.

4. Mathew V, Gersh B, Barron H, et al. In-hospital outcome of acute myocardial infarction in patients with prior coronary artery bypass surgery. Am Heart J. 2002;144(3):463-469.

5. Lee KL, Woodlief LH, Topol EJ, et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation. 1995;91(6):1659-1668.

6. Dittrich HC, Gilpin E, Nicod P, et al. Outcome after acute myocardial infarction in patients with prior coronary artery bypass surgery. Am J Cardiol. 1993;72(7):507-513.

7. Berry C, Pieper KS, White HD, et al. Patients with prior coronary artery bypass grafting have a poor outcome after myocardial infarction: an analysis of the VALsartan in acute myocardial iNfarcTion trial (VALIANT). Eur Heart J. 2009;30(12):1450-1456.

8. Grines CL, Booth DC, Nissen SE, et al. Mechanism of acute myocardial infarction in patients with prior coronary artery bypass grafting and therapeutic implications. Am J Cardiol. 1990;65(20):1292-1296.

9. Labinaz M, Sketch MH Jr, Ellis SG, et al. Outcome of acute ST-segment elevation myocardial infarction in patients with prior coronary artery bypass surgery receiving thrombolytic therapy. Am Heart J. 2001;141(3):469-477.

10. Peterson LR, Chandra NC, French WJ, Rogers WJ, Weaver WD, Tiefenbrunn AJ. Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2). Am J Cardiol. 1999;84(11):1287-1291.

11. Nguyen TT, O’Neill WW, Grines CL, et al. One-year survival in patients with acute myocardial infarction and a saphenous vein graft culprit treated with primary angioplasty. Am J Cardiol. 2003;91(10):1250-1254.

12. Al Suwaidi J, Velianou JL, Berger PB, et al. Primary percutaneous coronary interventions in patients with acute myocardial infarction and prior coronary artery bypass grafting, Am Heart J. 2001;142(3):452-459.

13. Stone GW, Brodie BR, Griffin JJ, et al. Clinical and angiographic outcomes in patients with previous coronary artery bypass graft surgery treated with primary balloon angioplasty for acute myocardial infarction. Second Primary Angioplasty in Myocardial Infarction Trial (PAMI-2) Investigators. J Am Coll Cardiol. 2000;35(3):605-611.

14. Labinaz M, Kilaru R, Pieper K, et al. Outcomes of patients with acute coronary syndromes and prior coronary artery bypass grafting: results from the platelet glycoprotein IIb/IIIa in unstable angina: receptor suppression using integrilin therapy (PURSUIT) trial. Circulation. 2002;105(3):322-327.

15. Gurfinkel EP, Perez de la Hoz R, Brito VM, et al. Invasive vs non-invasive treatment in acute coronary syndromes and prior bypass surgery. Int J Cardiol. 2007;119(1):65-72.

 

Other related studies on this subject published on this Open Access Online Scientific Journal include the following:

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

https://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. 12/31/2012 Renal Sympathetic Denervation: Updates on the State of Medicine

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

 

Lev-Ari, A. 9/2/2012 Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

https://pharmaceuticalintelligence.com/2012/09/02/imbalance-of-autonomic-tone-the-promise-of-intravascular-stimulation-of-autonomics/

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 https://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

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

 

Lev-Ari, A. 6/13/2012 Treatment of Refractory Hypertension via Percutaneous Renal Denervation

https://pharmaceuticalintelligence.com/2012/06/13/treatment-of-refractory-hypertension-via-percutaneous-renal-denervation/

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)

https://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

https://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

https://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/

 

Lev-Ari, A. 7/23/2012 Heart Remodeling by Design: Implantable Synchronized Cardiac Assist Device: Abiomed’s Symphony

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

 

Lev-Ari, A. (2006b). First-In-Man Stent Implantation Clinical Trials & Medical Ethical Dilemmas. Bouve College of Health Sciences, Northeastern University, Boston, MA 02115

 

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Accurate Identification and Treatment of Emergent Cardiac Events


Accurate Identification and Treatment of Emergent Cardiac Events

Author: Larry H Bernstein, MD, FCAP
In the immediately preceding article, I discussed the difficulties in predicting long-term safety for developing drugs, and the cost of failure in early identification.

It is not the same scale of issue as for the patient emergently presenting to the ED. Despite enormous efforts to reduce the development of and the complications of acute ischemia related cardiac events, the accurate diagnosis of the patient presenting to the emergency room is still, as always, reliant on clinical history, physical examination, effective use of the laboratory, and increasingly helpful imaging technology. The main issue that we have a consensus agreement that PLAQUE RUPTURE is not the only basis for a cardiac ischemic event. The introduction of  high sensitivity troponin tests has made it no less difficult after throwing out the receiver-operator characteristic curve (ROC) and assuming that any amount of cardiac troponin released from the heart is pathognomonic of an acute ischemic event.  This has resulted in a consensus agreement that

  • ctn measurement at a coefficient of variant (CV) measurement in excess of 2 Std dev of the upper limit of normal is a “red flag”
  • signaling AMI? or other cardiomyopathic disorder

This is the catch.  The ROC curve established AMI in ctn(s) that were accurate for NSTEMI – (and probably not needed with STEMI or new Q-wave, not previously seen) –

  1. ST-depression
  2. T-wave inversion
    • in the presence of other findings
    • suspicious for AMI

Wouldn’t it be nice if it was like seeing a robin on your lawn after a harsh winter?  Life isn’t like that.  When acute illness hits the patient may well present with ambiguous findings.   We are accustomed to relying on

  1. clinical history
  2. family history
  3. co-morbidities, eg., diabetes, obesity, limited activity?, diet?
    1. stroke and/or peripheral vascular disease
    2. hypertension and/or renal vascular disease
    3. aortic atherosclerosis or valvular heart disease
      • these are evidence, and they make up syndromic classes
  4. Electrocardiogram – 12 lead EKG (as above)
  5. Laboratory tests
    1. isoenzyme MB of creatine kinase (CK)… which declines after 12-18 hours
    2. isoenzyme-1 of LD if the time of appearance is > day-1 after initial symptoms (no longer used)
    3. cardiac troponin cTnI or cTnT
      • genome testing
      • advanced analysis of EKG

This may result in more consults for cardiologists, but it lays the ground for better evaluation of the patient, in the long run.  When you look at the amount of information that has to be presented to the physician, there is serious need for improvement in the electronic medical record to benefit the patient and the caregivers.  Recently, we have a publication on a new test that has been evaluated, closely related to the C-reactive protein (CRP), a test that has generated much discussion over the effect of treatment for patients who have elevated CRP in the absence of increased LDL cholesterol, diabetes, or obvious atherosclerotic comorbidities.  The serum pentraxin 3 test is related to cell mediated immunity, and an evaluation has been published in the Journal of Investigative Medicine.

Journal of Investigative Medicine Feb 2013; 61 (2): 278–285.
http://dx.doi.org/10.231/JIM.0b013e31827c2971

Serum Pentraxin 3 Levels Are Associated With the Complexity and Severity of Coronary Artery Disease in Patients With Stable Angina Pectoris
Karakas, Mehmet Fatih MD*; Buyukkaya, Eyup MD*; Kurt, Mustafa MD*; et al.
From the Departments of Cardiology and,Clinical Biochemistry, Mustafa Kemal University, Tayfur Ata Sokmen Medical School, Hatay, Turkey.
Reprints: Mehmet Fatih Karakas, MD, Antakya 31005, Turkey. E-mail: mfkarakas@hotmail.com.

Abstract
Background: Atherosclerosis is a complex inflammatory process. Although pentraxin 3 (PTX-3), a newly identified inflammatory marker, was associated with adverse outcomes in stable angina pectoris,

  • an association between PTX-3 and the complexity of coronary artery disease (CAD) has not been reported.

The aim of the present study is to assess

  • the association between the level of PTX-3 and
  • the complexity and severity of CAD assessed with
  • SYNTAX and Gensini scores in patients with stable angina pectoris.

Methods: The study population is 2 groups:

  • 161 patients with anginal symptoms and evidence of ischemia
    • who underwent coronary angiography and
  • 50 age- and sex- matched control subjects without evidence of ischemia .

Patients were grouped into 3 groups according to the complexity and severity of coronary lesions

  • assessed by the SYNTAX score (30 patients with a SYNTAX score of 0 were excluded).

Serum PTX-3 and high-sensitivity C-reactive protein (hs-CRP) levels were measured in both groups.

Results: The PTX-3 levels demonstrated

  • an increase from low to high SYNTAX groups (r = 0.72, P < 0.001).

Whereas the low SYNTAX group had statistically significantly higher PTX-3 levels when compared with the control group (0.50 ± 0.01 vs 0.24 ± 0.01 ng/mL, P < 0.001),

  • the hs-CRP levels were not different (0.81 ± 0.42 vs 0.86 ± 0.53 mg/dL, P = 0.96).
  • but  the intermediate SYNTAX group had higher hs-CRP levels compared with the low SYNTAX group (1.3 ± 0.66 vs 0.86 ± 0.53 mg/dL, P = 0.002).

Serum PTX-3 levels and hs-CRP levels were both correlated with the SYNTAX scores and Gensini scores (for SYNTAX: r = 0.87 [P < 0.001] and r = 0.36 [P = 0.01]; for Gensini: r = 0.75 [P < 0.001] and r = 0.27 [P = 0.002], respectively), and

  • according to the results of univariate and multivariate analyses, for “intermediate and high” SYNTAX scores, age, diabetes mellitus, low-density lipoprotein cholesterol, hs-CRP, and PTX-3
  • were found to be independent predictors, whereas
  • for the presence of “high” SYNTAX score only PTX-3 was found to be an independent predictor.
  • The receiver operating characteristic curve analysis further revealed that the PTX-3 level was
    • a strong indicator of high SYNTAX score with an area under the curve of 0.91 (95% confidence interval, 0.86–0.96).

Conclusions: Pentraxin 3, a novel inflammatory marker, was more tightly associated with the complexity and severity of CAD than hs-CRP and

    • it was found to be an independent predictor for high SYNTAX score.

The association between atherosclerosis and inflammation has been more understood during recent years. Currently, atherosclerosis is considered as a complex inflammatory process in which

    • leukocytes and inflammatory markers are involved.1

Several inflammatory markers

  1.  high-sensitivity C-reactive protein (hs-CRP),
  2. fibrinogen, and
  3. complement C3…. are associated with cardiovascular events.1–5

Pentraxin 3 (PTX-3), that resembles CRP both in structure and function,1 is produced both by

  • hematopoietic cells such as macrophages, dendritic cells, neutrophils, and by
  • nonhematopoietic cells such as fibroblasts and vascular endothelial cells.2

Plasma PTX-3 levels may be elevated in patients with

  1. vasculitis,6
  2. acute myocardial infarction,7,8 and
  3. systemic inflammation or sepsis,9
  4. psoriasis,
  5. unstable angina pectoris, and
  6. heart failure.10–13

Dubin et al14 reported that PTX-3 levels are associated with with adverse outcomes in stable angina pectoris (SAP). Despite reports about the association of PTX-3 and coronary artery disease (CAD),

an association between the level of PTX-3 and the complexity and severity of CAD is not established.15,16 Thus, the aim of this study was

  • to assess the association between the level of PTX-3 and the complexity and severity of CAD assessed with SYNTAX and Gensini scores in SAP patients.

MATERIALS AND METHODS

Of 211 patients were prospectively recruited,  161 SAP patients with evidence of ischemia (positive treadmill or myocardial perfusion scan) underwent coronary angiography for suspected CAD, and 50 age- and sex- matched outpatient subjects with a negative treadmill or myocardial perfusion scan test were taken as the control group. Patients were excluded if they had

  •  acute coronary syndrome
  • history of previous myocardial infarction;
  • coronary artery bypass grafting or percutaneous coronary intervention;
  • secondary hypertension (HT);
  • renal failure;
  • hepatic failure;
  • chronic obstructive lung disease and/or
  • manifest heart disease, such as
    • cardiac failure (left ventricular ejection fraction <50%),
    • atrial fibrillation, and
    • moderate to severe cardiac valve disease; and
    • SYNTAX score of zero

Similarly, patients were excluded with

  • infection,
  • acute stress, or chronic systemic inflammatory disease and
  • those who had been receiving medications affecting the number of leukocytes .

Thirty patients were excluded from the study because the coronary angiograms revealed normal coronary arteries (SYNTAX score of 0). All the participants included in the study were informed about the study, and they voluntarily consented to participate. The Serum PTX-3 level was measured on blood samples collected after 12-hour fast just prior to coronary angiography and kept at −80°C until the assays were performed. PTX3 was measured by enzyme immunoassay (EIA) using quantitative kit (human PTX-3/TSG-14 immunoassay, DPTX30; R&D Systems, Inc, Minneapolis, MN). The intra-assay and interassay coefficients of variation ranged from 3.8% to 4.4% and 4.1% to 6.1%, respectively (minimum detectable concentration, 0.025 ng/mL). High-sensitivity CRP was measured in serum by EIA (Immage hs-CRP EIA Kit; Beckman Coulter Inc, Brea, CA). Transthoracic echocardiography was performed, and biplane Simpson’s ejection fraction (%) was calculated before coronary angiography. Hypertension was defined as having at least 2 blood pressure measurements greater than 140/90 mm Hg or using antihypertensive drugs, whereas diabetes mellitus (DM) was defined as having at least 2 fasting blood sugar measurements greater than 126 mg/dL or using antidiabetic drugs. Smoking was categorized into current smokers and nonsmokers. Nonsmokers included ex-smokers who had quit smoking for at least 6 months before the study. Body mass index (BMI) values were calculated based on the height and weight of each patient. Medications used before the coronary angiography were noted. The study was approved by the local ethics committee.
SYNTAX and Gensini Scores
To grade the complexity of CAD, the SYNTAX score was used. Each coronary lesion with a stenosis diameter of 50% or greater in vessels of 1.5 mm or greater was scored. Parameters used in the SYNTAX scoring are shown in Table 1. The latest online updated version (2.11) was used in the calculation of the SYNTAX scores (www.syntaxscore.com).17 The SYNTAX score was classified as follows:

  1. low SYNTAX score (≤22),
  2. intermediate SYNTAX score (23–32)
  3. high SYNTAX score (≥33).

Table 1   http://images.journals.lww.com/jinvestigativemed/LargeThumb.00042871-201302000-00007.TT1.jpeg

The severity of CAD was determined by the Gensini score, which

  • measures the extent of coronary stenosis according to degree and location.18

In the Gensini scoring system,

  • larger segments are more heavily weighted ranging from 0.5 to 5.0
    • left main coronary artery × 5;
    • proximal segment of the left anterior descending coronary artery [LAD] × 2.5;
    • proximal segment of the circumflex artery × 2.5;
    • midsegment of the LAD × 1.5;
    • right coronary artery distal segment of the LAD,
    • posterolateral artery, and obtuse marginal artery × 1;
    • and others × 0.5.

The narrowing of the coronary artery lumen is rated

  1. 2 for 0% to 25% stenosis,
  2. 4 for 26% to 50%,
  3. 8 for 51% to 75%,
  4. 16 for 76% to 90%,
  5. 32 for 91% to 99%,
  6. 64 for 100%.

The Gensini index is the sum of the total weights for each segment. All angiographic variables of the SYNTAX and Gensini score were computed by

  • 2 experienced cardiologists who were blinded to the procedural data and clinical outcomes.

The final decision was reached by consensus when a conflict occurred.The number of diseased vessels with

  • greater than 50% luminal stenosis was scored from 1 to 3 (namely, 1-, 2-, or 3-vessel disease), and
  • a lesion greater than 50% in the left main coronary artery was regarded as a 2-vessel disease.

Statistical Analyses

Statistical analyses were conducted with SPSS 17 (SPSS Inc, Chicago, IL) software package program.
Continuous variables were expressed as mean ± SD or median ± interquartile range values, whereas categorical variables were presented as percentages.
The differences between normally distributed numeric variables were evaluated by Student t test or 1-way analysis of variance, whereas

  • non–normally distributed variables were analyzed by Mann-Whitney U test or Kruskal-Wallis variance analysis as appropriate.

χ2 Test was used for the comparison of categorical variables. Pearson test was used for correlation analysis.
To determine the independent predictors of “intermediate and high” SYNTAX scores and only “high” SYNTAX scores,

  • 2 different sets of univariate and multivariate analyses were performed
    • (in the first model SYNTAX cutoff was 22, whereas
    • in the second model SYNTAX cutoff was 33).

The standardized parameters that were found to have a significance (P < 0.10) in the univariate analysis were evaluated by stepwise logistic regression analysis.
Ninety-five percent confidence interval (CI) and odds ratio (OR) per SD increase were presented together. Interobserver and intraobserver variability for SYNTAX scores

  • was done by Bland-Altman analysis.

An exploratory evaluation of additional cut points was performed using the receiver operating characteristic (ROC) curve analysis.
All the P values were 2-sided, and a P < 0.05 was considered as statistically significant.
RESULTS
Baseline Characteristics
In total, 181 patients (50.2 ± 6.5 years, 52.5% were composed of males) were included in the study. Baseline clinical, angiographic, and laboratory characteristics of the patients
relative to SYNTAX score groups are shown in Table 2. Age, sex, HT, DM, BMI, and medication were not different between the groups. Baseline clinical and laboratory characteristics
of patients according to PTX-3 quartiles are shown in Table 3. The Bland-Altman analysis revealed that the degrees of intraobserver and interobserver variability for SYNTAX score
and Gensini score readings were 5% and 6% for SYNTAX and 8% and 9% for Gensini,
respectively.
Table 2   http://images.journals.lww.com/jinvestigativemed/Original.00042871-201302000-00007.TT2.jpeg
Table 3   http://images.journals.lww.com/jinvestigativemed/Original.00042871-201302000-00007.TT3.jpeg

The PTX-3 levels demonstrated an increase from the low SYNTAX group to the high SYNTAX group (r = 0.87, P < 0.001).
The low SYNTAX group had statistically significantly higher PTX-3 levels when compared with the control group (0.50 ± 0.01 vs 0.24 ± 0.01 ng/mL, P < 0.001); similarly,
the PTX-3 levels were higher in the high SYNTAX group than in both

  • the intermediate SYNTAX group (0.84 ± 0.08 vs 0.55 ± 0.01 ng/mL, P < 0.001) and
  • the low SYNTAX group (0.84 ± 0.08 vs 0.50 ± 0.01 ng/mL, P < 0.001).
  • there was no difference in levels of PTX-3 between the low and the intermediate SYNTAX group (0.50 ± 0.01 vs 0.55 ± 0.01 ng/mL, P = 0.09).

On the other hand, there was no difference in levels of hs-CRP between the control and the low SYNTAX group (0.81 ± 0.42 vs 0.86 ± 0.53 mg/dL, P = 0.96).
The intermediate SYNTAX group had statistically significantly higher hs-CRP levels

  • compared with the low SYNTAX group (1.3 ± 0.66 vs 0.86 ± 0.53 mg/dL, P = 0.002);
  • the hs-CRP levels were not different between the high SYNTAX group
    • and the intermediate SYNTAX group. (1.3 ± 0.66 vs 1.3 ± 0.43 mg/dL, P = 0.99).

Univariate correlation analysis revealed a positive correlation between serum PTX-3 levels and hs-CRP levels with

  • the SYNTAX and Gensini scores
    • for SYNTAX: r = 0.87 [P < 0.001] and r = 0.36 [P = 0.01];
    • for Gensini: r = 0.75 [P < 0.001] and r = 0.27 [P = 0.002],  (Fig. 1).

In addition to that, the Gensini and SYNTAX scores are found to be well correlated with each other (r = 0.80, P < 0.001).
When the SYNTAX score was taken as continuous variable, multivariate linear regression analysis revealed that

  • the SYNTAX score was correlated with PTX-3 and hs-CRP (for PTX-3: β = 0.84 [P < 0.001]; hs-CRP: β =0.08 [P = 0.032]).

Figure 1   http://images.journals.lww.com/jinvestigativemed/Original.00042871-201302000-00007.FF1.jpeg

For determining the predictors of intermediate and high SYNTAX scores and only-high SYNTAX scores,

  • 2 different sets of univariate and multivariate analyses were performed among the patients who underwent coronary angiography.

For predicting the intermediate and high SYNTAX scores, the SYNTAX score was dichotomized into

  • high (score ≥22) and
  • low (<22) groups,

whereas for predicting the only-high SYNTAX scores, the SYNTAX score was dichotomized into

  • 2 groups with a score of 33 or greater and a score of less than 33.

In the first multivariate analysis (where SYNTAX cutoff was 22), the parameters showing significance in the univariate analysis

  • age,
  • sex,
  • HT,
  • DM,
  • low-density lipoprotein cholesterol [LDL-C],
  • hs-CRP,
  • PTX-3

were evaluated by multivariate analysis to determine the

  • independent predictors of intermediate and high SYNTAX scores.

In the univariate analysis, higher values of

  • age (OR, 1.5 [95% CI, 1.1–2.0]; P = 0.01),
  • LDL-C (OR, 1.3 [95% CI, 0.98–1.8]; P = 0.068),
  • hs-CRP (OR, 2.6 [95% CI, 1.8–3.8]; P < 0.001), and
  • PTX-3 (OR, 13.6 [95% CI, 6.4–28.9]; P < 0.001)
    • were associated with higher SYNTAX scores,
  • HT (OR, 0.44 [95% CI, 0.24–0.80]; P = 0.008) and
  • DM (OR, 0.48 [95% CI, 0.25–0.91]; P = 0.02)
    • were associated with lower SYNTAX scores.

In the multivariate analysis – age, DM, LDL-C, hs-CRP, and PTX-3 – were found to be

  • independent predictors of “intermediate to high” SYNTAX score (Table 4).

Increased

  • age (OR, 2.5 [95% CI, 1.3–4.8]; P = 0.007),
  • LDL-C (OR, 2.8 [95% CI, 1.5–5.2]; P = 0.001),
  • hs-CRP (OR, 3.3 [95% CI, 1.8–6.1]; P < 0.001), and
  • PTX-3 (OR, 35.4 [95% CI, 10.1–123.6]; P < 0.001)
    • were associated with increased SYNTAX scores,

whereas DM (OR, 0.08 [95% CI, 0.02–0.33]; P < 0.001) was associated with lower SYNTAX score (Table 4).

In the second univariate and multivariate analyses (where SYNTAX cutoff was 33),

  • the parameters that showed significance in the univariate analysis were age, LDL-C, glucose, hs-CRP, and PTX-3.
  • In the univariate analysis, increased
    • age (OR, 1.5 [95% CI, 1.0–2.3]; P = 0.05),
    • LDL-C (OR, 1.5 [95% CI, 0.97–2.2]; P = 0.07),
    • hs-CRP (OR, 1.4 [95% CI, 0.97–2.1]; P = 0.072), and
    • PTX-3 (OR, 18.5 [95% CI, 6.6–51.8]; P < 0.001)
      • were found to be associated with increased SYNTAX scores.

When these parameters were evaluated with multivariate analysis, only PTX-3 (OR, 18.4 [95% CI, 6.2–54.2]; P < 0.001)

    • was found to be an independent predictor for high SYNTAX score (Table 4).

Table 4   http://images.journals.lww.com/jinvestigativemed/Original.00042871-201302000-00007.TT4.jpeg

The ROC curve analysis further revealed that the PTX-3 level was a strong indicator of high SYNTAX score with

  • an area under the curve (AUC) of 0.91 (95% CI, 0.86–0.96) (Fig. 2).

The optimal cutoff of PTX-3 for the high SYNTAX score was 0.75 ng/mL.
Sensitivity, specificity, positive predictive value, and negative predictive value to identify high SYNTAX score for the PTX-3 level

  • were 90%, 84%, 97%, and 60%, respectively.
  • the ROC curve analysis of PTX-3 for intermediate-high SYNTAX score revealed that the AUC value was 0.82 (95% CI, 0.75–0.89).

The optimal threshold of PTX-3 level that

  • maximized the combined specificity and sensitivity to predict
    • intermediate to high SYNTAX score was 0.73 ng/mL.

For the cutoff value of 0.73 ng/mL, sensitivity, specificity, positive predictive value, and negative predictive value

  • to identify intermediate-high SYNTAX score were 56%, 98%, 97%, and 56%, respectively.

Figure 2   http://images.journals.lww.com/jinvestigativemed/Original.00042871-201302000-00007.FF2.jpeg

In the ROC analysis of hs-CRP for high SYNTAX scores, the AUC value was found to be 0.68 (95% CI, 0.59–0.77; P < 0.001).
The optimal threshold of hs-CRP that maximized the combined specificity and sensitivity to predict for high SYNTAX scores was 0.89 mg/dL.
Similarly, the ROC analysis of hs-CRP for the intermediate-high SYNTAX scores revealed an AUC of 0.74 (95% CI, 0.65–0.83; P = 0.001).
The cutoff value of hs-CRP to predict the intermediate-high SYNTAX scores with a maximized sensitivity and specificity was 0.66 mg/dL.
DISCUSSION
In this particular study, we investigated the relationship between the serum PTX-3 level and the severity of CAD

  • assessed by SYNTAX and Gensini scores in patients with SAP.

The PTX-3, was significantly higher than control group in the patients with CAD, and the serum PTX-3 levels

  • were associated with the SYNTAX and Gensini scores.

When compared with the hs-CRP, the PTX-3 was found to be more tightly associated with the complexity and severity of CAD in the patients with SAP.
Pentraxin 3, an acute-phase reactant that is functionally and structurally similar to CRP,1 is produced both by different kinds of cells such as

  • macrophages, dendritic cells, neutrophils, fibroblasts, and vascular endothelial cells.2
  • Pentraxin 3 is released following the inflammatory stimuli19; therefore, it may reflect the local inflammatory status in tissues.20

Serum PTX-3 levels were shown to be elevated in patients with

  • vasculitis,6 acute myocardial infarction,7,8 and systemic inflammation or sepsis,9 psoriasis, unstable angina pectoris, and heart failure.10–13

Higher PTX3 levels were reported to be associated with worse cardiovascular outcomes

  1. after acute coronary syndromes,8,21
  2. in the elderly people without known cardiovascular disease22 and
  3. associated with overall mortality in patients with stable coronary disease,
  4. independent of systemic inflammation.14

There are 2 reports investigating the association of PTX-3 level and the atherosclerotic burden.15,16 In one of these reports,

  • Knoflach et al.15 took B-mode ultrasonography as the atherosclerosis index.

They did not provide any information about coronary anatomy, and in the other report, Soeki et al.16 evaluated 40 patients who

  • underwent coronary angiography and measured their Gensini scores.

However, in none of the studies were the SYNTAX score and Gensini score used together to assess the degree of coronary atherosclerotic burden.
To our knowledge, this is the first report that showed the association of PTX-3 levels with the complexity and severity of CAD assessed by

  • SYNTAX and Gensini scores in patients with stable coronary disease.

Chronic low-grade inflammation has been thought to play a major role in the pathogenesis of atherosclerosis.23,24 Previous studies have reported that

  • levels of inflammatory markers such as hs-CRP, interleukin 6, and so on were increased in atherosclerosis.25

In the present study, both the SYNTAX and the Gensini scores were found to be correlated with serum PTX-3 and hs-CRP levels,

  • which in turn might reflect the degree of inflammation.

The SYNTAX score is an important tool in the classification of complex CAD26 and can give predictive information about short- and long-term outcomes

  • in patients with stable CAD who undergo percutaneous coronary intervention.27–30

Although the SYNTAX score is currently used for assessing the angiographic complexity of CAD rather than the severity of coronary atherosclerotic burden,

  • because more complex lesions tend to have more atherosclerotic burden,
  • the SYNTAX scores may also reflect the severity of coronary atherosclerotic burden.

The Gensini score, a well-known and widely used scoring system to evaluate the severity of CAD,18 was measured and

  • found to be well correlated with the SYNTAX score,
    • which supports the idea that angiographically more complex lesions tend to have more atherosclerotic burden.

When compared with the hs-CRP,

  • the PTX-3 seems to be more tightly associated with coronary disease burden (r = 0.36 vs r = 0.87).

We found out that the serum PTX-3 levels were higher than those in the control group, even in the low SYNTAX group.
On the other side, the serum hs-CRP levels were not different in the control and the low SYNTAX groups.
It was reported that the leukocytes mainly found in the coronary artery lumen are the neutrophils.31
It is also known that PTX-3 is stored in specific granules of neutrophils and released in response to inflammatory signals.32
The reason why serum PTX-3 levels seem more tightly associated with the coronary disease burden

  • when compared with serum hs-CRP levels may be the association of the
  • on-site presence of neutrophils and local inflammatory signal–triggered release of  PTX-3.

On the other hand, some human studies revealed that PTX-3 was produced more in areas of atherosclerosis and may contribute to its pathogenesis.31
Some other studies suggested that PTX-3 may be part of a protective mechanism in

  • vascular repair via inhibiting fibroblast growth factor 2 or some other growth factors responsible for smooth muscle proliferation.33,34

But still, the exact role of PTX-3 in the pathophysiology of atherosclerosis seems to be obscure for the time being. It is well established that atherosclerosis
has an inflammatory background in most of the cases. In addition to that, high blood CRP level is known as an indicator of future cardiovascular disease risk
even in healthy individuals.35 According to the results of univariate and multivariate analyses, for intermediate and high SYNTAX scores,

  1. age, DM, LDL-C, hs-CRP, and PTX-3 were found to be independent predictors, whereas for the presence of
  2. high SYNTAX score, only PTX-3 was found to be an independent predictor.

Because of the tighter association with atherosclerotic burden and the on-site vascular presence,

    • PTX-3 may be a promising candidate marker for vascular inflammation and future cardiovascular events.

LIMITATIONS
The major limitation of the current study is the number of patients included. It would be better to include more patients to increase the statistical power.

Besides, the SYNTAX and Gensini scores give us an idea about the complexity and severity of coronary atherosclerosis; however,
with coronary angiography alone, it is not possible to understand the extent of coronary plaque. In addition to that, the coronary anatomy of the
control group was not known, which was another limitation. Our selected population was free of other confounders of systemic inflammation, and
we did not have data about inflammatory markers other than hs-CRP, such as interleukin 6, tumor necrosis factor α, and so on, which may be accepted
as a limitation. Another limitation of the current study is that because there was no long-term follow-up of the patients, it did not provide any prognostic
data in terms of future cardiovascular events.
CONCLUSIONS
Pentraxin 3, a novel inflammatory marker, is associated with the complexity and severity of the CAD assessed by the SYNTAX and the Gensini scores in patients with SAP and seems to be more tightly associated with coronary atherosclerotic burden than hs-CRP.

REFERENCES

1. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005; 352: 1685–1695.
2. Brown DW, Giles WH, Croft JB. White blood cell count: an independent predictor of coronary heart disease mortality among a national cohort. J Clin Epidemiol. 2001; 54: 316–322.
3. Kannel WB, Anderson K, Wilson PW. White blood cell count and cardiovascular disease. Insights from the Framingham Study. JAMA. 1992; 267: 1253–1256.
4. Muscari A, Bozzoli C, Puddu GM, et al.. Association of serum C3 levels with the risk of myocardial infarction. Am J Med. 1995; 98: 357–364.
5. Ridker PM, Cushman M, Stampfer MJ, et al.. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997; 336: 973–979.
6. Fazzini F, Peri G, Doni A, et al.. PTX3 in small-vessel vasculitides: an independent indicator of disease activity produced at sites of inflammation. Arthritis Rheum. 2001; 44: 2841–2850.
7. Peri G, Introna M, Corradi D, et al.. PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans. Circulation. 2000; 102: 636–641.
8. Latini R, Maggioni AP, Peri G, et al.. Prognostic significance of the long pentraxin PTX3 in acute myocardial infarction. Circulation. 2004; 110: 2349–2354.
9. Muller B, Peri G, Doni A, et al.. Circulating levels of the long pentraxin PTX3 correlate with severity of infection in critically ill patients. Crit Care Med. 2001; 29: 1404–1407.
10. Bevelacqua V, Libra M, Mazzarino MC, et al.. Long pentraxin 3: a marker of inflammation in untreated psoriatic patients. Int J Mol Med. 2006; 18: 415–423.
11. Inoue K, Sugiyama A, Reid PC, et al.. Establishment of a high sensitivity plasma assay for human pentraxin3 as a marker for unstable angina pectoris. Arterioscler Thromb Vasc Biol. 2007; 27: 161–167.
12. Suzuki S, Takeishi Y, Niizeki T, et al.. Pentraxin 3, a new marker for vascular inflammation, predicts adverse clinical outcomes in patients with heart failure. Am Heart J. 2008; 155: 75–81.
13. Matsubara J, Sugiyama S, Nozaki T, et al.. Pentraxin 3 is a new inflammatory marker correlated with left ventricular diastolic dysfunction and heart failure with normal ejection fraction. J Am Coll Cardiol. 2011; 57: 861–869.
14. Dubin R, Li Y, Ix JH, et al.. Associations of pentraxin-3 with cardiovascular events, incident heart failure, and mortality among persons with coronary heart disease: data from the Heart and Soul Study. Am Heart J. 2012; 163: 274–279.
16. Soeki T, Niki T, Kusunose K, et al.. Elevated concentrations of pentraxin 3 are associated with coronary plaque vulnerability. J Cardiol. 2011; 58: 151–157.
17. SYNTAX working group. SYNTAX score calculator. Available at http://www.syntaxscore.com. Accessed May 20, 2012.
18. Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol. 1983; 51: 606.
20. Mantovani A, Garlanda C, Bottazzi B, et al.. The long pentraxin PTX3 in vascular pathology. Vascul Pharmacol. 2006; 45: 326–330.
21. Matsui S, Ishii J, Kitagawa F, et al.. Pentraxin 3 in unstable angina and non-ST-segment elevation myocardial infarction. Atherosclerosis. 2010; 210: 220–225.
22. Jenny NS, Arnold AM, Kuller LH, et al.. Associations of pentraxin 3 with cardiovascular disease and all-cause death: the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol. 2009; 29: 594–599.
26. Serruys PW, Morice MC, Kappetein AP, et al.. Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009; 360: 961–972.
27. van Gaal WJ, Ponnuthurai FA, Selvanayagam J, et al.. The SYNTAX score predicts peri-procedural myocardial necrosis during percutaneous coronary intervention. Int J Cardiol. 2009; 135: 60–65.
28. Lemesle G, Bonello L, de Labriolle A, et al.. Prognostic value of the SYNTAX score in patients undergoing coronary artery bypass grafting for three-vessel coronary artery disease. Catheter Cardiovasc Interv. 2009; 73: 612–617.
29. Capodanno D, Di Salvo ME, Cincotta G, et al.. Usefulness of the SYNTAX score for predicting clinical outcome after percutaneous coronary intervention of unprotected left main coronary artery disease. Circ Cardiovasc Interv. 2009; 2: 302–308.
30. Kim YH, Park DW, Kim WJ, et al.. Validation of SYNTAX (Synergy between PCI with Taxus and Cardiac Surgery) score for prediction of outcomes after unprotected left main coronary revascularization. JACC Cardiovasc Interv. 2010; 3: 612–623.
32. Jaillon S, Peri G, Delneste Y, et al.. The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps. J Exp Med. 2007; 204: 793–804.
33. Inforzato A, Baldock C, Jowitt TA, et al.. The angiogenic inhibitor long pentraxin PTX3 forms an asymmetric octamer with two binding sites for FGF2. J Biol Chem. 2010; 285: 17681–17692.
34. Camozzi M, Zacchigna S, Rusnati M, et al.. Pentraxin 3 inhibits fibroblast growth factor 2–dependent activation of smooth muscle cells in vitro and neointima formation in vivo. Arterioscler Thromb Vasc Biol. 2005; 25: 1837–1842.
35. Koenig W, Sund M, Frohlich M, et al.. C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. Circulation. 1999; 99: 237–242.
Keywords:  pentraxin 3; coronary artery disease; SYNTAX score; hs-CRP; inflammation

This is not the only recent finding that adds to the ability to evaluate these patients.  An as yet unpublished paper, expected to be published soon reports on

QRS fragmentation as a Prognostic test in Acute Coronary Syndrome,  and this reviewer expects the work to have a high impact.  The authors state that
QRS complex fragmentation is a promising bed-side test for assessment of prognosis in those patients.  Presence of fragmented QRS in surface ECG during ACS

  • represents myocardial scar or fibrosis and reflect severity of coronary lesions and a correlation between fQRS and depression of Lv function is established.

There are still other indicators that need to be considered, such as the mean arterial blood pressure.

There has been review and revisions of the guidelines for treatment of UA/NSTEMI within the last year, with differences being resolved among the Europeans and US.

Guidelines Updated for Unstable Angina/Non-ST Elevation Myocardial Infarction
According to the current study by Jneid and colleagues, new evidence is available on the management of unstable angina. This report replaces the 2007 American College of Cardiology Foundation/American Heart Association (ACC/AHA) Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (UA/NSTEMI) that were updated by the 2011 guidelines.

This guideline was reviewed by

  • 2 official reviewers each nominated by the ACCF and the AHA, as well as
  • 1 or 2 reviewers each from the American College of Emergency Physicians; the Society for Cardiovascular Angiography and Interventions; and the Society of Thoracic Surgeons; and
  • 29 individual content reviewers, including members of the ACCF Interventional Scientific Council.

The recommendations in this focused update are considered current

  • until they are superseded in another focused update or the full-text guideline is revised, and are official policy of both the ACCF and the AHA.

STUDY SYNOPSIS AND PERSPECTIVE
American cardiology societies have caught up with the European Society of Cardiology by

  • issuing their second update to the UA/NSTEMI guidelines in 18 months,
  • with the 2012 focused update replacing the 2011 guidelines [1].

The new recommendations include ticagrelor (Brilinta) as one of the options for antiplatelet therapy alongside prasugrel (Effient) and clopidogrel, bringing them in line with European.
The European guidance, however, gave precedence to the new antiplatelets over clopidogrel, whereas the American update “places ticagrelor on an equal footing with the other two antiplatelets available
this is the main reason for the update,” lead author Dr Hani Jneid (Baylor College of Medicine, Houston, TX), told heartwire . “Doctors now have a choice for second-line therapy after aspirin, depending on

  • the patient’s clinical scenario,
  • physician preference, and cost,”
    • now that clopidogrel is available generically.

The US decision to recommend

  • first prasugrel–in its 2011 update to the UA/NSTEMI guidelines–and
  • now ticagrelor as equivalent antiplatelet therapy choices to clopidogrel after aspirin
    • puts it somewhat at odds with the Europeans,
    • who reserve clopidogrel use for those who cannot take the newer agents.

The reason for the Americans differing stance is that because while they are faster acting and more potent–

  • the cost-effectiveness of the new agents is not known.
  • it isn’t clear how the efficacy observed in pivotal clinical trials of these agents is going to translate into real-world benefit,
  • and issues such as bleeding with prasugrel and compliance with a twice-daily drug such as ticagrelor remain concerns.

Bulk of 2012 Update on How to Use Ticagrelor
The 2012 ACCF/AHA focused update for the management of UA/NSTEMI stresses that

  • all patients at medium/high risk should receive dual antiplatelet therapy on admission,
  • with aspirin being first-line, indefinite therapy.

The bulk of the update centers on how to use ticagrelor which–

  • like prasugrel or clopidogrel–
  • can be added to aspirin for up to 12 months (or longer, at the discretion of the treating clinician).

Jneid notes it’s important to remember that prasugrel can only be used in the cath lab

  • in patients undergoing percutaneous coronary intervention (PCI),
  • whereas ticagrelor, like clopidogrel, can be used in medically managed or PCI patients.

And he emphasizes that, in line with the FDA’s black-box warning on ticagrelor,

The 81-mg aspirin dose is also considered a reasonable option in preference to a higher maintenance dose of 325 mg in

  • any acute coronary syndrome (ACS) patient following PCI, he adds, as
  • this strategy is believed to result in equal efficacy and lower bleeding risk.

With regard to how long antiplatelet therapy should be stopped before planned cardiac surgery, the recommendation is

  • five days for ticagrelor–the same as that advised for clopidogrel.
  • and seven days prior to surgery for prasugrel.

Jneid also highlights other important recommendations from the 2011 focused update carried over to 2012:

It is “reasonable” to proceed with cardiac catheterization and revascularization within

  • 12–24 hours of admission in initially stable, very high-risk patients with ACS.

An invasive strategy is “reasonable” in patients with

  • mild and moderate chronic kidney disease.

In those with diabetes hospitalized with ACS, insulin use should target glucose levels <180 mg/dL,

  • a less-intensive reduction than previously recommended.

Platelet function or genotype testing for clopidogrel resistance are both considered “reasonable”

  • if clinicians think the results will alter management,
  • but Jneid acknowledged that “there is not much evidence to support these assays” .

Committee Encourages Participation in Registries
Jneid observes that unstable angina and NSTEMI are “very common” conditions that carry a high risk of death and recurrent heart attacks,

  • which is why “the AHA and ACCF constantly update their guidelines so that physicians can provide patients with
  • the most appropriate, aggressive therapy with the goal of improving health and survival.”

To this end, he notes that the writing panel encourages

  • clinicians and hospitals to participate in quality-of-care registries designed
  • to track and measure outcomes, complications, and
  • adherence to evidence-based medicines.

Conflicts of interest for the writing committee are listed in the paper.

References

Jneid H, Anderson JL, Wright SR, et al. 2012 ACCF/AHA focused update on the guideline for the management of patients with unstable angina/non-ST elevation myocardial infarction (Updating the 2007 guideline and replacing the 2011 focused update): A report of the ACCF/AHA.
Circulation 2012;      Available at: http://circ.ahajournals.org/  http://dx.doi.org/10.1161/CIR0b013e3182566fleo
source   http://www.medscape.org

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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)
Age-standardised disability-adjusted life year...

Age-standardised disability-adjusted life year (DALY) rates from Cardiovascular diseases by country (per 100,000 inhabitants). (Photo credit: Wikipedia)

English: Cardiovascular disease: PAD therapy w...

English: Cardiovascular disease: PAD therapy with stenting Deutsch: PAVK Therapie: Kathetertherapie mit stenting (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)

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