Objectives This study sought to ascertain the relationship of 9p21 locus with: 1) angiographic coronary artery disease (CAD) burden; and 2) myocardial infarction (MI) in individuals with underlying ...CAD. Background Chromosome 9p21 variants have been robustly associated with coronary heart disease, but questions remain on the mechanism of risk, specifically whether the locus contributes to coronary atheroma burden or plaque instability. Methods We established a collaboration of 21 studies consisting of 33,673 subjects with information on both CAD (clinical or angiographic) and MI status along with 9p21 genotype. Tabular data are provided for each cohort on the presence and burden of angiographic CAD, MI cases with underlying CAD, and the diabetic status of all subjects. Results We first confirmed an association between 9p21 and CAD with angiographically defined cases and control subjects (pooled odds ratio OR: 1.31, 95% confidence interval CI: 1.20 to 1.43). Among subjects with angiographic CAD (n = 20,987), random-effects model identified an association with multivessel CAD, compared with those with single-vessel disease (OR: 1.10, 95% CI: 1.04 to 1.17)/copy of risk allele). Genotypic models showed an OR of 1.15, 95% CI: 1.04 to 1.26 for heterozygous carrier and OR: 1.23, 95% CI: 1.08 to 1.39 for homozygous carrier. Finally, there was no significant association between 9p21 and prevalent MI when both cases (n = 17,791) and control subjects (n = 15,882) had underlying CAD (OR: 0.99, 95% CI: 0.95 to 1.03)/risk allele. Conclusions The 9p21 locus shows convincing association with greater burden of CAD but not with MI in the presence of underlying CAD. This adds further weight to the hypothesis that 9p21 locus primarily mediates an atherosclerotic phenotype.
Abstract Background 12-lead ECG is a critical component of initial evaluation of cardiac ischemia, but has traditionally been limited to large, dedicated equipment in medical care environments. ...Smartphones provide a potential alternative platform for the extension of ECG to new care settings and to improve timeliness of care. Objective To gain experience with smartphone electrocardiography prior to designing a larger multicenter study evaluating standard 12-lead ECG compared to smartphone ECG. Methods 6 patients for whom the hospital STEMI protocol was activated were evaluated with traditional 12-lead ECG followed immediately by a smartphone ECG using right (VnR) and left (VnL) limb leads for precordial grounding. The AliveCor™ Heart Monitor was utilized for this study. All tracings were taken prior to catheterization or immediately after revascularization while still in the catheterization laboratory. Results The smartphone ECG had excellent correlation with the gold standard 12-lead ECG in all patients. Four out of six tracings were judged to meet STEMI criteria on both modalities as determined by three experienced cardiologists, and in the remaining two, consensus indicated a non-STEMI ECG diagnosis. No significant difference was noted between VnR and VnL. Conclusions Smartphone based electrocardiography is a promising, developing technology intended to increase availability and speed of electrocardiographic evaluation. This study confirmed the potential of a smartphone ECG for evaluation of acute ischemia and the feasibility of studying this technology further to define the diagnostic accuracy, limitations and appropriate use of this new technology.
Mortality and morbidity in acute coronary syndromes (ACSs), caused principally by plaque erosion or rupture leading to thrombus formation and myocardial ischemia, have been reduced by a combination ...of antithrombotic agents (antiplatelet drugs and anticoagulants) and early revascularization. Aspirin is the foundation antiplatelet agent. New P2Y12 receptor inhibitors (prasugrel and ticagrelor) have clear benefits compared with clopidogrel for dual antiplatelet therapy, and cangrelor or vorapaxar, a thrombin receptor inhibitor, may be of value in specific settings. Anticoagulation uses 1 of 4 choices: bivalirudin, unfractionated heparin, enoxaparin, and fondaparinux. Moreover, some patients (such as those who have chronic atrial fibrillation) require triple therapy with aspirin, clopidogrel, plus an anticoagulant, frequently a vitamin K antagonist. New oral anticoagulants have been shown to be at least as effective as vitamin K antagonists in atrial fibrillation and led to fewer bleeding complications. Finally, the combination of aspirin, clopidogrel, and low-dose rivaroxaban has recently been approved by the European Medicines Agency (but not the Food and Drug Administration) for secondary prevention after ACS. Several strategies have been developed to balance the potential benefit of antithrombotic therapy against the risk of bleeding complications, for example, radial access in coronary angiography or restricted use of combination therapy, and others are under investigation, such as discontinuation of aspirin. This overview summarizes the current status of antithrombotic therapy in ACS and describes strategies currently explored to optimize its benefit/risk ratio.
(Level of Evidence: C) Intravenous administration of digitalis glycosides or nondihydropyridine calcium channel antagonists to patients with AF and a preexcitation syndrome may paradoxically ...accelerate the ventricular response and is not recommended.\n Slotwiner North Shore, Long Island Jewish Health Care System--Associate Director, Electrophysiology Laboratory None None None None None None William G. Stevenson Brigham and Women's Hospital, Cardiovascular Division--Director, Clinical Cardiac Electrophysiology Program None None None None None None Cynthia M. Tracy George Washington University Medical Center--Associate Director, Division of Cardiology; George Washington University Hospital--Director, Cardiac Service None None None None None None * This table represents the relevant relationships of committee members with industry that were reported orally at the initial writing committee meeting/conference call and updated in conjunction with all meetings and conference calls of the writing committee during the document development process. Committee Member Research Grant Speakers Bureau Stock Ownership Board of Directors Consultant/Advisory Member David S. Cannom Guidant AstraZeneca L.P. Guidant Medtronic None None Cardionet Cryden DSMB Guidant Harry J. Crijns AstraZeneca L.P. Guidant Medtronic Sanofi-aventis None None None AstraZeneca L.P. Sanofi-aventis Anne B. Curtis Medtronic St. Jude Guidant Medtronic St. Jude Medical None None Medtronic Kenneth A. Ellenbogen AstraZeneca Bristol Myers Squibb/Sanofi Partnership Guidant Medtronic Pfizer St. Jude Medical None None None Ablation Frontiers Biosense Webster Stereotaxis Valentin Fuster None None None GlaxoSmithKline GlaxoSmithKline Kereos Vasogen Jonathan L. Halperin None None None None Astellas Pharama AstraZeneca Bayer AG Healthcare Boehringer Ingelheim Daiichi Medical Research GlaxoSmithKline Sanofi-aventis Vasogen Jean-Yves Le Heuzey Sanofi-aventis Medtronic None None None 3M AstraZeneca L.P. GlaxoSmithKline Guidant G. Neal Kay None None None None None James E. Lowe None None None None None S. Bertil Olsson AstraZeneca L.P. None AstraZeneca L.P. Upjohn None AstraZeneca L.P. Boehringer-Ingelheim Eric N. Prystowsky Sanofi-aventis Reliant CardioNet CardioNet Bard Guidant Sanofi-aventis Stereotaxis Lars E. Ryden AFA Insurance AstraZeneca Pfizer Sanofi-aventis Swedish Heart Lung Foundation Occasional lectures at various meetings None Chair SBU Alert (A governmental Swedish HTA organization evaluating new medical technology Sanofi-aventis Juan Luis Tamargo None None None None None L. Samuel Wann None None None None None * DSMB, Data and Safety Monitoring Board.This table represents the actual or potential relationships with industry that were reported at the initial writing committee meeting on August 27, 2004.This table will be updated in conjunction with all meetings and conference calls of the writing committee.
Data routinely captured in clinical registries may be leveraged to enhance efficiency of prospective research. The quality of registry data for this purpose has not been studied, however. We ...evaluated the completeness and accuracy of perioperative data within congenital heart centers' local surgical registries.
Within 12 Pediatric Heart Network (PHN) sites, we evaluated 31 perioperative variables (and their subcategories, totaling 113 unique fields) collected via sites' local clinical registries for submission to The Society of Thoracic Surgeons Database, compared with chart review by PHN research coordinators. Both used standard STS definitions. Data were collected on 10 subjects for 2 to 5 procedures/site and adjudicated by the study team. Completeness and accuracy (agreement of registry data with medical record review by PHN coordinator, adjudicated by the study team) were evaluated.
A total of 56,500 data elements were collected on 500 subjects. With regard to data completeness, 3.1% of data elements were missing from the registry, 0.6% from coordinator-collected data, and 0.4% from both. Overall, registry data accuracy was 98%. In total, 94.7% of data elements were both complete/non-missing and accurate within the registry, although there was variation across data fields and sites. Mean total time for coordinator chart review per site was 49.1 hours versus 7.0 hours for registry query.
This study suggests that existing surgical registry data constitute a complete, accurate, and efficient information source for prospective research. Variability across data fields and sites also suggest areas for improvement in some areas of data quality.
2011 Writing Group Members*Writing group members are required to recuse themselves from voting on sections where their specific relationships with industry and other entities may apply; see Appendix ...1 for recusal information Thom W. Rooke, MD, FACC, ChairdaggerACCF/AHA Representative Alan T. Hirsch, MD, FACC, Vice Chair* Sanjay Misra, MD, FAHA, FSIR, Vice Chair*double daggerSociety of Interventional Radiology Representative Anton N. Sidawy, MD, MPH, FACS, Vice Chair§Society for Vascular Surgery Representative Joshua A. Beckman, MD, FACC, FAHA*||Society for Vascular Medicine Representative Laura Findeiss, MDdouble dagger Jafar Golzarian, MDdagger Heather L. Gornik, MD, FACC, FAHA*dagger Jonathan L. Halperin, MD, FACC, FAHA*¶ACCF/AHA Task Force on Practice Guidelines Liaison Michael R. Jaff, DO, FACC*dagger Gregory L. Moneta, MD, FACSdagger Jeffrey W. Olin, DO, FACC, FAHA*#ACCF/AHA Task Force on Performance Measures Liaison James C. Stanley, MD, FACSdagger Christopher J. White, MD, FACC, FAHA, FSCAI***Society for Cardiovascular Angiography and Interventions Representative John V. White, MD, FACSdagger R. Eugene Zierler, MD, FACSdagger 2005 Writing Committee Members Alan T. Hirsch, MD, FACC, Chair Ziv J. Haskal, MD, FAHA, FSIR, Co-Chair Norman R. Hertzer, MD, FACS, Co-Chair Curtis W. Bakal, MD, MPH, FAHA Mark A. Creager, MD, FACC, FAHA Jonathan L. Halperin, MD, FACC, FAHA Loren F. Hiratzka, MD, FACC, FAHA, FACS William R.C. Murphy, MD, FACC, FACS Jeffrey W. Olin, DO, FACC Jules B. Puschett, MD, FAHA Kenneth A. Rosenfield, MD, FACC David Sacks, MD, FSIR James C. Stanley, MD, FACS Lloyd M. Taylor, Jr, MD, FACS Christopher J. White, MD, FACC, FAHA, FSCAI John V. White, MD, FACS Rodney A. White, MD, FACS Table of Contents Introduction... .1569 Introduction This document is a compilation of the current American College of Cardiology Foundation/American Heart Association (ACCF/AHA) practice guideline recommendations for peripheral artery disease from the "ACC/AHA 2005 Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic)"*J Am Coll Cardiol 2006;47:1239-12, http://dx.doi.org/10.1016/j.jacc.2005.10.009 and the "2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (Updating the 2005 Guideline)".daggerJ Am Coll Cardiol 2011;58:2020-45, http://dx.doi.org/10.1016/j.jacc.2011.08.023 Updated and new recommendations from 2011 are noted and outdated recommendations have been removed. The ACCF/AHA Task Force on Practice Guidelines chooses to republish the recommendations in this format to provide the complete set of practice guideline recommendations in a single resource. Because this document includes recommendations only, please refer to the respective 2005 and 2011 articles for all introductory and supportive content until the entire full-text guideline is revised. (Level of Evidence: C) Individuals with asymptomatic lower extremity PAD should be identified by examination and/or measurement of the ankle-brachial index (ABI) so that therapeutic interventions known to diminish their increased risk of myocardial infarction (MI), stroke, and death may be offered.\n5.1 2.6.1.6 2.6.3 Sanjay Misra, Vice Chair Mayo Clinic: Division of Vascular and Interventional Radiology--Associate Professor of Radiology Johnson & Johnson None None None None None 2.6.3 Anton N. Sidawy, Vice Chair George Washington University--Professor and Chairman, Department of Surgery None None None None None None None Joshua A. Beckman Brigham and Women's Hospital Cardiovascular Division: Cardiovascular Fellowship Bristol-Myers Squibb Sanofi-aventis None None None None None 2.6.1.6 Laura K. Findeiss University of California, Irvine: Chief, Division of Vascular and Interventional Radiology--Associate Professor of Radiology and Surgery None None None None None None None Jafar Golzarian University of Minnesotra Medical School--Professor of Radiology and Surgery None None None None None None None Gregory L. Moneta Oregon Health & Science University--Chief and Professor of Vascular Surgery None None None None None None None Jeffrey W. Olin Mount Sinai School of Medicine--Professor of Medicine and Director of the Vascular Medicine Program Genzyme None None BMS/sanofi-aventis Colorado Prevention Center (DSMB) None Defendant; pulmonary embolism; 2009 2.6.1.6 James C. Stanley University of Michigan, Division of Vascular Surgery, University Hospital--Handleman Professor of Surgery None None None None None None None Christopher J. White Ochsner Clinical Foundation: Department of Cardiology--Chairman None None None Boston Scientific Neovasc St. Jude Medical None None 2.6.3 5.2.6 John V. White Advocate Lutheran General Hospital--Chief of Surgery None None None None None None None R. Eugene Zierler University of Washington--Professor of Surgery None None None None None None None * This table represents the relationships of writing group members with industry and other entities that were determined to be relevant to this document.
Background While beta-blockers increase survival in acute coronary syndrome (ACS) patients, the doses used in trials were higher than doses used in practice and recent data do not support an ...advantage of higher doses. We hypothesized that rates of major adverse cardiac events (MACE), all-cause death, myocardial infarction (MI), and stroke is equivalent for patients on low-dose and high-dose beta-blocker. Methods Patients admitted to Intermountain Healthcare with ACS and diagnosed with ≥70% coronary stenosis between 1994 and 2013 were studied (n = 7834). We classified low-dose as ≤25% and high-dose as ≥50% of an equivalent daily dose of 200 mg of metoprolol. Multivariate analyses were used to test association between low-dose vs high-dose beta-blocker dosage and MACE at 0–6 months and 6–24 months. Results 5287 ACS subjects were discharged on beta-blockers (87% low-dose, 12% high-dose and 1% intermediate-dose). The 6-month MACE outcomes rates for the beta-blocker dosage (low vs high) were not equivalent ( P = .18) (hazard ratio HR =0.76; 95% CI: 0.52–1.10). However, subjects on low-dose beta-blocker therapy did have a significantly decreased risk of MI for 0–6 months (HR = 0.53; 95% CI: 0.33–0.86). The rates of MACE events during the 6–24 months after presentation with ACS were equivalent for the two doses ( P = .009; HR = 1.03 95% CI: 0.70–1.50). Conclusions In ACS patients, rates of MACE for high-dose and low-dose beta-blocker doses are similar. These findings question the importance of achieving a high-dose of beta-blocker in ACS patients and highlight the need of further investigation of this clinical question.
A consensus panel was formed to review the rapidly emerging literature on the vascular-specific inflammatory marker lipoprotein-associated phospholipase A2 (Lp-PLA2 ) and to update recommendations ...for the appropriate use of this novel biomarker in clinical practice. The recommendations of the panel build on guidelines of the Adult Treatment Panel III (ATP III) and the American Heart Association/Centers for Disease Control (AHA/CDC) for cardiovascular risk assessment. Consistent with the ATP III guideline recommendations for the use of inflammatory markers, Lp-PLA2 is recommended as an adjunct to traditional risk assessment in patients at moderate and high 10-year risk. A simplified framework for traditional Framingham risk factor assessment is proposed. As a highly specific biomarker for vascular inflammation, elevated Lp-PLA2 levels should prompt consideration of increasing the cardiovascular risk category from moderate to high or high to very high risk, respectively. Because intensification of lifestyle changes and low-density lipoprotein (LDL) cholesterol lowering is beneficial in high-risk patients, regardless of baseline LDL cholesterol levels, consideration should be given to lowering the LDL cholesterol target by 30 mg/dL (1 mg/dL = 0.02586 mmol/L) in patients with high levels of Lp-PLA2 . Lp-PLA2 is recommended as a diagnostic test for vascular inflammation to better identify patients at high or very high risk who will benefit from intensification of lipid-modifying therapies. However, at this time Lp-PLA2 cannot be recommended as a target of therapy.
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