Michael D. Winniford

2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery

Alice K. Jacobs, MD, FACC, FAHA, Chair Jeffrey L. Anderson, MD, FACC, FAHA, Chair-Elect Nancy Albert, PhD, CCNS, CCRN, FAHA Mark A. Creager, MD, FACC, FAHA Steven M. Ettinger, MD, FACC Robert A. Guyton, MD, FACC Jonathan L. Halperin, MD, FACC, FAHA Judith S. Hochman, MD, FACC, FAHA

2011 ACCF/AHA guideline for coronary artery bypass graft surgery: Executive summary

2011;58;2584-2614; originally published online Nov 7, 2011; J. Am. Coll. Cardiol. Winniford Joseph F. Sabik, Ola Selnes, David M. Shahian, Jeffrey C. Trost, and Michael D. A. Lange, Martin J. London, Michael J. Mack, Manesh R. Patel, John D. Puskas, Adolph M. Hutter, Jr, Michael E. Jessen, Ellen C. Keeley, Stephen J. Lahey, Richard Bridges, John G. Byrne, Joaquin E. Cigarroa, Verdi J. DiSesa, Loren F. Hiratzka, L. David Hillis, Peter K. Smith, Jeffrey L. Anderson, John A. Bittl, Charles R. Surgeons Surgery, Society of Cardiovascular Anesthesiologists, and Society of Thoracic Developed in Collaboration With the American Association for Thoracic Foundation/American Heart Association Task Force on Practice Guidelines Executive Summary: A Report of the American College of Cardiology 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: This information is current as of January 22, 2012 http://content.onlinejacc.org/cgi/content/full/58/24/2584 located on the World Wide Web at: The online version of this article, along with updated information and services, is

Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling

The cardiac extracellular matrix (ECM) fills the space between cells, supports tissue organization, and transduces mechanical, chemical, and biological signals to regulate homeostasis of the left ventricle (LV). Following myocardial infarction (MI), a multitude of ECM proteins are synthesized to replace myocyte loss and form a reparative scar. Activated fibroblasts (myofibroblasts) are the primary source of ECM proteins, thus playing a key role in cardiac repair. A balanced turnover of ECM through regulation of synthesis by myofibroblasts and degradation by matrix metalloproteinases (MMPs) is critical for proper scar formation. In this review, we summarize the current literature on the roles of myofibroblasts, MMPs, and ECM proteins in MI-induced LV remodeling. In addition, we discuss future research directions that are needed to further elucidate the molecular mechanisms of ECM actions to optimize cardiac repair.

Impact of Clinical and Therapeutic Factors on Incident Cardiovascular and Cerebrovascular Events in a Population‐Based Cohort of HIV‐Infected and Non–HIV‐Infected Adults

Cardiovascular and cerebrovascular (CVD) events/diseases are a common cause of non–acquired immunodeficiency syndrome (AIDS)‐related mortality in the aging human immunodeficiency virus (HIV)‐infected population. The incidence rate and clinical correlates of CVD in people living with HIV/AIDS compared to the general population warrants further investigation.

Cigarette Smoking and Incident Heart Failure: Insights From the Jackson Heart Study

Background: Cigarette smoking has been linked with several factors associated with cardiac dysfunction. We hypothesized that cigarette smoking is associated with left ventricular (LV) structure and function, and incident heart failure (HF) hospitalization. Methods: We investigated 4129 (never smoker n=2884, current smoker n=503, and former smoker n=742) black participants (mean age, 54 years; 63% women) without a history of HF or coronary heart disease at baseline in the Jackson Heart Study. We examined the relationships between cigarette smoking and LV structure and function by using cardiac magnetic resonance imaging among 1092 participants, cigarette smoking and brain natriuretic peptide levels among 3325 participants, and incident HF hospitalization among 3633 participants with complete data. Results: After adjustment for confounding factors, current smoking was associated with higher mean LV mass index and lower mean LV circumferential strain (P<0.05, for both) in comparison with never smoking. Smoking status, intensity, and burden were associated with higher mean brain natriuretic peptide levels (all P<0.05). Over 8.0 years (7.7–8.0) median follow-up, there were 147 incident HF hospitalizations. After adjustment for traditional risk factors and incident coronary heart disease, current smoking (hazard ratio, 2.82; 95% confidence interval, 1.71–4.64), smoking intensity among current smokers (≥20 cigarettes/d: hazard ratio, 3.48; 95% confidence interval, 1.65–7.32), and smoking burden among ever smokers (≥15 pack-years: hazard ratio, 2.06; 95% confidence interval, 1.29–3.3) were significantly associated with incident HF hospitalization in comparison with never smoking. Conclusions: In blacks, cigarette smoking is an important risk factor for LV hypertrophy, systolic dysfunction, and incident HF hospitalization even after adjusting for effects on coronary heart disease.

Modifying matrix remodeling to prevent heart failure

Abstract: In the USA, cardiovascular disease is the leading cause of morbidity and mortality, accounting for approximately 40% of all deaths. Myocardial infarction or its sequelae is the primary cause of cardiovascular disease death. Despite advances in novel therapeutic strategies over the past 30 years, heart failure morbidity and mortality remain high for the post-myocardial infarction patient. Extracellular matrix remodeling and its role in heart failure are explored in this chapter: the key players involved, current therapeutic options and future trends are discussed.

Elevated serum osteoprotegerin is associated with increased left ventricular mass index and myocardial stiffness

Aim Osteoprotegerin (OPG) is associated with a poor prognosis in patients with heart failure with preserved ejection fraction (HFpEF). OPG has also been associated with fibrosis and collagen cross-linking, which increase arterial and left ventricle (LV) myocardial stiffness. Little is known about the relation of OPG and LV structure and function in African-Americans who are disproportionately affected by HFpEF. Methods and results Our analysis included 1172 participants with preserved LV ejection fraction (>50%) from the African-American cohort in the Genetic Epidemiology Network of Arteriopathy Study (mean age 63 years, 72% female). We used diastolic wall strain indicator measured by echocardiography to assess LV myocardial stiffness. Diastolic wall strain was calculated as (LV posterior thickness at end-systole − LV posterior thickness at end-diastole)/LV posterior thickness at end-systole. Associations between OPG levels and indices of arterial and LV structure and function were evaluated by using generalized linear mixed models and adjusted for possible confounders. OPG levels were correlated with age, female sex, presence of hypertension and diabetes, and lower estimated glomerular filtration rate (P < 0.05 for all). Multivariable analysis revealed that higher OPG levels were associated with greater LV mass index, increased LV myocardial stiffness, and higher N-terminal prohormone brain natriuretic peptide levels (P < 0.05 for all). Conclusion In African-Americans, higher OPG levels were associated with characteristics common in patients with HFpEF and were significantly associated with known precursors to HFpEF. These findings indicate a potential role for OPG in the pathophysiology of HFpEF in African-Americans.