Volume 73 Number 6 October 2006	back to contents

1Cardiology Fellow, Zena and Michael A. Wiener Cardiovascular Institute Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, and 2Assistant Professor of Medicine and Cardiology and Director, Advanced Heart Failure and Transplant Program, Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY.

Address all correspondence to Satish R. Tiyyagura, M.D., Cardiology, Box 1030, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029-6574; email: satish.tiyyagura@mssm.edu

Abstract

Medical advances in the care of cardiac patients have resulted in more patients surviving an acute myocardial infarction (MI) than ever before. Each year hundreds of thousands of these survivors undergo remodeling of their left ventricle and often progress to clinical congestive heart failure. The extent of remodeling has been linked to the size of the infarct, whether or not the myocardium has been revascularized, and the control of loading conditions. The extent of infarction can be measured several ways, including the amount of enzyme released as well as infarct imaging with nuclear perfusion or magnetic resonance imaging. Methods to prevent adverse remodeling of the ventricle have included pharmacotherapy with beta-blockers, nitrates, and modulators of the renin-angiotensin-aldosterone system. Surgical intervention has proven useful for select patients with aneurysmal areas of remodeling. Researchers are now investigating several approaches to preventing and reversing cardiac remodeling. These include the use of stem cells to regenerate myocardium and post-infarct pacing to prevent remodeling. Improved therapies are needed to help reduce the number of patients progressing from myocardial infarction to end-stage heart failure.

Key Words

Heart failure, left ventricle, remodeling, myocardial infarction.

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