Volume 73 Number 4 July 2006	back to contents

1Fellow, 2Instructor, and 3Professor, Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY.

Address all correspondence to Juan J. Badimon, Ph.D., Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, Box 1030, Mount Sinai School of Medicine, One East 100 th Street, New York, NY 10029; email: juan.badimon@mssm.edu

Grant Support: BGC: Ruth L. Kirschstein National Research Service Award (National Institutes of Health), and GV: Beca Formación en Investigación (Spanish Ministry of Health).

Adapted from a Grand Rounds presentation to the Department of Medicine, Mount Sinai School of Medicine, New York, NY on May 3, 2005, and updated as of June 2005.

Abstract

Despite considerable progress in the development of new therapies to control atherosclerosis and its complications, coronary heart disease (CHD) remains the number one cause of death in the Western world. While low high-density lipoprotein (HDL) has been associated with increased risk for CHD, raising HDL to reduce risk of disease has yet to be accepted as a standard therapeutic strategy. Currently available drugs that raise HDL (e.g., nicotinic acid, fibric acid derivatives, peroxisome proliferator-activated receptor agonists, and statins) also affect low-density lipoprotein (LDL) and other lipid constituents, making independent interpretation of their HDL-raising effect difficult to tease apart. Nevertheless, basic science studies suggest that HDL has multiple beneficial effects, and current efforts to develop new pharmacologic products with potent HDL-elevating effects may herald a day when HDL elevation becomes part of standard management of atherosclerotic diseases.

Key Words

High-density lipoprotein cholesterol, atherosclerosis, coronary heart disease, HDL elevating therapy, dyslipidemia, nicotinic acid, fibrate, statin, cholesterol ester transfer protein inhibitor, peroxisome proliferator-activated receptor ligands.

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