Volume 71 Number 3 May 2004	back to contents

From the 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 100th Street, New York, NY 10029; email: juan.badimon@mssm.edu

Adapted from a Grand Rounds presentation to the Zena and Michael A. Wiener Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, NY, on December 9, 2002, and updated as of November 2003.

ABSTRACT
Crucial advances in our understanding of the pathogenesis of atherothrombosis, defined as atherosclerosis and its thrombotic complications, have been achieved during the past two decades. The historical hypothesis of pathogenesis (“lipid accumulation”) has evolved to integrate several factors contributing to the initiation and evolution of this complex disease. Endothelial dysfunction is considered to be the earliest event in atherogenesis. Inflammation and apoptosis play critical roles in its progression and onset. Tissue factor is postulated to be a central actor in determining plaque thrombogenicity. A hyperreactive state of the blood (”vulnerable blood”) may be responsible for one-third of all the acute coronary syndromes. This review will discuss emerging concepts in the pathogenesis of and therapeutic approaches to atherothrombotic disease.

KEY WORDS
Atherothrombosis, atherosclerosis, antithrombotic therapy, coronary artery disease, acute coronary syndromes, tissue factor, inflammation, apoptosis, endothelial dysfunction.

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