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J Am Coll Cardiol, 2003; 41:7-14 © 2003 by the American College of Cardiology Foundation |
* Zena and Michael A. Wiener Cardiovascular Institute, The Mount Sinai School of Medicine, New York, New York, USA
Manuscript received May 7, 2002; accepted August 4, 2002.
*
Reprint requests and correspondence: Dr. Valentin Fuster, Mount Sinai School of Medicine, Box 1030, New York, New York 10029 USA.
valentin.fuster{at}mssm.edu
The propensity of plaque to disrupt is a major determinant of future ischemic events. Although they are distinct from one another, the atherosclerotic and thrombotic processes appear to be interdependent and may be integrated under the term "atherothrombosis." It is now clear that plaque composition, rather than the percent stenosis, is a major determinant of plaque vulnerability. Plaque disruption seems to depend on both passive and active phenomena and is not purely mechanical. Inflammation (activation of monocytes/macrophages) is a major determinant of both plaque vulnerability and thrombogenicity as they relate to plaque disruption. In one-third of acute coronary syndromes, there is, however, no plaque disruption but only superficial erosion of a markedly stenotic, fibrotic plaque. In these cases, thrombus formation may be exacerbated by a hyperthrombogenic state present in patients with certain systemic risk factors. The endothelium plays a pivotal role in vascular homeostasis and hemostasis. This dynamic organ regulates blood thrombogenicity as well as contractile, secretory, and mitogenic activities in the vessel wall. Some classic risk factors induce endothelial dysfunction by reducing the bioavailability of nitric oxide, increasing tissue endothelin-1, and activating pro-inflammatory signaling pathways. Vascular hemostasis, which is the maintenance of blood fluidity and vascular integrity, is achieved by counter-balancing the intrinsic clotting tendency of blood. As a consequence of the central role of endothelial cells in hemostatic control, a dysfunctional endothelium will generate a pro-thrombotic environment favoring development of atherosclerotic lesions and thrombotic complications.
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