PLAQUE DISRUPTION AND THROMBOSIS : Potential Role of Inflammation and Infection - 08/09/11
Resumen |
Ischemic heart disease, a consequence of coronary atherosclerosis, is the leading cause of death in the United States and developing countries. The clinical manifestations of coronary atherosclerosis range from asymptomatic state and stable angina, to acute coronary syndromes, such as unstable angina, acute myocardial infarction (MI), and many cases of sudden cardiac death. Acute coronary events are the first clinical expression of coronary atherosclerosis in 30% to 40% of cases. A better understanding of the pathophysiology of acute coronary syndromes could provide improved preventive and therapeutic strategies against coronary artery disease.
Recent studies have challenged the old paradigm, which was based on the notion that coronary syndromes resulted from gradual and progressively luminal obstruction (stenosis) caused by growth of the atherosclerotic plaque. In the new paradigm, plaque disruption and thrombosis, the vulnerability to which is determined by intrinsic characteristics of the plaque (plaque vulnerability) and extrinsic triggers rather than the stenosis severity, are the most important determinants of the more lethal clinical manifestations of coronary atherosclerosis.* Coronary artery disease progresses in a nonlinear and often unpredictable fashion leading to a rapid worsening of coronary luminal obstruction, including the sudden development of total or near total occlusion. This rapid change is largely related to superimposition of a thrombus on top of a disrupted plaque.25 Several studies have demonstrated a high prevalence of coronary thrombosis in acute coronary syndromes with an underlying substrate of plaque-cap fissure or rupture in 60% to 80% or superficial plaque-endothelial erosions in 20% to 40%.* Serial angiography has revealed an interesting angiographic-clinical paradox whereby 60% to 70% of acute coronary syndromes (and by inference plaque disruptions with thrombosis leading to total or subtotal occlusion) evolve from lesions that are non–flow-limiting with only a mild to moderate luminal stenosis even though severely stenotic lesions are more likely to progress to total occlusion over time.1, 2, 36, 61 Stress testing in patients with known chronic coronary artery disease has also shown that MI often occurs in coronary territories that did not produce stress-induced ischemia months prior to development of MI.77 The apparent paradox may be largely explained by the fact that mildly stenotic lesions outnumber the severely stenotic lesions by a factor of 5 to 10 and that angiography often underestimates the extent of the plaque as well as the severity of anatomic cross-sectional narrowing that is observed in autopsy studies.82 Furthermore, a rapid transition of a mildly stenotic lesion to total occlusion is more likely to result in a clinical event, because of a low likelihood of protective collaterals, compared with when a severely stenotic lesion becomes totally occluded. Finally, mildly obstructive plaques are often large and may be subject to a greater degree of wall stress because of a larger luminal diameter.62, 81, 96
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| Address reprint requests to Prediman K. Shah, MD, Division of Cardiology and the, Atherosclerosis Research Center, Room 5347, Cedars-Sinai Medical Center, Los Angeles, CA 90048, e-mail: [email protected] |
Vol 17 - N° 2
P. 271-281 - mai 1999 Regresar al número
Artículo precedente
- HISTOPATHOLOGY OF PLAQUE RUPTURE
- Hanne Berg Ravn, Erling Falk
- THROMBOSIS AND COAGULATION ABNORMALITIES IN THE ACUTE CORONARY SYNDROMES
- Avi Fischer, David E. Gutstein, Valentin Fuster
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