Pathophysiology and clinical significance of atherosclerotic plaque rupture.
Atherosclerotic plaque rupture and resulting intracoronary thrombosis are thought to account for most acute coronary syndromes. These syndromes include unstable angina, non-Q-wave myocardial infarction (MI) and Q-wave MI. In addition, many cases of sudden cardiac death may be attributable to atherosclerotic plaque disruption and its immediate complications. Our understanding of the atherosclerotic process and the pathophysiology of plaque disruption has advanced remarkably. Despite these advances, event rates after acute coronary syndromes remain unacceptably high. This review will focus on the pathophysiology underlying atherosclerotic plaque development, the sequellae of coronary plaque rupture, and current therapies designed to treat the acute coronary syndromes. It is hoped that as our understanding of the atherosclerotic plaque improves, treatment strategies for the acute coronary syndromes will advance.
Gutstein
D E
DE
Cardiovascular Institute, Mount Sinai Medical Center, New York, NY 10029-6574, USA.
Fuster
V
V
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology
D000319:Adrenergic beta-Antagonists; D000924:Anticholesteremic Agents; D005343:Fibrinolytic Agents