The role of the vulnerable plaque in acute coronary syndromes
- Frank Kolodgie, PhD
Frank Kolodgie, PhD
- Associate Director
- CVPath Institute, Inc.
- Aloke Finn, MD
Aloke Finn, MD
- Associate Professor of Medicine
- University of Maryland
- Medical Director
- CVPath Institute Inc
- Renu Virmani, MD
Renu Virmani, MD
- President & Medical Director
- CVPath Institute, Inc.
- Clinical Professor of Pathology
- Georgetown University
- Clinical Professor of Pathology
- George Washington University
- Section Editors
- Christopher P Cannon, MD
Christopher P Cannon, MD
- Section Editor — Coronary Heart Disease
- Professor of Medicine
- Harvard Medical School
- Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
- Section Editor — Coronary Heart Disease
- Professor of Cardiovascular Science
- Director, Cardiovascular and Cell Sciences Research Institute
- St. George's, University of London
- Peter Libby, MD
Peter Libby, MD
- Section Editor — Coronary Heart Disease
- Chief, Cardiovascular Medicine
- Brigham and Women's Hospital
- Professor, Harvard Medical School
Acute coronary syndromes (ACS) represent a spectrum in the clinical manifestations of acute coronary artery disease that includes unstable angina, acute myocardial infarction, and sudden coronary arrest. (See "Classification of unstable angina and non-ST elevation myocardial infarction" and "Criteria for the diagnosis of acute myocardial infarction" and "Pathophysiology and etiology of sudden cardiac arrest" and "Pathophysiology and etiology of sudden cardiac arrest", section on 'Myocardial ischemia and infarction'.)
Coronary artery thrombosis is the final pathogenic mechanism of most cases with ACS, as documented by angiographic and pathologic studies [1,2]. For example, coronary artery thrombi are found in 50 to 75 percent of cases of sudden cardiac death. (See "The role of platelets in coronary heart disease".)
The formation of an intraluminal clot is thought to result from the loss of integrity of a protective covering over an atherosclerotic plaque. In healthy arteries, a single layer of endothelial cells separates the blood from potentially thrombogenic components of the arterial medial layer. With atherogenic plaque in the underlying intima, there is loss of integrity of the protective covering, referred to as plaque rupture or erosion. This disruption allows blood to come in contact with the highly thrombogenic contents of the necrotic core of the plaque and luminal thrombosis to occur [3,4]. Intraluminal thrombosis after exposure of blood to calcified nodules has also been observed. Other mechanisms of ACS, such as a supply-demand mismatch, have been postulated.
Plaque rupture or erosion often occurs at sites where luminal stenosis is angiographically modest [5,6]. Autopsy studies of sudden coronary death victims have shown that approximately 40 percent of plaque ruptures occur at lesion sites with less than 50 percent diameter stenosis . In instances when rupture or erosion does not lead to thrombotic occlusion of the vessel, such an event may not necessarily cause symptoms and plaque healing results in plaque progression and greater luminal narrowing [8,9].
This topic focuses on the contribution of plaque rupture to the development of ACS as well as potential strategies to detect and treat vulnerable plaques. The underlying pathology and pathogenesis of coronary plaque progression, including rupture, are reviewed separately. (See "Pathology and pathogenesis of the vulnerable plaque".)
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- PLAQUE FEATURES RESPONSIBLE FOR ACUTE THROMBOSIS
- Plaque rupture
- Plaque erosion
- Calcified nodule
- PLAQUE MORPHOLOGY IN ACUTE CORONARY SYNDROMES
- Sudden cardiac death
- Acute myocardial infarction
- Unstable angina
- Age and sex differences
- Other correlates
- Repeat plaque ruptures
- OBSERVATIONS IN PATIENTS WITH PLAQUE RUPTURE
- VULNERABLE PLAQUES AND FUTURE RUPTURE
- Identification of vulnerable plaque by CT
- Natural history
- RISK FACTORS AND FATAL PLAQUES
- STATIN THERAPY