Pathology and pathogenesis of the vulnerable plaque
- Frank Kolodgie, PhD
Frank Kolodgie, PhD
- Associate 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
- Aloke Finn, MD
Aloke Finn, MD
- Associate Professor of Medicine
- University of Maryland
- Medical Director
- CVPath Institute Inc
- Section Editors
- Christopher P Cannon, MD
Christopher P Cannon, MD
- Section Editor — Coronary Heart Disease
- Professor of Medicine
- Harvard Medical School
- 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 represent a clinical spectrum of acute coronary artery disease that includes unstable angina, acute myocardial infarction, and sudden coronary death.(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'.)
Most acute coronary syndromes are believed to result from the loss of integrity of a protective covering over an atherosclerotic plaque; this occurs with plaque rupture when the fibrous cap overlying the plaque gets disrupted or with erosion when the endothelial lining of the plaque is disturbed. This disruption of the protective covering allows blood to come in contact with the highly thrombogenic contents of the necrotic core (in cases of plaque rupture) or collagen of the plaque, which promotes the formation of luminal thrombus [1,2]. Intraluminal thrombosis after exposure of the blood to calcified nodules has also been observed. Acute coronary syndrome can also result from other mechanisms such as a supply-demand mismatch (so called type 2 myocardial infarction).
Autopsy studies have shown that when intraluminal thrombi are identified in patients with sudden cardiac death and acute myocardial infarction, the underlying pathology is rupture 55 to 75 percent of the time, erosion 25 to 40 percent of the time, and 2 to 7 percent for calcified nodules [1,3-10]. In vivo studies in patients presenting with ST-segment elevation myocardial infarction using high resolution optical coherence tomography intravascular imaging of culprit plaques have shown a similar distribution of plaque morphologies .
This topic focuses on the process of plaque progression and the development of the vulnerable plaque. The contribution of plaque rupture to the development of acute coronary syndromes, including the mechanisms of coronary thrombosis, and potential strategies to detect and treat rupture-prone vulnerable plaques, are discussed separately. (See "The role of the vulnerable plaque in acute coronary syndromes".)
PATHOLOGY OF CORONARY ATHEROSCLEROSIS
Atherosclerosis is a dynamic process with multiple stages: intimal thickening, fibrous cap atheroma (fibroatheroma) formation, thin-cap fibroatheroma formation, and plaque rupture (figure 1A-B) . To understand plaque rupture, it is useful to review the stages of development of a plaque .To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- PATHOLOGY OF CORONARY ATHEROSCLEROSIS
- Intimal thickening and intimal xanthoma
- Pathologic intimal thickening
- Fibrous cap atheroma
- Thin-cap fibroatheroma (vulnerable plaque)
- - Reconsideration of the definition
- Plaque rupture
- Plaque erosion
- Calcified nodule
- Healed rupture
- MECHANISMS OF PLAQUE PROGRESSION
- Inflammation and plaque progression
- Formation and expansion of the necrotic core
- Apoptosis and necrotic core expansion
- Intraplaque hemorrhage
- Coronary arterial remodeling
- MECHANISMS OF PLAQUE RUPTURE
- Collagen synthesis and breakdown in the fibrous cap
- Apoptosis and plaque rupture
- Local mechanical stress and plaque rupture
- MECHANISMS OF EROSION AND PROGRESSION