Pathophysiology of coronary thrombosis: role of plaque rupture and plaque erosion
1Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute, and Department of Medicine, Cedars Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA.
Insights
Coronary artery disease, a leading cause of death, involves plaque buildup in arteries. Stabilizing these plaques may reduce serious events like heart attacks and sudden death.
Area of Science:
- Cardiovascular Medicine
- Pathology
Background:
- Coronary artery disease (CAD) is a major global health concern, primarily caused by atherosclerotic plaques.
- Plaque disruption, leading to thrombus formation, precipitates acute coronary syndromes such as myocardial infarction and unstable angina.
Purpose of the Study:
- To elucidate the characteristics of vulnerable atherosclerotic plaques.
- To explore the implications of plaque stabilization on clinical outcomes in coronary artery disease.
Main Methods:
- Review of pathological features of disrupted and vulnerable plaques.
- Analysis of the relationship between plaque composition and clinical events.
Main Results:
- Vulnerable plaques exhibit outward remodeling, large lipid cores, thin fibrous caps, reduced collagen, and inflammation.
- Plaque stabilization, achieved through lipid-lowering and risk-factor modification, correlates with fewer acute vaso-occlusive events.
Conclusions:
- Understanding vulnerable plaque characteristics is crucial for managing CAD.
- Interventions targeting plaque stabilization show promise in reducing acute cardiovascular events.
Abstract:
Coronary artery disease is the leading cause of death in much of the western world. Atherosclerotic plaques in the coronary arteries contribute to luminal obstruction leading to myocardial ischemia; however, abrupt coronary artery occlusion most frequently results from superimposition of a thrombus on a disrupted plaque, leading to the most serious clinical manifestations of coronary artery disease, ie, unstable angina, acute myocardial infarction, and sudden death. Plaque that have undergone disruption and, by inference, plaques at risk for disruption (vulnerable plaques), tend to demonstrate outward vessel remodeling, contain a large lipid core, thinned out fibrous cap, reduced collagen content, and increased inflammatory cell infiltration. Plaque stabilization through change in plaque composition may be responsible for reduced frequency of acute vaso-occlusive events observed with lipid and other risk-factor modifying interventions.
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