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[Ischemic heart disease]
H Mokuno1, H Daida, H Yamaguchi
1Juntendo University, Division of Cardiology.
Insights
Atherosclerotic plaque rupture and thrombosis can cause coronary artery disease. Plaque composition and thrombus stability influence whether rupture leads to unstable angina or acute myocardial infarction.
Area of Science:
- Cardiovascular Pathology
- Atherosclerosis Research
- Thrombosis Mechanisms
Context:
- Atherosclerotic plaque rupture is a key event in cardiovascular disease progression.
- Plaque rupture and superimposed thrombosis are dynamic and can occur repeatedly.
- Healed ruptures often contribute to plaque growth without causing symptoms.
Purpose:
- To elucidate the mechanisms of atherosclerotic plaque rupture and thrombosis.
- To differentiate the pathogenesis of unstable angina and acute myocardial infarction based on thrombus characteristics.
- To identify factors contributing to plaque vulnerability and rupture.
Summary:
- Plaque rupture, particularly of soft, lipid-rich plaques with eccentric lipid cores, initiates thrombosis.
- Acute mural occlusive thrombi overlying plaque ruptures cause acute coronary syndromes.
- Thrombus composition, stability, vessel injury, and blood flow dynamics dictate clinical outcomes, differentiating unstable angina from acute myocardial infarction.
- Macrophages within plaques can promote rupture through protease release.
Impact:
- Understanding these mechanisms is crucial for developing targeted therapies for atherosclerosis and thrombosis.
- This research informs strategies to prevent acute coronary events.
- Identifies plaque characteristics and thrombus properties as critical determinants of clinical presentation and severity.
Abstract:
During the progression of early atherosclerotic lesions, atherosclerotic plaque rupture, with intraluminal thrombosis superimposed, which is one of the principle mechanisms of evolving atherosclerosis, may lead to thrombotic occlusion and ischemic coronary syndrome. Pathologic studies suggest that plaque rupture and overlying thrombi, which are dynamic and repetitive may frequently occur. In most cases, healed ruptures and incorporation of thrombi produce plaque progression without manifestation of clinical symptoms. However, acute mural occlusive thrombi, overlying plaque ruptures, cause unstable angina and acute myocardial infarction. The different pathogenesis between unstable angina and acute myocardial infarction might depend on the composition and stability of the thrombus resulting from the degree of vessel injury and blood flow. Soft lipid-rich plaques appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages in the plaque may also facilitate plaque rupture by releasing proteases.