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The pathogenesis of coronary plaques, thromboses, and hemorrhages: an evaluative review
Insights
Coronary plaque development involves cholesterol, thrombi, and trauma. Plaque rupture causes life-threatening thrombosis and hemorrhage, leading to potential canalization and new vascular issues.
Area of Science:
- Cardiovascular Science
- Pathology
- Medical Research
Background:
- Coronary plaque formation is a complex process.
- Plaque rupture is a critical event in cardiovascular disease.
- Thrombosis plays a key role in acute coronary events.
Purpose of the Study:
- To elucidate the mechanisms of coronary plaque development and rupture.
- To understand the role of thrombosis in acute coronary syndromes.
- To describe the consequences of coronary thrombosis and subsequent vascular changes.
Main Methods:
- Review of existing literature on coronary atherosclerosis.
- Analysis of pathological mechanisms of plaque formation and rupture.
- Description of thrombotic processes and vascular remodeling.
Main Results:
- Coronary plaque progression is driven by hemodynamic stress, cholesterol deposition, and thrombogenic factors.
- Plaque rupture, often due to necrosis and calcification, triggers acute thrombosis and hemorrhage.
- Survival from coronary thrombosis can lead to canalization, forming new vessels prone to further complications.
Conclusions:
- Coronary plaque rupture is the primary cause of acute coronary thrombosis and associated events.
- The development of luminal collateral vascularization post-thrombosis presents new risks.
- Understanding these processes is crucial for managing cardiovascular disease.
Abstract:
The initial appearance and continuous development of a coronary plaque depends on a combination of hemodynamic trauma, deposition of excess cholesterol, and accretion and incorporation of thrombogenic elements as well as fully formed mural thrombi. Plaques become life-threatening when rupture of their intimal surface due to internal necrosis and calcification leads to acute thrombosis and/or intramural hemorrhage. Although infarcts can and do occur in the absence of acute thrombi, the latter are caused not by the occurrence of infarcts, but almost always by plaque rupture. Following the occurrence of and survival from an acute occlusive coronary thrombosis, canalization of the thrombus frequently takes place, leading to the formation of a "luminal collateral vascularization." The vessels making up such complexes are prone in turn to hemorrhage and thrombosis.
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