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Published on: August 18, 2016
Atherosclerosis and acute coronary events
S Dalager-Pedersen1, H B Ravn, E Falk
1Department of Cardiology and Institute of Experimental Clinical Research, Aarhus University Hospital, Denmark.
Insights
Coronary atherosclerosis becomes dangerous due to plaque rupture and subsequent thrombosis, not just plaque size. Identifying vulnerable plaques and optimizing antithrombotic therapy are key to preventing heart attacks and sudden death.
Area of Science:
- Cardiovascular Medicine
- Pathology
- Thrombosis Research
Background:
- Coronary atherosclerosis is typically benign unless plaque disruption occurs.
- Plaque rupture leads to thrombosis, causing serious clinical events like myocardial infarction and sudden death.
Purpose of the Study:
- To highlight the critical role of plaque composition and vulnerability in rupture.
- To emphasize the importance of thrombotic response in clinical outcomes.
- To advocate for improved methods in identifying and treating vulnerable plaques and optimizing antithrombotic strategies.
Main Methods:
- Review of existing literature on coronary atherosclerosis, plaque rupture, and thrombosis.
- Analysis of factors influencing plaque vulnerability and rupture triggers.
- Examination of the thrombotic response mechanisms, including platelet reactivity and coagulation/fibrinolysis balance.
Main Results:
- Plaque composition and vulnerability are more critical than plaque size or stenosis in determining rupture risk.
- Extensive plaque rupture can lead to severe clinical manifestations, including unstable angina, myocardial infarction, and sudden death.
- The thrombotic response is influenced by platelet reactivity and the hemostatic balance.
Conclusions:
- Vulnerable plaque identification and targeted treatment are crucial for preventing life-threatening coronary thrombosis.
- Optimizing antithrombotic treatment is essential for managing patients with coronary atherosclerosis.
- Further research is needed to develop novel strategies for vulnerable plaque detection and intervention.
Abstract:
Without thrombosis, coronary atherosclerosis is generally benign. It is plaque disruption, or fissuring, and subsequent thrombosis that make coronary atherosclerosis dangerous. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may cause the development of unstable angina, myocardial infarction, and sudden death. The risk of plaque disruption depends more on plaque type (composition) than on plaque size and stenosis severity. Both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The resultant thrombotic response, which affects the clinical presentation and outcome, is partly determined by the reactivity of the circulating platelets and the balance between the coagulation and fibrinolytic systems. To prevent and treat life-threatening coronary thrombosis, the medical community should seek new ways to identify and treat dangerous, vulnerable plaques and to optimize antithrombotic treatment.
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