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Pathogenesis of thrombosis in coronary artery disease
J H Chesebro1, U Rauch, V Fuster
1Cardiovascular Institute, Mount Sinai Medical Center, New York, NY 10029-6574, USA.
Insights
Acute coronary syndromes involve arterial thrombosis due to plaque disruption. Therapy with aspirin and anticoagulation reduces thrombotic events, myocardial infarction, and death.
Area of Science:
- Cardiovascular Medicine
- Hematology
Background:
- Acute coronary syndromes (ACS) are often caused by arterial thrombosis.
- Plaque disruption in vulnerable lesions initiates this process.
Purpose of the Study:
- To describe the mechanisms of arterial thrombosis in ACS.
- To evaluate the efficacy of acute and subacute antithrombotic therapy.
Main Methods:
- Analysis of pathological features of disrupted arterial lesions.
- Review of therapeutic strategies involving aspirin and anticoagulation (e.g., low-molecular-weight heparin).
Main Results:
- Plaque rupture with lipid-rich cores and thin fibrous caps triggers thrombosis.
- Therapy with aspirin plus anticoagulation significantly reduces thrombotic occlusion, myocardial infarction, and mortality.
Conclusions:
- Understanding plaque vulnerability is key to managing ACS.
- Combined aspirin and anticoagulation therapy is effective in preventing adverse thrombotic outcomes in ACS patients.
Abstract:
Arterial thrombosis in the acute coronary syndromes is precipitated by plaque disruption. This occurs in lesions with a large lipid core, a thin fibrous cap, macrophages infiltrating the fibrous cap, and a lipid core with a high tissue-factor content. This results in acute platelet deposition and rapid growth of mural thrombus which unfavorably influences the rheology of blood flow to produce more thrombus, and propagates additional thrombosis by the high thrombogenicity of the mural thrombus overlying the disrupted culprit arterial lesion. Acute therapy in the hospital and subacute therapy beyond the hospital phase for as long as 1.5-3 months with aspirin plus anticoagulation, such as low-molecular-weight heparin, or oral anticoagulation, reduces thrombotic occlusion, myocardial infarction, death, and need for coronary revascularization.