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Published on: June 29, 2015
Thrombosis in ischemic heart disease
1Department of Medicine, Mount Sinai Medical Center, New York, NY, USA.
Insights
Thrombus formation in atherosclerosis drives acute coronary syndromes and disease progression. Current treatments dissolve or prevent thrombus extension, while new strategies focus on plaque stabilization and reduced hypercoagulability.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Interventional Cardiology
Background:
- Atherosclerotic plaque disruption initiates thrombus formation, a key mechanism in acute coronary syndromes like myocardial infarction and unstable angina.
- Thrombus formation contributes to chronic atherosclerotic disease progression and restenosis after coronary angioplasty.
- Current therapeutic strategies for thrombus involve pharmacological agents and intracoronary interventions.
Purpose of the Study:
- To review the pathogenetic mechanisms of thrombus formation in atherosclerosis.
- To outline current therapeutic approaches for managing intracoronary thrombus.
- To discuss emerging strategies for the primary prevention of thrombus formation.
Main Methods:
- Literature review of pathogenetic mechanisms of thrombus formation.
- Analysis of current pharmacological and interventional treatments for thrombus.
- Examination of ongoing and recent clinical trials for plaque stabilization and hypercoagulability reduction.
Main Results:
- Thrombus formation is central to myocardial infarction (arterial occlusion) and unstable angina (mural thrombus).
- Therapeutic interventions aim to prevent thrombus extension, dissolve fibrin, inhibit platelet aggregation, or mechanically open arteries.
- Primary prevention strategies, including plaque stabilization and reducing hypercoagulability, are under investigation.
Conclusions:
- Thrombus formation is a critical determinant in acute coronary syndromes and atherosclerotic disease progression.
- Effective management requires a combination of antithrombotic therapies and revascularization techniques.
- Future research focuses on primary prevention through plaque modification and modulation of coagulation pathways.
Abstract:
Thrombus formation on a fissured or disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression and in restenosis following coronary angioplasty. Therapeutic measures to treat thrombus rely on the ability of drugs to either prevent thrombus extension, dissolve its fibrin component, or prevent further platelet aggregation. Other measures rely on the ability of intracoronary techniques to open coronary arteries. The primary prevention of intracoronary thrombus formation is evolving. Measures to stabilize plaques or to reduce hypercoagulability are being tested or have been tested in recent trials.
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