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Prothrombotic determinants of coronary atherothrombosis
Frederick L Ruberg1, Joseph Loscalzo
1Evans Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Insights
Acute coronary syndrome (ACS) results from plaque destabilization and thrombus formation. Modifying risk factors reduces atherosclerotic disease and the prothrombotic state, preventing atherothrombotic events.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Thrombosis
Background:
- Acute coronary syndrome (ACS) arises from thrombotic events in atherosclerotic coronary arteries.
- Plaque destabilization initiates thrombus formation, driven by local hemostatic imbalances.
- Established risk factors contribute to both atherosclerosis and a prothrombotic environment.
Purpose of the Study:
- To review traditional and emerging risk factors for ACS.
- To examine the pathological effects of these risk factors on local hemostatic balance.
- To highlight the role of risk factor modification in preventing atherothrombotic events.
Main Methods:
- Literature review of traditional and emerging risk factors for ACS.
- Analysis of the impact of risk factors on atherosclerotic plaque stability.
- Examination of the prothrombotic milieu within the atherosclerotic microenvironment.
Main Results:
- Risk factors promote atherosclerotic plaque development and instability.
- These factors create a prothrombotic state favoring thrombus formation.
- Aggressive risk factor modification mitigates these pathological processes.
Conclusions:
- Understanding risk factors' role in hemostasis is crucial for ACS prevention.
- Modifying risk factors reduces atherosclerotic disease progression.
- Targeting risk factors ameliorates the prothrombotic state, lowering atherothrombotic event risk.
Abstract:
An acute coronary syndrome (ACS) is the clinical manifestation of a thrombotic event occurring within a coronary artery narrowed by atherosclerosis. This atherothrombotic event is thought to occur following destabilizing changes within the atherosclerotic plaque, rendering it a surface on which thrombus can develop. The development and progression of this thrombus are determined by deleterious perturbations in the hemostatic equilibrium within the local environment of the plaque that favor thrombosis. Major risk factors for the development of atherosclerotic disease have been clearly established and are targets of aggressive modification in an effort to impede the development or slow the progression of disease. While conferring an increased risk for plaque development, these and other risk factors also establish a prothrombotic milieu within the microenvironment of the atherosclerotic plaque that favors thrombosis. This review seeks to address these traditional and emerging risk factors from the context of their pathologic effects on local hemostatic balance. Aggressive risk factor modification not only reduces atherosclerotic disease development and progression, but also ameliorates the prothrombotic state, and ultimately serves to reduce atherothrombotic events.