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Published on: June 4, 2021
[The hemostatic system in the acute coronary syndromes: physiopathological and therapeutic implications]
J A Páramo Fernández1, J Orbe Lopategui
1Servicio de Hematología, Clínica Universitaria, Facultad de Medicina, Universidad de Navarra, Pamplona. japaramo@anav.es
Insights
Acute coronary syndromes (ACS) involve plaque disruption and thrombus formation. Combining antithrombotic therapies significantly reduces ischemic events and prevents recurrences in ACS patients.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pathophysiology
Context:
- Acute coronary syndromes (ACS), including unstable angina and myocardial infarction, stem from vulnerable atherosclerotic plaque rupture.
- Atherothrombosis pathogenesis involves platelet activation and clotting cascade initiation at sites of endothelial injury.
- Tissue factor plays a critical role in initiating thrombin generation and fibrin formation, stabilizing platelet-rich thrombi.
Purpose:
- To elucidate the pathophysiological mechanisms underlying acute coronary syndromes.
- To highlight the role of platelet aggregation and the coagulation cascade in atherothrombosis.
- To underscore the therapeutic benefits of combined antithrombotic strategies in managing ACS.
Summary:
- ACS pathogenesis is driven by the interaction between disrupted atherosclerotic plaques and subsequent thrombus formation.
- Platelet adhesion, aggregation, and coagulation activation are key events following endothelial injury.
- Tissue factor initiates the coagulation cascade, leading to thrombin generation and fibrin clot formation to stabilize the thrombus.
Impact:
- Combined antithrombotic therapies, including fibrinolytics, antiplatelets, and anticoagulants, are crucial for managing ACS.
- These strategies significantly reduce ischemic events and prevent recurrent episodes in patients with ACS.
- Understanding atherothrombosis mechanisms informs the development of more effective ACS treatments.
Abstract:
The interaction between the vulnerable atherosclerotic plaque prone to disruption and thrombus formation is the cornerstone of acute coronary syndromes (ACS): unstable angina and acute myocardial infarction with and without ST-segment elevation. Platelet adhesion and aggregation and clotting activation, at the level of injured endothelium lacking thromborresistance properties, and directly implicated in the pathogenesis of atherothrombosis. Tissue factor emerges as the initial mechanism leading to thrombin generation and fibrin formation to stabilize the platelet-rich thrombus. The combination of several antithrombotic strategies, including fibrinolytics, antiplatelets (aspirin, clopidogrel, and GpIIb/IIIa antagonists), and anticoagulants (mainly low-molecular-weight heparins) has proven to be of great benefit in the reduction of ischemic events and in the prevention of recurrences after ACS.
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