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[Unstable atherosclerotic plaque and acute coronary syndromes]
1II. interná klinika Lekárskej fakulty Univerzity Komenského v Bratislave, Slovakia.
Insights
Acute coronary syndromes stem from unstable atherosclerotic plaques causing coronary artery obstruction. Comprehensive prevention and therapy, focusing on endothelium protection and antithrombotic strategies, are crucial for managing these life-threatening cardiovascular events.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Pharmacology
Context:
- Acute coronary syndromes (ACS), including unstable angina pectoris, myocardial infarction, and sudden cardiac death, are major contributors to cardiovascular morbidity and mortality.
- The common pathway involves the disruption of atherosclerotic plaques, leading to thrombus formation, vasoconstriction, and dynamic coronary artery obstruction.
Purpose:
- To elucidate the pathogenetic mechanisms underlying acute coronary syndromes, emphasizing the role of unstable atherosclerotic plaques and thrombogenesis.
- To highlight the necessity for complex, multi-faceted prevention and therapeutic strategies for atherosclerosis and ACS.
Summary:
- ACS pathogenesis is linked to atherosclerotic plaque instability and thrombus formation, influenced by vascular, rheologic, thrombotic, and antithrombotic factors.
- The formation of unstable plaques is a critical determinant in the development of myocardial ischemia.
- Current research focuses on novel antithrombotic agents to address residual thrombosis and thrombin activity.
Impact:
- Effective prevention and therapy require a combination of antiatherogenic, endothelium-protective, cellulo-protective, antilipidogenic, and antithrombogenic approaches.
- Therapeutic strategies cannot be substituted; a comprehensive approach is essential for managing atherosclerosis and preventing ACS.
- Ongoing investigation into new antithrombotic substances is vital for improving outcomes in patients with or at risk for ACS.
Abstract:
Acute coronary syndromes (unstable angina pectoris, acute myocardial infarction, sudden cardiac death) participate significantly in cardiovascular and general morbidities and mortalities. Their common pathogenetic mechanism resides in the disturbance of the integrity of atherosclerotic plaque by a fissure, rupture, or ulceration and the origin of unstable atherosclerotic plaque by the formation of thrombi, which together with vasoconstriction, causes a varying degree of the dynamic obstruction of the coronary artery. Thrombogenesis takes place in coincidence with the factors of vascular wall, rheologic, thrombotic (proaggregatory and procoagulatory), and antithrombotic (antiaggregatory and anticoagulatory-fibrinolytic) factors. The formation of unstable atherosclerotic plaque is a critical point of the dissociation of both stable and unstable myocardial ischaemiae. The prevention and therapy of atherosclerosis must be complex, namely antiatherogenic, however most of all endothelium-protective, or cellulo-protective, antilipidogenic and antithrombogenic. They cannot be alternative; one therapy will not substitute another. Regarding the importance of even residual thrombosis and thrombin, new antithrombotic substances are being intensively investigated.