Atherosclerotic plaque rupture and thrombosis. Evolving concepts

Area of Science:

• Cardiovascular Research
• Pathophysiology
• Thrombosis

Background:

• Atherosclerotic plaque rupture is fundamental to ischemic coronary syndromes, often involving plaques with mild-to-moderate stenosis and high lipid content.
• Macrophages play a critical role in atherogenesis, influencing plaque stability through lipoprotein metabolism and enzyme production.
• Plaque composition, configuration, and hemodynamic forces influence susceptibility to rupture, initiating thrombotic events.

Purpose of the Study:

• To elucidate the mechanisms underlying atherosclerotic plaque rupture and subsequent thrombotic vessel occlusion.
• To highlight the role of plaque characteristics and cellular components in the development of ischemic coronary syndromes.
• To review current and emerging therapeutic strategies targeting atherosclerosis and thrombosis.

Main Methods:

• Review of existing literature on atherosclerotic plaque rupture, thrombosis, and ischemic coronary syndromes.
• Analysis of the pathophysiological processes involved in plaque disruption and thrombus formation.
• Examination of the role of macrophages and lipoproteins in atherogenesis.

Main Results:

• Plaque rupture, particularly in lipid-rich, eccentrically located plaques, leads to thrombotic occlusion and myocardial infarction or unstable angina.
• Thrombus formation involves platelet activation and the coagulation cascade, with potential for reocclusion after lysis.
• Research is advancing on antithrombotic agents targeting thrombin, thromboxane, serotonin, and platelet receptors.

Conclusions:

• Atherosclerotic plaque rupture is a critical event in ischemic heart disease, driven by plaque vulnerability and thrombotic processes.
• Further research into atherogenesis and thrombosis is essential for developing effective therapeutic interventions.
• Novel antithrombotic therapies show promise for managing acute thrombotic events in atherosclerosis.