Pathogenesis of atherosclerosis

Area of Science:

• Cardiovascular Medicine
• Immunology
• Pathology

Background:

• Atherosclerosis is a chronic inflammatory disease of arteries, characterized by lipid accumulation and involving endothelial cells, leukocytes, and smooth muscle cells.
• The most severe outcomes of atherosclerosis, heart attack and stroke, result from superimposed thrombosis on plaques.
• The critical question is not the development of atherosclerosis but the transition from indolent plaque growth to acute thrombosis.

Purpose of the Study:

• To elucidate the pathogenesis of atherosclerosis and its link to thrombosis.
• To identify characteristics of rupture-prone plaques for potential in vivo detection.
• To explore strategies for preventing thrombosis and mitigating atherosclerosis complications.

Main Methods:

• Review of the pathogenesis of atherosclerosis, focusing on immunoinflammatory mechanisms.
• Analysis of the pathological features of ruptured plaques, including lipid core size, fibrous cap thickness, cellular composition, and associated vascular changes.
• Discussion of imaging modalities for detecting thrombosis-prone plaques.

Main Results:

• Plaque rupture is the primary cause of fatal coronary thrombi (76%), more common in men (80%) than women (60%).
• Ruptured plaques exhibit distinct features: large lipid-rich cores, thin fibrous caps with macrophages, angiogenesis, adventitial inflammation, and outward remodeling.
• These pathoanatomical features offer potential targets for in vivo imaging and detection of vulnerable plaques.

Conclusions:

• Understanding atherosclerosis pathogenesis is key to preventing thrombotic complications.
• Detection of thrombosis-prone plaques through their characteristic features is a promising strategy.
• Averting plaque rupture and thrombosis could significantly reduce the morbidity and mortality associated with atherosclerosis.