Mechanistic Insights and Clinical Implications of Atherosclerotic Plaque Progression

Atherosclerosis is a chronic, progressive disease of the arterial wall and a leading cause of cardiovascular morbidity and mortality worldwide. The development and progression of atherosclerotic plaques involve endothelial injury, LDL oxidation, foam cell formation, vascular smooth muscle cell proliferation, and extracellular matrix deposition, ultimately resulting in fibrous cap formation over lipid-rich cores. Plaque vulnerability is influenced by factors such as cap thickness, lipid content, intraplaque hemorrhage, and neovascularization, increasing the risk of acute events such as myocardial infarction and ischemic stroke. The heterogeneity of plaque morphology, driven by genetic, hemodynamic, and metabolic factors, complicates risk prediction but highlights the importance of individualized assessment. Advances in imaging modalities, including MRI, CT, and intravascular ultrasound, combined with computational modeling approaches such as finite element analysis and fluid-structure interaction, allow detailed evaluation of plaque biomechanics and rupture risk. Early detection and management of cardiovascular risk factors, alongside targeted therapeutic strategies addressing lipid levels, inflammation, and angiogenesis, are critical for reducing disease burden. Integrating mechanistic insights with precise diagnostics and patient-specific interventions offers a pathway toward improved prevention and treatment of atherosclerotic cardiovascular disease.

کلیدواژه ها:

Atherosclerosis ، Plaque Vulnerability ، Oxidized LDL ، Computational Modeling ، Cardiovascular Risk