Atherosclerosis, which underlies most cases of coronary artery disease (CAD), is a chronic cardiovascular condition characterized by lipid deposition and persistent inflammation within the walls of large arteries. Over time, these pathological changes may lead to serious clinical outcomes, including myocardial infarction (MI) and stroke. Although atherosclerosis develops gradually over many years and is more commonly associated with older age, it remains a major cause of death worldwide, despite reductions in its incidence in certain regions. The development of atherosclerotic plaques involves the progressive accumulation of lipids, inflammatory cells, vascular smooth muscle cells, and cellular debris within the arterial intima beneath the endothelial lining. As these lesions enlarge, they may narrow the arterial lumen by more than 50%, restricting blood flow and producing symptoms such as angina, particularly during physical exertion or emotional stress. In some cases, plaques with a high lipid content and substantial inflammatory activity become vulnerable to rupture. Plaque disruption in a coronary artery can trigger thrombus formation, potentially leading to complete vessel occlusion and acute myocardial infarction. If thrombotic material travels through the circulation to the cerebral vessels, it may obstruct blood flow to the brain and cause an ischemic stroke.
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M.I. et al. (2026) studied this question.
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