Atherosclerosis is the most common pathological mechanism underlying coronary artery disease (CAD), encompassing both acute coronary syndromes (ACS) and chronic coronary syndromes (CCS). Traditionally, the plaque formation process has been perceived as a consequence of cholesterol accumulation (particularly scavenger receptor-mediated uptake of modified low-density lipoprotein), leading to continuous plaque growth. Subendothelial intimal layer build-up further leads to progressive stenosis, reduced blood flow, and, eventually, tissue hypoxia. In addition, spontaneous thrombotic vessel occlusion and embolic events may constitute the common pathophysiological […]