In the previous chapter, we learned that atherosclerosis is characterized by the accumulation of lipids, fibrous elements, and immune cells within the arterial wall, leading to the formation of atheroma and progressively developing into vulnerable plaque. Advanced plaques can undergo calcification, necrosis, and rupture. Plaque rupture exposes thrombogenic material to the bloodstream, leading to thrombus formation and potential arterial occlusion, causing acute cardiovascular events.