From a mechanistic perspective, Lp(a) promotes atherothrombosis through multiple pathways: the carriage of oxidized phospholipids, activation of inflammatory cascades (including NLRP3 inflammasome and IL-1β/IL-18), endothelial dysfunction, and smooth muscle cell proliferation, all of which contribute to diffuse atherosclerotic progression. Here, IL18 is linked to endothelial dysfunction.