Acute coronary syndrome and postprandial delayed hyperchylomicronemia

levels have been established as a risk factor for fatal cardiovascular (CV) events, including acute coronary syndrome (ACS), whose principal pathogenesis is the disruption of culprit plaques composed of a large lipid core under a thin fibrous cap. This structure, termed thin-cap fibroatheroma (TCFA), is considered vulnerable. Statins or 3-hydroxy-methylglutaryl coenzyme A reductase inhibitors can stabilize vulnerable coronary plaques by lowering LDL-C levels, and this stabilization prevents the occurrence of ACS. Clinical trials involving more than 170,000 participants conducted over two decades have demonstrated the beneficial effects of statins in reducing the risk of CV events by 25%; however, 75% of coronary events manifest despite treatment, possibly because of underlying residual risk [1].