Data presented in this week’s issue of Blood shed new light on the interaction between lipoproteins and platelets that may lead to heart attack.
In the manuscript, Chan and colleagues report that L5, the most highly electronegative fraction of low-density lipoprotein (LDL), is markedly elevated in patients with ST-elevation myocardial infarction (STEMI). Utilizing in vitro studies, investigators demonstrate that L5 increased adenosine diphosphate (ADP)-induced platelet aggregation, platelet P-selectin expression, GPIIb/IIIa activation, and platelet-endothelial cell adhesion. When injected into mice, L5 also activated platelets.
These findings suggest that elevated L5 may promote coronary artery thrombosis leading to STEMI, offer further insight into the role of platelets in coronary artery occlusion, and provide a potential entry point for future therapies.