The Lipid–Platelet Interplay: Unraveling the Effects of PCSK9 Inhibition on Platelet Reactivity

The interaction of circulating lipoproteins with platelets can increase platelet reactivity, promoting platelet activation, aggregation, and thrombus formation.[1] This can explain why patients with hypercholesterolemia, especially those with familial hypercholesterolemia, and increased levels of low-density lipoprotein (LDL-C) have heightened platelet reactivity.[1] However, the mechanism(s) explaining these observations are not completely elucidated. Among the prevailing hypotheses, it has been postulated that the LDL-C and oxidized LDL-C modulate platelet membrane lipid composition and interact directly via multiple platelet receptors (e.g., CD36 and lectin-like oxidized LDL receptor 1), resulting in hyper-reactivity, morphologic changes, and increased aggregation.[1]