Key result
PCSK9 inhibitors show potential anti-thrombotic effects beyond lipid lowering by modulating platelets and coagulation.
Why the study?
The inhibitory effect of PCSK9 inhibitors on atherosclerosis progression appears driven not only by lipid modification but also by LDL-independent mechanisms, warranting a review of their anti-thrombotic effects.
This narrative review highlights that PCSK9 inhibitors may exert anti-thrombotic effects by reducing platelet activation, improving endothelial function, and modulating coagulation, beyond their established lipid-lowering benefits.
May support LDL-independent benefits of PCSK9 inhibitors; leaves open whether effects alter thrombotic outcomes or practice.
Atherosclerosis is the primary process that underlies cardiovascular disease. The connection between LDL cholesterol and the formation of atherosclerotic plaques is established by solid evidence. PCSK9 inhibitors have proven to be a valuable and practical resource for lowering the LDL cholesterol of many patients in recent years. Their inhibitory effect on atherosclerosis progression seems to be driven not just by lipid metabolism modification but also by LDL-independent mechanisms. We review the effect of PCSK9 inhibitors on various mechanisms involving platelet activation, inflammation, endothelial dysfunction, and the resultant clot formation. The main effectors of PCSK9 activation of platelets are CD36 receptors, lipoprotein(a), oxidised LDL particles, tissue factor, and factor VIII. Many more molecules are under investigation, and this area of research is growing rapidly.
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Péč et al. (2023) conducted a review in Cardiovascular disease and thrombosis. PCSK9 inhibitors was evaluated. PCSK9 inhibitors demonstrate potential pleiotropic anti-thrombotic effects beyond lipid lowering by reducing platelet activation, improving endothelial function, and modulating coagulation factors.
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