Lipoprotein(a) and Atrial Fibrillation: Mechanistic Insights and Therapeutic Approaches

Elevated lipoprotein(a) [Lp(a)] levels are increasingly recognized as a significant risk factor for cardiovascular diseases and may also contribute to atrial fibrillation (AF). This review investigated the indirect mechanisms through which Lp(a) may influence AF, including proatherogenic, prothrombotic, and proinflammatory pathways. Traditional lipid-lowering therapies, such as lifestyle modifications and statins, have limited effects on Lp(a) levels. Emerging treatments, such as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, lipoprotein apheresis, small interfering RNA, antisense oligonucleotides, cholesterol ester transfer protein inhibitors, and interleukin-6 receptor monoclonal antibodies, are promising alternatives. Notably, only PCSK9 inhibitors and lipoprotein apheresis have been shown to reduce both Lp(a) levels and cardiovascular events. Research indicates varying associations between Lp(a) and AF across different populations, underscoring the need for diverse, large-scale studies to elucidate these differences. Ongoing trials aim to provide clearer insights into these relationships. Addressing these gaps is essential for developing targeted therapies to manage elevated Lp(a) and mitigate the risk of AF and associated cardiovascular events.