Cardiovasc Ther. 2026;2026(1):e7328020. doi: 10.1155/cdr/7328020.
ABSTRACT
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel contributor to atrial fibrillation (AF) pathophysiology. Recent studies suggest that elevated PCSK9 levels may promote AF through multiple mechanisms, including platelet activation, oxidative stress, vascular calcification, and structural atrial remodeling. PCSK9 inhibitors such as alirocumab, evolocumab, and newer agents like inclisiran have shown potential in reducing AF incidence and cardiovascular events, particularly in high-risk populations. However, evidence from randomized controlled trials with AF as a primary clinical endpoint is limited. Further mechanistic and interventional research is warranted to establish optimized therapeutic strategies targeting PCSK9 in AF prevention and management.
PMID:42935110 | DOI:10.1155/cdr/7328020