Atrial Fibrillation, Thromboembolic Risk, and Anticoagulation in Cardiac Amyloidosis: A Review

Cardiac amyloidosis (CA) is caused by extracellular myocardial deposition of amyloid fibrils that are primary derived either from misfolding of transthyretin (ATTR) or light-chain (AL) proteins. CA is associated with atrial fibrillation, potentiated by electromechanical changes as a result of amyloid infiltration in the myocardium. CA also predisposes to thromboembolism and could potentially simultaneously elevate bleeding risk. In this review, we aim to explore and compare the prevalence and pathophysiological mechanisms of atrial fibrillation and thromboembolism in ATTR and AL, examine bleeding risk and factors that promote bleeding, and compare anticoagulation strategies in CA. Finally, we highlight knowledge gaps in the field of thromboembolism in CA to guide future research.

Automated summary

Cardiac amyloidosis (CA) is characterized by the deposition of amyloid fibrils derived from misfolding of transthyretin (ATTR) or light-chain (AL) proteins in the myocardium, leading to atrial fibrillation and thromboembolism. It also increases the risk of bleeding. This review explores the prevalence, pathophysiological mechanisms, bleeding risk, and anticoagulation strategies in CA, aiming to identify knowledge gaps for future research on thromboembolism in CA.