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

• Published in: Journal of cardiac failure Vol. 29; no. 1; pp. 76 - 86
• Main Authors: BUKHARI, SYED, KHAN, SYED ZAMRAK, BASHIR, ZUBAIR
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-01-2023
• Subjects: Amyloid; Amyloid Neuropathies, Familial - complications; Amyloid Neuropathies, Familial - drug therapy; Amyloid Neuropathies, Familial - epidemiology; Amyloidosis - complications; Amyloidosis - drug therapy; Amyloidosis - epidemiology; Anticoagulants - therapeutic use; anticoagulation; atrial fibrillation; Atrial Fibrillation - complications; Atrial Fibrillation - drug therapy; Atrial Fibrillation - epidemiology; Cardiac amyloidosis; Heart Failure - complications; Humans; thromboembolic risk; Thromboembolism - epidemiology; Thromboembolism - etiology; Thromboembolism - prevention & control; atrial fibrillation; thromboembolic risk; Cardiac amyloidosis; anticoagulation
• ISSN: 1071-9164; 1532-8414
• DOI: 10.1016/j.cardfail.2022.08.008

•Cardiac amyloidosis (CA) is associated with higher prevalence of atrial fibrillation compared with age-matched population without CA, and the prevalence is higher in wild-type transthyretin cardiac amyloidosis compared with hereditary transthyretin cardiac amyloidosis and AL variants.•CA causes elevated risk of thromboembolism, regardless of atrial fibrillation status and CHA2DS2Vasc score, and can potentiate bleeding simultaneously.•Both direct oral anticoagulants and vitamin K antagonists can be used to provide thromboembolic protection in CA, and have comparable efficacy and bleeding rates.
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.