Ventricular arrhythmias occurs in 20-50% of patients supported with left ventricular assist devices (LVAD). Ventricular arrhythmias are well tolerated with LVAD support but long-term consequences include worsening right ventricular function. Management of ventricular arrhythmias in LVAD patients includes use of antiarrhythmic agents or ablation. Amiodarone has been used a first-line agent to treat ventricular arrhythmias post-LVAD implantation. Chronic treatment with amiodarone for arrhythmias can result in hyperthyroidism and hypothyroidism in 5-10% of patients. Hyperthyroidism is known to cause endothelial dysfunction, alterations in coagulation, and fibrinolytic pathways favoring hypercoagulable state. We describe two cases of left ventricular assist device (LVAD) thrombosis potentiated by amiodarone-induced hyperthyroidism (AIT) and discuss pathophysiological mechanisms for hypercoagulable state induced by hyperthyroidism.
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