Open AccessLeft Ventricular Assist Device Thrombosis—Amiodarone-Induced Hyperthyroidism: Causal Link?
Author(s) -
Indranee Rajapreyar,
Deepak Acharya,
José Tallaj,
Lauren Hornbuckle,
Jessica L. Sharpton,
Joanna M. Joly,
Salpy V. Pamboukian
Publication year - 2019
Publication title -
asaio journal
Language(s) - Uncategorized
Resource type - Journals
eISSN - 1538-943X
pISSN - 1058-2916
DOI - 10.1097/mat.0000000000000773
Subject(s) - amiodarone , medicine , cardiology , ventricular assist device , ventricular function , thrombosis , ablation , heart failure , atrial fibrillation
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.