Abstract

Introduction: Aortic valve insufficiency (AI) is associated with left ventricular assist device (LVAD) implantation. We report a patient with end-stage heart failure secondary to hypertrophic cardiomyopathy on LVAD support who developed severe AI. He was initially treated by TAVI, which was complicated by CoreValve migration into the left ventricular outflow tract (LVOT) post-procedure. He subsequently underwent emergency sternotomy with explantation of the CoreValve and aortic valve stitch closure. Case report description: A 49-year-old male patient with hypertrophic cardiomyopathy developed AI 10 months after Heartmate II LVAD implantation as a bridge to heart transplant. He presented with increasing dyspnea. A right heart study demonstrated a cardiac output of 2.9L/min with a corresponding high LVAD pump flow. Transesophageal echocardiogram confirmed severe AI. He was planned for open surgical aortic valve closure. Prior to surgery, he developed cardiac decompensation and pneumonia, which necessitated ICU care and rendered him high risk for surgery. In view of heart failure symptoms refractory to medical therapy, he underwent TAVI via the transfemoral approach. Post-deployment, transesophageal echocardiogram and fluoroscopy demonstrated satisfactory CoreValve position, and mild paravalvular AI. Two hours post procedure, the patient became hypotensive, and bedside echocardiogram showed severe AI and migration of the CoreValve towards the LVOT. He underwent emergency sternotomy with explantation of the CoreValve and suture closure of the aortic valve. Discussion: AI can occur in patients with long-standing LVAD. However, there is no consensus on the optimal management of AI in LVAD patients. Options include medical management, suture repair or closure of the native valve, prosthetic valve replacement, and patch closure of the LVOT. Case reports of successful percutaneous treatment of AI in LVAD patients using TAVI and Amplatzer devices have also been previously described. The use of TAVI in our patient was complicated by migration of the CoreValve into the LVOT shortly after the procedure. Likely contributory factors include suboptimal anchoring of the prosthesis due to absence of aortic root and valve calcification and the continuous suction by the continuous flow LVAD in the left ventricular apex. Conclusions: AI remains a significant complication of long term LVAD support. Surgical aortic valve closure remains the definitive treatment for this problem. While percutaneous therapy remains a potentially viable option, further studies on the feasibility of each of these methods in LVAD patients is required.

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