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Case Report

Late Right Heart Failure After Left Ventricular Assist Device Implant: VAD or Valve?

Faris G. Araj, MD; Alpesh A. Amin, MD; Robert M. Morlend, MD; Pradeep P.A. Mammen, MD

University of Texas Southwestern Medical Center, Dallas, Texas

November 2020

Case Report

A 76-year-old woman with a history of advanced heart failure and a bi-ventricular pacemaker-defibrillator underwent intra-pericardial left ventricular assist device (LVAD) implant as destination therapy (Figure 1). Pre-implant hemodynamics are shown in Table 1. Echocardiographic right ventricular systolic function at the time was normal and there was only mild tricuspid regurgitation (TR). Three years later, she presented with recurrent hospitalizations for low LVAD flows and bilateral lower extremity edema. Her examination was notable for a prominent C-V wave on jugular venous exam and bilateral, lower extremity pitting edema. A right heart catheterization was performed in order to better characterize the etiology of her decompensation (Table 1). The right atrial pressure tracing was suggestive of severe TR. This was a new finding, and was persistent despite aggressive diuretic therapy and a reduction in device speed (Figure 2). Transesophageal echocardiography confirmed severe TR with incomplete coaptation of primarily the tricuspid valve septal leaflet, secondary to impingement by the implantable cardioverter defibrillator lead (Figure 3). The patient was considered for transcatheter edge-to-edge tricuspid valve repair with lead extraction; however, she declined. In light of that decision, and after completion of intravenous (IV) diuretic therapy, efforts were made to maintain optimization of the right ventricular preload, afterload, and contractility. This was accomplished by use of oral torsemide (which has a better bioavailability than oral furosemide) in addition to scheduled metolazone, ensuring that the pump speed was not excessive to result in interventricular septum bowing leftward with worsening tricuspid valve annular dilatation and TR, and finally by adding digoxin. The use of a phosphodiesterase-5 inhibitor was felt to be of minimal benefit given the absence of significant pulmonary hypertension. As of this time, the readmission rate for volume overload has not been entirely eliminated; however, the frequency has decreased.

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