Case report
A 58-year-old obese man with end-stage nonischemic cardiomyopathy underwent implantation of a HeartWare left ventricular assist device (LVAD) as destination therapy. Post-operative transesophageal and transthoracic echocardiography (TTE) demonstrated appropriate device positioning and neutral septal configuration without valvular abnormalities, including aortic insufficiency (AI). LVAD parameters were optimized with ramp echocardiography, and the patient was discharged home.
Three months later, the patient was hospitalized with progressively worsening shortness of breath, a 40-pound weight gain over 3 months, and peripheral edema. He weighed 387 pounds. The physical exam revealed a continuous hum of the LVAD, diffuse inspiratory crackles, and lower extremity pitting edema. Jugular venous pulsations could not be visualized due to body habitus.
Chest radiograph demonstrated bilateral pleural effusions and vascular congestion. Pertinent serum studies included N-terminal proBNP 13,613 pg/mL, LDH 329 IU/L, INR 2.1, negative urobilinogen, and negative serum free hemoglobin. Daily monitoring of LDH was consistent with the patient’s baseline elevated LDH. An LVAD interrogation revealed no alarms, power spikes, or increased flow, a consistent speed of 2700 rpm, flow of 5.5 L/min, and power of 5.1 watts.
Considering the patient’s presentation and initial work up, he had signs of right heart failure including elevated CVP and lower extremity edema, but also had evidence of left heart failure with dyspnea and diffuse crackles. The continuous hum of the LVAD was not suggestive of pump motor failure. Pump thrombosis was less likely given no alarms or power spikes, negative urobilinogen, and negative serum free hemoglobin. A left ventricular suction event or inflow obstruction were also ruled out. Furthermore, he received aggressive diuresis for over 1 week with marked volume loss, yet his symptoms persisted, which suggested the presence of a separate pathology.
A ramp echocardiogram demonstrated a neutral septal position and an ill-defined aortic regurgitant jet in the parasternal and short axis views. Upon increasing the LVAD speed, AI and mitral regurgitation persisted (Figure 1). Considering heightened suspicion of AI with concomitant recirculation syndrome (1), invasive testing was performed to assess the significance of AI.
A right heart catheterization demonstrated a mean right atrial pressure (mRAP) of 16 mmHg with a mean pulmonary capillary wedge pressure (mPCWP) of 21 mmHg (CI 2.6 L/min/m2) at baseline speed (2700 rpm). With increased speed (2800 rpm), the mRAP was 18 mmHg and the mPCWP was 23 mmHg (CI 2.3 L/min/m2), consistent with possible recirculation syndrome (1). Considering the mixed hemodynamic picture and difficult echocardiographic parameters, intracardiac echocardiography (ICE) was performed. The ultrasound tipped catheter was advanced via the right femoral vein into the right atrium. While in the right atrium, the probe was rotated to obtain a long axis view of the left ventricular outflow tract, which demonstrated flow turbulence within the aortic annulus but no evidence of AI (Video 1).
Based on the findings with ICE, the patient was continued on aggressive intravenous diuresis. LVAD parameters were optimized. After achieving euvolemia, he was discharged with additional oral diuretics and encouragement for medication and dietary compliance. He weighed 356 pounds on the day of discharge. The patient was regularly seen at the heart failure clinic on follow-up. He was stable at 355-360 pounds and remained compliant with diet and medications.