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.