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We sought to determine hemodynamic mechanisms of exercise intolerance in a group of patients with the HeartWare ventricular assist device (VAD) compared to a group of heart failure patients. Twenty VAD and 22 heart failure patients underwent symptom-limited active straight leg raising exercise during right heart catheterization with thermodilution (TD), and upright cycling cardiopulmonary stress testing with cardiac output measurement by inert gas rebreathing (IGR) method. The TD and IGR exercise cardiac indexes were higher in VAD compared with heart failure group (both P < 0.05), although there was only a borderline increase in peak exercise oxygen consumption (VO2) (P = 0.06). Baseline and exercise right heart catheterization pressures were not significantly different between the two groups. The only significant independent predictors of peak VO2 in the heart failure group were exercise heart rate and cardiac index (both P < 0.05). In contrast, for the VAD group only, resting pulmonary arterial wedge and pulmonary arterial mean pressures were independently related to peak VO2 (both P < 0.05). Thus, in heart failure, exercise cardiac index is an important limitation to exercise capacity, and VADs increase exercise cardiac index. However, in VAD patients, this only produces limited benefits as increased pulmonary and pulmonary wedge pressures limit increases in exercise capacity.

To manage myocardial recovery in patients with the HeartWare left ventricular assist device (HVAD), we describe a minimally invasive approach (decommissioning) that involves disconnecting the driveline and occluding the outflow tract through a small left thoracotomy incision, leaving the device in situ, in conjunction with optimal medical therapies and comprehensive assessment of left ventricular recovery. Nine patients (all male, 37 ± 12 years, all nonischemic dilated cardiomyopathy) had an HVAD implanted for 766 ± 343 days. When left ventricular function improved to mild impairment by echocardiography, patients underwent assessment at reduced flow (2578 ± 148 to 1822 ± 67 rpm) with documentation of compensated right heart hemodynamics and ejection fraction 52 ± 8%. Eight of nine patients underwent decommissioning, and 1 patient had a hybrid procedure of percutaneous occlusion of outflow graft and surgical division of driveline. Two patients died postoperatively at 413 days (sepsis) and 810 days (heart failure). In conclusion, in selected patients with nonischemic dilated cardiomyopathy, a prolonged period of HVAD support in conjunction with heart failure medications can lead to recovery of left ventricular function. Surgical decommissioning is then an option to remove these patients from support. These patients are, however, not cured and remain at risk for future deterioration in ventricular function and infections.