Case Report: Rescue with Impella 5.5 after HeartMate 3 failure- a bridge to heart transplantation

Background We present the first reported case of simultaneous HeartMate 3 (HM3) and Impella 5.5 support as a bridge to heart transplantation. Case presentation A 35-year-old male with a history of non-ischemic cardiomyopathy presented to our facility for the evaluation of low-flow alarms 2 years post-HM3 implantation. The HM3 device was set to 5,200 RPM (2.9 L/min); the patient was asymptomatic and had no edema or orthopnea. He was actively listed for heart transplantation at the time of presentation. A chest CT scan revealed evidence of hypoattenuation next to the bend relief portion of the outflow cannula, and therefore, the patient was admitted for monitoring and transplant evaluation. Bivalirudin (0.12 mg/kg/h) was initiated. Over the next 18 days, the patient remained clinically stable with a pulsatility index ranging between 3 and 4. An echocardiogram performed on day 18 to assess clot burden revealed eccentric left ventricular hypertrophy with septum deviation to the right and a left ventricular internal diameter in diastole (LVIDd) of 70 mm, and hence, milrinone (0.25 µg/kg/min) was initiated. Right heart catheterization revealed a right atrial (RA) pressure of 18 mmHg, a right ventricle (RV) pressure of 54/2 mmHg, a pulmonary artery (PA) pressure of 55/28 (37) mmHg, a pulmonary capillary wedge pressure of 32, a pulmonary artery pulsatility index of 1.5, a Fick cardiac output of 7.7 L/min, and a Fick cardiac input of 3.4 L/min/m 2 . On day 40, the patient complained of cough, fever (38.1°C), and shortness of breath, following which he was intubated and started on meropenem (2 mg) intravenously (IV) three times a day (TID). His left ventricular assist device (LVAD) flow rate decreased to 1.2 L/min, with increasing alarm frequency and worsening hemodynamics. CT angiography revealed extensive near-occlusive hypodense filling defects in the proximal outflow cannula consistent with thrombosis, leaving only a 1–2 mm residual lumen. The team chose to support the patient’s worsening hemodynamics and cardiogenic shock with an Impella 5.5 device rather than take him for emergent surgical exploration for his outflow graft obstruction. The Impella 5.5 device was placed in a standard fashion via the left axillary artery, and it delivered flow rates of 2.6–3.1 L/min. Concurrently, HM3 was maintained at flow rates of 1.5–2.0 L/min. Despite persistent low-flow alarms on HM3, the patient's hemodynamics improved after the Impella 5.5 device was implanted [heart rate, 101 beats per minute; BP, 104/77 (88) mmHg; RA, 2 mmHg; PA, 35/19 (24) mmHg; venous oxygen saturation (SvO 2 )], 69%), and he became ambulatory. His United Network for Organ Sharing (UNOS) status was upgraded to status 1e because of the risk of stroke. Over the next 6 days, the patient was maintained under close observation, and he remained clinically stable in the ICU. The estimated glomerular filtration rate remained between 41 and 50 mL/min/1.73 m 2 . Six days after Impella 5.5 placement, the patient underwent a prolonged and complex heart transplant. One week post-transplant, the patient had normal biventricular graft function and stable renal function, was extubated, and was ambulatory on dobutamine medication (4 µg/kg/min). Two weeks later, the patient was discharged, with stable cardiac function and standard immunosuppression. Two months post-transplant, he showed grade 2R rejection, which was adequately treated. Currently, 6 months post-transplant, he remains stable while being maintained on the standard post-transplant immunosuppression and cardiac rehabilitation. Conclusion This is the first reported case highlighting the feasibility of Impella 5.5 support after HM3 failure as a bridge to transplantation for short-term hemodynamic stabilization in the setting of LVAD outflow obstruction and cardiogenic shock without the need for extracorporeal membrane oxygenation or emergent chest exploration, which may complicate or delay transplantation.