Case report
A 53 year - old African American with class 1 obesity , hypertension ( HTN ), diabetes mellitus DM2, gout with chronic systolic (congestive) heart failure secondary to nonischemic cardiomyopathy who underwent initial implantation of a Left ventricular Assist device HeartMate III ( LVAD ) on 3/17/2017
The patient had been quite active running his company until October 2016 when he presented with progressively worsening dyspnea on exertion, lower extremity edema, and orthopnea. He was diagnosed with heart failure and his ejection fraction (EF) of < 10%. He underwent cardiac catheterization on 8/3/2016 which demonstrated near-normal coronary arteries, right dominant system, Left ventricular end-diastolic Pressure (LVEDP) of 18, and normal pulmonary pressures. He was optimized with medical therapy but failed to respond. He underwent automatic implantable cardioverter defibrillator (AICD) placement for primary prevention after failing to respond to medical therapies. He subsequently had multiple readmissions for heart failure despite complete compliance with medication. During one of his hospitalizations, Right heart catheterization pressures (RHC) demonstrated the following right atrium (RA) 21, right ventricle ( RV ) 64/42, Pulmonary capillary wedge pressure (PCWP )35, cardiac output (CO )4.9, Cardiac Index ( CI ) 2.2, pulmonary pressure (PA )55%. He had been on inotropes since 1/2017. He presented on 2/28/2017 with cardiogenic shock and required an intra-aortic balloon pump.
On 3/17/2017 He underwent Heartmate III LVAD placement and needed chest tube 2 days later after developing acute anemia during epicardial lead removal. Chest exploration was remarkable for many clots along the diaphragmatic surface of the heart extending around the lateral wall presumed to be related to the previously removed pacing wire. His postoperative course was remarkable for RV failure needing prolonged milrinone and fever of unknown origin. Work-up for infection was unrevealing except for nonspecific mediastinal and retroperitoneal lymphadenopathy. He was commenced on aspirin and warfarin
Three years later, on 7/20/2021, our patient presented to the emergency department (ED) with dyspnea. He was found to be COVID positive (he was unvaccinated) with a heart rate of 100, respiratory rate of 29, SPO2 87 %, and MAP of 63 mmHg. He was admitted to the ICU for acute hypoxic respiratory failure. Zosyn and Azithromycin, dexamethasone, Remdesivir, and Tocilizumab were incited. His respiratory requirements increased, requiring BiPAP
During the night of 7/22, his LVAD alarmed, and it was found that the flow had decreased to 0.5 L/min. CT Cardiac Angiogram with IV Contrast showing LV Complete distal thrombosis of the outflow conduit from LVAD (Figure 1), diffuse ground-glass disease of lungs due to edema versus infection/inflammation, and laboratory changes (Table 1). Our patient was not a surgical candidate as he was too unstable with multiple organ failures including heart, liver, kidney, and lung. As an obstructive clot in the LVAD would be fatal, it was decided to start tPA to try to dissolve the clot. After tPA was started, he had increased bleeding from a central venous catheter (CVC) and began to have melena. His LVAD flow did not significantly increase despite tPA, and on the morning of 7/24, it was 0.4 L/min. After discussion with the family, he was transitioned to comfort care. His LVAD was turned off, and later that morning he stopped breathing and became pulseless.