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.