Abstract

Background The HeartMate 3 (HM3) left ventricular assist device (LVAD) has a low reported rate of pump thrombosis. In this case series, we report two HM3 LVAD recipients who developed acute pump thrombosis in the early post-operative period. Case 1 A 69 M with ischemic cardiomyopathy who underwent HM 3 implant as destination therapy (DT). Apical calcium was noted intra-operatively and was removed at the time of surgery. On post-operative day 3, the patient developed low flows alarms, high powers, and increased arterial line pulsatility. Lactate dehydrogenase (LDH) was within normal limits and heparin was therapeutic. Pump interrogation demonstrated rising pump temperature (70°C) with intermittent pump stops. The decision was made to return to the operating room (OR) and during this time the patient developed hypotension and lactic acidosis. In the OR fresh thrombus of the inflow, pump and outflow graft was encountered. The pump was exchanged to a new HM3 and the patient had full recovery with no further thrombotic events. Case 2 A 58-year-old woman with Adriamycin associated cardiomyopathy underwent DT HM3 implantation with tricuspid valve annuloplasty. The LV cavity size decreased from 5.9 cm pre- operatively to 4.0 cm post-operatively, causing septal contact with the inflow cannula and intermittent ventricular tachycardia. On post-operative day 3 the patient developed low flow alarms, followed by elevated pump flows and powers and return of arterial line pulsatility. LVAD interrogation demonstrated a high pump temperature (75 °C) with intermittent pump stops. Similar to the first patient, the second patient had a normal LDH, was therapeutic on a heparin drip, and developed hemodynamic instability. The same findings (inflow, outflow, and intra pump thrombus) were present at in the OR. This second patient's pump was re-positioned reduce septal contact at the time of exchange. Discussion Here we report 2 cases of acute HM3 pump thrombosis shortly after LVAD implantation. Full investigation into these events internally and with the manufacturer did not reveal pump malfunction. The first event was felt to be caused by ingestion of calcified material from the left ventricle leading to rotor misplacement and subsequent thrombus formation. The second case was thought to be triggered by sustained low flow from the septal contact with subsequent thrombus formation. In each case, the patients developed high powers, return arterial line pulsatility, and dangerously high internal pump temperatures. The purpose of this case series is to help the community develop pattern recognition in order to be able to quickly diagnose this rare but serious event.

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