Abstract

IntroductionAlthough less common with the HeartMate 3 (HM3), pump thrombosis remains a life-threatening complication of durable left ventricular assist devices (LVAD). We present what we believe is the first case of suspected pump thrombosis in a patient with a HM3 LVAD that was successfully managed with tissue plasminogen activator (tPA).Case ReportA 22-year-old man who underwent HM3 implantation for end stage heart failure due to left ventricular non-compaction presented after experiencing two low flow alarms. His physical examination was notable for tachycardia at 125 beats per minute and an elevated Doppler mean blood pressure of 92 mm Hg. LVAD interrogation revealed low flows without power spikes (Figure 1A). Within 24 hours, he developed persistent hypotension requiring vasopressor support and multiple low flow alarms. Serial laboratory results were notable for rising LDH, peaking at 4,741 U/L and acute liver injury with AST 2,712 U/L, ALT 798 U/L and INR 5.2. Transthoracic echocardiography and computed tomography (CT) angiography did not reveal any obvious thrombus. Given this constellation of findings, pump thrombosis was suspected. Following multidisciplinary discussion, unfractionated heparin bolus and infusion were started. After an unremarkable head CT, heparin was stopped and systemic tPA was given at a dose of 5 mg over one minute followed by 10 mg over 10 minutes due to ongoing liver dysfunction. Heparin was resumed after PTT returned to therapeutic range. Immediately post tPA infusion, his LVAD flows improved from 2.3 L/min to 4.1 L/min (Figure 1B). Vasopressor support was quickly weaned. LDH, creatinine, and liver enzymes improved over the following days. Warfarin was resumed on day 14 of admission. He was discharged on aspirin, clopidogrel and warfarin.SummaryThrombolytics may be a potential therapeutic option in select cases of HM 3 pump thrombosis. Further research is warranted to delineate LVAD parameters that facilitate early recognition of pump thrombosis and successful medical management. Although less common with the HeartMate 3 (HM3), pump thrombosis remains a life-threatening complication of durable left ventricular assist devices (LVAD). We present what we believe is the first case of suspected pump thrombosis in a patient with a HM3 LVAD that was successfully managed with tissue plasminogen activator (tPA). A 22-year-old man who underwent HM3 implantation for end stage heart failure due to left ventricular non-compaction presented after experiencing two low flow alarms. His physical examination was notable for tachycardia at 125 beats per minute and an elevated Doppler mean blood pressure of 92 mm Hg. LVAD interrogation revealed low flows without power spikes (Figure 1A). Within 24 hours, he developed persistent hypotension requiring vasopressor support and multiple low flow alarms. Serial laboratory results were notable for rising LDH, peaking at 4,741 U/L and acute liver injury with AST 2,712 U/L, ALT 798 U/L and INR 5.2. Transthoracic echocardiography and computed tomography (CT) angiography did not reveal any obvious thrombus. Given this constellation of findings, pump thrombosis was suspected. Following multidisciplinary discussion, unfractionated heparin bolus and infusion were started. After an unremarkable head CT, heparin was stopped and systemic tPA was given at a dose of 5 mg over one minute followed by 10 mg over 10 minutes due to ongoing liver dysfunction. Heparin was resumed after PTT returned to therapeutic range. Immediately post tPA infusion, his LVAD flows improved from 2.3 L/min to 4.1 L/min (Figure 1B). Vasopressor support was quickly weaned. LDH, creatinine, and liver enzymes improved over the following days. Warfarin was resumed on day 14 of admission. He was discharged on aspirin, clopidogrel and warfarin. Thrombolytics may be a potential therapeutic option in select cases of HM 3 pump thrombosis. Further research is warranted to delineate LVAD parameters that facilitate early recognition of pump thrombosis and successful medical management.

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