Repeated Successful Thrombolysis of a Jarvik 2000 Left Ventricular Assist Device in a Patient With Noncompaction Cardiomyopathy
28-year-old white man with history of end-stage heart failure caused by isolated left ventricular (LV) noncompaction cardiomyopathy had been implanted with the Jarvik 2000 LV assist device 3 years previously as a bridge to survival and to decision via a left posterolateral thoracotomy, off-pump, with outflow graft anastomosis to the descending aorta and postauricular pedestal. The patient had an excellent postoperative course free of adverse events for 1.5 years. The pump was operated at a rotational speed of 9000 rounds per minute. Anticoagulation included acenocoumarol aiming for an international normalized ratio of 3 to 3.5 and 100 mg of aspirin daily.
On the 20th month of support, the patient presented with symptoms and signs of cardiogenic shock associated with a sudden increase in power consumption by the device. His international normalized ratio was 3.3, but during the previous week, his international normalized ratio was 2.2. Echocardiography revealed LV thrombus obstructing the pump inflow (the Figure, A and online-only Data Supplement Movie I), LV distension, and systolic opening of the aortic valve during each cardiac cycle, suggesting device malfunction. Echocardiographically titrated intravenous thrombolysis was used, with a door-to-needle time of 2 hours. A 15-mg bolus of recombinant tissue plasminogen activator was followed by infusion of 85 mg recombinant tissue plasminogen activator over 90 minutes on continuous echocardiographic monitoring, during which progressive thrombus fragmentation (the Figure, B and C and online-only Data Supplement Movies II and III) was witnessed. Thrombolysis resulted in clinical improvement and return of device power consumption to baseline within 15 minutes. Complete thrombus resolution (the Figure, D and online-only Data Supplement Movie IV) was achieved after an additional intravenous infusion of 50 mg over 30 minutes. The patient was discharged on intensified anticoagulation aiming to international normalized ratio of 3 to 4, as well as antiplatelet treatment with aspirin (100 mg) and clopidogrel (75 mg).
One repeated episode of thrombosis on the 23rd month of support was successfully treated with the same regimen. During a third episode, after partial thrombolysis and during heparin infusion, hemorrhagic shock resulting from a ruptured splenic hematoma was treated successfully with splenectomy and supportive therapy. Currently on the 31st month of support, the patient remains free of clinically evident episodes of thrombosis on the triple antithrombotic regimen.
Despite the recurrent thrombotic episodes, there was no clinically evident cerebrovascular accident or other site embolization. Outflow graft anastomosis to the descending aorta might be an important safety feature, and it may lessen the chances of cerebral embolization of pump thrombi. The design of the pump inflow (the triple-arch cage guarding the inflow) also seemed to be advantageous by restraining the entrance of large thrombus into the pump. Furthermore, the apical position of the device in the LV allowed an excellent echocardiographic window and facilitated close monitoring and titration of the dose of the thrombolytic regimen.
In conclusion, administration of intravenous thrombolysis under echocardiographic guidance is a feasible option for hemodynamically significant thrombosis of the Jarvik 2000 LV assist device. To the best of our knowledge, this is the first case of long-term support with the Jarvik 2000 in a patient with noncompaction cardiomyopathy and the first case of successfully treated recurrent thrombosis of the Jarvik 2000 with an intravenous thrombolytic regimen.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/121/3/e13/DC1.