ASAIO Journal 2014
Case Reports
Ventricular Assist Device Thrombosis Following Recovery of Left Ventricular Function Andrew R. Sifain, Karl Q. Schwarz, William Hallinan, H. Todd Massey, and Jeffrey D. Alexis
Although ventricular assist devices (VADs) are lifesaving therapy for patients with severe heart failure, complications such as pump thrombosis can occur. In this report, we present a case of VAD thrombosis following recovery of left ventricular (LV) function. The patient had been supported with a VAD for 8 months, and at the time of presentation, echocardiography revealed near normal native systolic function, aortic valve opening with significant native heart ejection, reduced systolic flow in the outflow and inflow cannulae, and no forward flow through the VAD during diastole. The patient underwent successful VAD explant and examination of the pump revealed thrombus on the rotor. We propose that abnormal flow through the VAD seen with recovery of LV function may contribute to VAD thrombosis. ASAIO Journal 2014; 60:243–245.
Patient History A 30-year-old woman presented with a 2 week history of dyspnea on exertion and orthopnea following delivery of twins 2 months before presentation. On examination, she had a third heart sound and estimated jugular venous pressure of 16 mm Hg. An echocardiogram revealed LV ejection fraction (LVEF) of 10%, LV end-diastolic diameter 6.4 cm, and moderate-to-severe right ventricular (RV) dysfunction. Heart failure medications could not be titrated due to hypotension. Right heart catheterization revealed right atrial pressure 23 mm Hg, pulmonary artery pressure 48/37 mm Hg, pulmonary capillary wedge pressure 31 mm Hg, and cardiac index 1.03 L/min/m2. She received a HeartMate II LVAD as a bridge to transplantation and a Centrimag RV assist device (RVAD; Thoratec, Pleasanton, CA). Her RVAD was weaned 6 days later, and she was discharged home 19 days after VAD implant. Lactate dehydrogenase level at 3 months post VAD implant routine visit was 849 unit/L. Five months after VAD implantation, a transesophageal echocardiogram (TEE) revealed an LVEF of 47%. As she had a dilated and hypocontractile RV, the decision was made to continue to follow her clinically and not attempt explant. Eight months after VAD implant, she presented with lightheadedness, high power readings (12–12.7 watts), and a low pulsatility index (2.0) at her baseline VAD speed of 8,800 revolutions per minute (rpm). Blood work revealed lactate dehydrogenase level of 2,900 unit/L and a haptoglobin less than 20 mg/dl. Hemoglobin level was low at 7.6 g/dl. Her medications included aspirin and warfarin (international normalized ratio was 3.2 on admission and had been therapeutic previously). TEE demonstrated pump dysfunction, as systolic Doppler flow velocities in both the inflow and outflow cannulae were about half that expected and there was essentially no diastolic flow through the VAD (Figure 1, A and B). Left ventricular ejection fraction was 55%, the aortic valve opened vigorously with each native ventricular systole, and there was significant native heart ejection. There was no change in LVEF as VAD flow speed setting was decreased to a speed of 6,000 rpm. The absence of forward diastolic flow in the VAD outflow cannula changed to flow reversal when the speed setting was reduced to 6,000 rpm (Figure 1C). Quantitative assessment of flow in the outflow cannula over a spectrum of VAD speed settings showed that the minute flow rate was less than half that expected for a HeartMate II3 (Figure 1D). Doppler flow velocity through the outflow cannula was normal 3 months earlier (see Supplemental Digital Content 1, http://links.lww. com/ASAIO/A46). RV ejection fraction was mildly reduced. The clinical impression was VAD thrombosis.
Key Words: ventricular assist device, left ventricular recovery, peripartum cardiomyopathy, ventricular assist device thrombosis
Left ventricular assist devices (LVADs) have been a major
advancement in the treatment of end-stage heart failure and have been shown to decrease morbidity and mortality in comparison with optimal medical management.1 Recovery of left ventricular (LV) function, while not common, can occur following ventricular assist device (VAD) implant and allow for VAD explantation.2 In this report, we present the case of a patient with a history of cardiogenic shock, supported by a HeartMate II LVAD (Thoratec, Pleasanton, CA), who demonstrated VAD thrombosis following recovery of LV function and underwent successful VAD explant. We show the utility of echocardiography for assessing blood flow through a VAD and discuss the risk of VAD thrombosis associated with recovery of LV function.
From the Department of Medicine, Department of Surgery, and Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York. Submitted for consideration July 2013; accepted for publication in revised form November 2013. Disclosure: The authors have no conflicts of interest to report. Reprint Requests: Andrew R. Sifain, MD, Department of Anesthesia, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 604, Rochester, NY. Email: andrew_sifain@urmc. rochester.edu. Copyright © 2014 by the American Society for Artificial Internal Organs DOI: 10.1097/MAT.0000000000000036
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Figure 2. Thrombus formation in the ventricular assist device (VAD). Evaluation of the VAD revealed thrombus formation on the rotor assembly, occluding two of the three rotor pathways (printed with permission from Thoratec).
min). Aerosolized epoprostenol was administered via inhalation to decrease RV afterload. The chest was closed and she was taken to the intensive care unit for continued care. Lactate dehydrogenase level was 845 unit/L on postoperative day 4. She tolerated the explant well and was discharged home 9 days after explant. Examination of the pump revealed thrombus on the rotor (Figure 2). She has returned to work and continues to do well 18 months after explant. Discussion
Figure 1. Echocardiographic evidence of ventricular assist device (VAD) dysfunction. A: Doppler signal through the VAD inflow cannula at 7,800 revolutions per minute (rpm) reveals flow during systole (single white arrow) and no flow during diastole (double white arrows). B: Doppler signal through the VAD outflow cannula at 7,800 rpm reveals flow during systole (single white arrow) and no flow during diastole (double white arrows). C: Doppler signal through the VAD outflow cannula at 6,000 rpm reveals flow during systole (single white arrow) and reversal of flow in diastole (double white arrows). D: Doppler derived measurement of flow (Q corrected) through the VAD at varying pump speeds. Calculated flow rates are less than half expected based on rpm (Methods for detection of flow are described in the study by Schwarz et al.3).
The patient was taken to the operating room for LVAD exploration and possible explant. After placement of a radial arterial line, general anesthesia was induced with the patient remaining hemodynamically stable. A TEE demonstrated LVEF approximately 45%, with a moderately dilated and hypokinetic RV. Spectral Doppler identified only minimal low-velocity flow exiting the outflow graft into the aorta. The inflow cannula was in good position without discernable obstruction. The aortic valve opened with every beat, and there was trace aortic insufficiency. The patient was heparinized and placed on cardiopulmonary bypass to remove the LVAD. The inflow cannula was removed from the apex, and a complex plug constructed from felt and bovine pericardium was used to close the hole. The outflow graft was stapled in multiple layers; the drive line was divided as close to the fascia as possible, and the entire VAD assembly was removed en bloc. The patient was weaned off cardiopulmonary bypass on epinephrine (0.02 μg/kg/min) and milrinone (0.5 μg/kg/
Thrombosis remains a feared complication associated with VAD implantation. Issues such as decreased blood volume through the pump and altered blood flow through the pump, as seen with recovery of LV function, may be causal factors. In our patient, there was evidence of near normal native systolic function with vigorous aortic valve opening and significant native heart ejection. This would lead to decreased flow through the pump in systole. There was also abnormal diastolic flow through the pump. Higher diastolic suction pressure in the recovered ventricle “robs” the VAD of blood due to a combination of native diastolic ventricular volume expansion and higher pressure differential between the LV cavity and aorta. Volume that is expanding the ventricle is volume that is not going into the VAD, and recovered ventricles with significant native ventricular ejection have higher diastolic aortic pressures. We propose that with recovery of LV function (including improved diastolic function), decreased systolic flow through the VAD and diastolic reversal of flow through the VAD can occur, and this abnormal flow can contribute to thrombosis. In our patient, there were four echo-Doppler findings that suggested pump malfunction: 1) the systolic flow velocities in the outflow and inflow cannulae were about half that expected,3 2) no forward flow was noted during diastole at the baseline speed setting, 3) the lack of forward diastolic flow turned to flow reversal at lower speed settings, and 4) quantitative assessment of VAD output showed less than half the expected volumetric flow rate at all settings. The performance of rotational VAD pumps is dependent on the pump’s efficiency and the pressure differential between the LV and aorta. The finding of low systolic outflow cannula flow velocity illustrated the effect of low pump efficiency, as the pump was not able to achieve normal systolic flow rates even during native ventricular systole when the pressure gradient between the LV
THROMBOSIS FOLLOWING RECOVERY OF LV FUNCTION
cavity and the aorta is lowest. The finding of absent diastolic outflow cannula flow also illustrates the low pump efficiency, as the VAD was not able to overcome the pressure differential between the aorta and LV cavity. The finding of diastolic flow reversal in the outflow cannula at the lowest tested VAD speed illustrates the return of normal LV diastolic suction, which was able to overcome the weak VAD pump, which itself was fighting to keep flow in the forward direction. Finally, the quantitative assessment of VAD output showed clearly low pump efficiency over a wide range of speed settings. Recovery of LV function is not common after placement of an LVAD but can occur. In an analysis of patients supported on a HeartMate II LVAD, Goldstein et al.2 recently reported that recovery of LV function was most common in patients who were young (age less than 40), with nonischemic cardiomyopathy of less than 1 year in duration. Survival for explanted patients was 95% at 12 months and 85% at 42 months. Reimplant-free and transplant-free survival was 74% at 42 months. Similar to the findings by Goldstein et al.,2 our patient was young, had a nonischemic cardiomyopathy (peripartum), and was ill for less than 1 year. This case demonstrates that VAD thrombosis as indicated by echocardiographic Doppler assessments may occur in association with recovery of LV function, and we propose that
245
recovery of LV function should be considered in patients presenting with VAD thrombosis. Our patient had RV dysfunction but did well with VAD explant. This suggests that LVAD explant can be done in patients with mild RV dysfunction. We recommend the use of echocardiography to assess LV recovery in patients with substrate for recovery such as young age, nonischemic cardiomyopathy of less than 1 year, and peripartum cardiomyopathy. In patients with recovery of LV function, VAD explant can be done as the procedure is usually well tolerated with good outcomes and explant may help prevent VAD thrombosis or thromboembolism. References 1. Slaughter MS, Rogers JG, Milano CA, et al; HeartMate II Investigators: Advanced heart failure treated with c ontinuous-flow left ventricular assist device. N Engl J Med 361: 2241–2251, 2009. 2. Goldstein DJ, Maybaum S, MacGillivray TE, et al; HeartMate II Clinical Investigators: Young patients with nonischemic cardiomyopathy have higher likelihood of left ventricular recovery during left ventricular assist device support. J Card Fail 18: 392–395, 2012. 3. Schwarz KQ, Parikh SS, Chen X, et al: Non-invasive flow measurement of a rotary pump ventricular assist device using quantitative contrast echocardiography. J Am Soc Echocardiogr 23: 324–329, 2010.
Case Reports
Ventricular Assist Device Thrombosis Following Recovery of Left Ventricular Function Andrew R. Sifain, Karl Q. Schwarz, William Hallinan, H. Todd Massey, and Jeffrey D. Alexis
Although ventricular assist devices (VADs) are lifesaving therapy for patients with severe heart failure, complications such as pump thrombosis can occur. In this report, we present a case of VAD thrombosis following recovery of left ventricular (LV) function. The patient had been supported with a VAD for 8 months, and at the time of presentation, echocardiography revealed near normal native systolic function, aortic valve opening with significant native heart ejection, reduced systolic flow in the outflow and inflow cannulae, and no forward flow through the VAD during diastole. The patient underwent successful VAD explant and examination of the pump revealed thrombus on the rotor. We propose that abnormal flow through the VAD seen with recovery of LV function may contribute to VAD thrombosis. ASAIO Journal 2014; 60:243–245.
Patient History A 30-year-old woman presented with a 2 week history of dyspnea on exertion and orthopnea following delivery of twins 2 months before presentation. On examination, she had a third heart sound and estimated jugular venous pressure of 16 mm Hg. An echocardiogram revealed LV ejection fraction (LVEF) of 10%, LV end-diastolic diameter 6.4 cm, and moderate-to-severe right ventricular (RV) dysfunction. Heart failure medications could not be titrated due to hypotension. Right heart catheterization revealed right atrial pressure 23 mm Hg, pulmonary artery pressure 48/37 mm Hg, pulmonary capillary wedge pressure 31 mm Hg, and cardiac index 1.03 L/min/m2. She received a HeartMate II LVAD as a bridge to transplantation and a Centrimag RV assist device (RVAD; Thoratec, Pleasanton, CA). Her RVAD was weaned 6 days later, and she was discharged home 19 days after VAD implant. Lactate dehydrogenase level at 3 months post VAD implant routine visit was 849 unit/L. Five months after VAD implantation, a transesophageal echocardiogram (TEE) revealed an LVEF of 47%. As she had a dilated and hypocontractile RV, the decision was made to continue to follow her clinically and not attempt explant. Eight months after VAD implant, she presented with lightheadedness, high power readings (12–12.7 watts), and a low pulsatility index (2.0) at her baseline VAD speed of 8,800 revolutions per minute (rpm). Blood work revealed lactate dehydrogenase level of 2,900 unit/L and a haptoglobin less than 20 mg/dl. Hemoglobin level was low at 7.6 g/dl. Her medications included aspirin and warfarin (international normalized ratio was 3.2 on admission and had been therapeutic previously). TEE demonstrated pump dysfunction, as systolic Doppler flow velocities in both the inflow and outflow cannulae were about half that expected and there was essentially no diastolic flow through the VAD (Figure 1, A and B). Left ventricular ejection fraction was 55%, the aortic valve opened vigorously with each native ventricular systole, and there was significant native heart ejection. There was no change in LVEF as VAD flow speed setting was decreased to a speed of 6,000 rpm. The absence of forward diastolic flow in the VAD outflow cannula changed to flow reversal when the speed setting was reduced to 6,000 rpm (Figure 1C). Quantitative assessment of flow in the outflow cannula over a spectrum of VAD speed settings showed that the minute flow rate was less than half that expected for a HeartMate II3 (Figure 1D). Doppler flow velocity through the outflow cannula was normal 3 months earlier (see Supplemental Digital Content 1, http://links.lww. com/ASAIO/A46). RV ejection fraction was mildly reduced. The clinical impression was VAD thrombosis.
Key Words: ventricular assist device, left ventricular recovery, peripartum cardiomyopathy, ventricular assist device thrombosis
Left ventricular assist devices (LVADs) have been a major
advancement in the treatment of end-stage heart failure and have been shown to decrease morbidity and mortality in comparison with optimal medical management.1 Recovery of left ventricular (LV) function, while not common, can occur following ventricular assist device (VAD) implant and allow for VAD explantation.2 In this report, we present the case of a patient with a history of cardiogenic shock, supported by a HeartMate II LVAD (Thoratec, Pleasanton, CA), who demonstrated VAD thrombosis following recovery of LV function and underwent successful VAD explant. We show the utility of echocardiography for assessing blood flow through a VAD and discuss the risk of VAD thrombosis associated with recovery of LV function.
From the Department of Medicine, Department of Surgery, and Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York. Submitted for consideration July 2013; accepted for publication in revised form November 2013. Disclosure: The authors have no conflicts of interest to report. Reprint Requests: Andrew R. Sifain, MD, Department of Anesthesia, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 604, Rochester, NY. Email: andrew_sifain@urmc. rochester.edu. Copyright © 2014 by the American Society for Artificial Internal Organs DOI: 10.1097/MAT.0000000000000036
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244 SIFAIN et al.
Figure 2. Thrombus formation in the ventricular assist device (VAD). Evaluation of the VAD revealed thrombus formation on the rotor assembly, occluding two of the three rotor pathways (printed with permission from Thoratec).
min). Aerosolized epoprostenol was administered via inhalation to decrease RV afterload. The chest was closed and she was taken to the intensive care unit for continued care. Lactate dehydrogenase level was 845 unit/L on postoperative day 4. She tolerated the explant well and was discharged home 9 days after explant. Examination of the pump revealed thrombus on the rotor (Figure 2). She has returned to work and continues to do well 18 months after explant. Discussion
Figure 1. Echocardiographic evidence of ventricular assist device (VAD) dysfunction. A: Doppler signal through the VAD inflow cannula at 7,800 revolutions per minute (rpm) reveals flow during systole (single white arrow) and no flow during diastole (double white arrows). B: Doppler signal through the VAD outflow cannula at 7,800 rpm reveals flow during systole (single white arrow) and no flow during diastole (double white arrows). C: Doppler signal through the VAD outflow cannula at 6,000 rpm reveals flow during systole (single white arrow) and reversal of flow in diastole (double white arrows). D: Doppler derived measurement of flow (Q corrected) through the VAD at varying pump speeds. Calculated flow rates are less than half expected based on rpm (Methods for detection of flow are described in the study by Schwarz et al.3).
The patient was taken to the operating room for LVAD exploration and possible explant. After placement of a radial arterial line, general anesthesia was induced with the patient remaining hemodynamically stable. A TEE demonstrated LVEF approximately 45%, with a moderately dilated and hypokinetic RV. Spectral Doppler identified only minimal low-velocity flow exiting the outflow graft into the aorta. The inflow cannula was in good position without discernable obstruction. The aortic valve opened with every beat, and there was trace aortic insufficiency. The patient was heparinized and placed on cardiopulmonary bypass to remove the LVAD. The inflow cannula was removed from the apex, and a complex plug constructed from felt and bovine pericardium was used to close the hole. The outflow graft was stapled in multiple layers; the drive line was divided as close to the fascia as possible, and the entire VAD assembly was removed en bloc. The patient was weaned off cardiopulmonary bypass on epinephrine (0.02 μg/kg/min) and milrinone (0.5 μg/kg/
Thrombosis remains a feared complication associated with VAD implantation. Issues such as decreased blood volume through the pump and altered blood flow through the pump, as seen with recovery of LV function, may be causal factors. In our patient, there was evidence of near normal native systolic function with vigorous aortic valve opening and significant native heart ejection. This would lead to decreased flow through the pump in systole. There was also abnormal diastolic flow through the pump. Higher diastolic suction pressure in the recovered ventricle “robs” the VAD of blood due to a combination of native diastolic ventricular volume expansion and higher pressure differential between the LV cavity and aorta. Volume that is expanding the ventricle is volume that is not going into the VAD, and recovered ventricles with significant native ventricular ejection have higher diastolic aortic pressures. We propose that with recovery of LV function (including improved diastolic function), decreased systolic flow through the VAD and diastolic reversal of flow through the VAD can occur, and this abnormal flow can contribute to thrombosis. In our patient, there were four echo-Doppler findings that suggested pump malfunction: 1) the systolic flow velocities in the outflow and inflow cannulae were about half that expected,3 2) no forward flow was noted during diastole at the baseline speed setting, 3) the lack of forward diastolic flow turned to flow reversal at lower speed settings, and 4) quantitative assessment of VAD output showed less than half the expected volumetric flow rate at all settings. The performance of rotational VAD pumps is dependent on the pump’s efficiency and the pressure differential between the LV and aorta. The finding of low systolic outflow cannula flow velocity illustrated the effect of low pump efficiency, as the pump was not able to achieve normal systolic flow rates even during native ventricular systole when the pressure gradient between the LV
THROMBOSIS FOLLOWING RECOVERY OF LV FUNCTION
cavity and the aorta is lowest. The finding of absent diastolic outflow cannula flow also illustrates the low pump efficiency, as the VAD was not able to overcome the pressure differential between the aorta and LV cavity. The finding of diastolic flow reversal in the outflow cannula at the lowest tested VAD speed illustrates the return of normal LV diastolic suction, which was able to overcome the weak VAD pump, which itself was fighting to keep flow in the forward direction. Finally, the quantitative assessment of VAD output showed clearly low pump efficiency over a wide range of speed settings. Recovery of LV function is not common after placement of an LVAD but can occur. In an analysis of patients supported on a HeartMate II LVAD, Goldstein et al.2 recently reported that recovery of LV function was most common in patients who were young (age less than 40), with nonischemic cardiomyopathy of less than 1 year in duration. Survival for explanted patients was 95% at 12 months and 85% at 42 months. Reimplant-free and transplant-free survival was 74% at 42 months. Similar to the findings by Goldstein et al.,2 our patient was young, had a nonischemic cardiomyopathy (peripartum), and was ill for less than 1 year. This case demonstrates that VAD thrombosis as indicated by echocardiographic Doppler assessments may occur in association with recovery of LV function, and we propose that
245
recovery of LV function should be considered in patients presenting with VAD thrombosis. Our patient had RV dysfunction but did well with VAD explant. This suggests that LVAD explant can be done in patients with mild RV dysfunction. We recommend the use of echocardiography to assess LV recovery in patients with substrate for recovery such as young age, nonischemic cardiomyopathy of less than 1 year, and peripartum cardiomyopathy. In patients with recovery of LV function, VAD explant can be done as the procedure is usually well tolerated with good outcomes and explant may help prevent VAD thrombosis or thromboembolism. References 1. Slaughter MS, Rogers JG, Milano CA, et al; HeartMate II Investigators: Advanced heart failure treated with c ontinuous-flow left ventricular assist device. N Engl J Med 361: 2241–2251, 2009. 2. Goldstein DJ, Maybaum S, MacGillivray TE, et al; HeartMate II Clinical Investigators: Young patients with nonischemic cardiomyopathy have higher likelihood of left ventricular recovery during left ventricular assist device support. J Card Fail 18: 392–395, 2012. 3. Schwarz KQ, Parikh SS, Chen X, et al: Non-invasive flow measurement of a rotary pump ventricular assist device using quantitative contrast echocardiography. J Am Soc Echocardiogr 23: 324–329, 2010.
