J CARD SURG 2015;30:869–873
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
selected patients.8 Prognosis of cardiac sarcomas underwent transplantation could be better than any surgical methods with good survival range of 48 months more.1,8 However, many patients are not transplanted because of the high risk of tumor recurrence or metastasis and the possible enhancement of tumor growth by immunosuppressive drugs. In this case, heart transplantation was considered as a treatment option because complete surgical resection of the tumor would result in the inability to repair the heart and the patient underwent the same immunosuppression protocol as other usual transplantation patients in our hospital. Resection and reconstruction is rather difficult when the tumor is deeply infiltrated into the left upper pulmonary vein. In such cases, fresh or bovine pericardial angioplasty of the pulmonary veins is an option.5 In many cases, cardiac sarcoma is so widespread that only palliative surgery can be performed. Although a few patients in the current studies underwent cardiac transplantation, this procedure might be described to have a potential to provide disease control for selected patients with primary cardiac sarcoma. REFERENCES 1. Gowdamarajan A, Michler RE: Therapy for primary cardiac tumors: Is there a role for heart transplantation? Curr Opin Cardiol 2000;15:121–125. 2. Catton C: The management of malignant cardiac tumors: Clinical considerations. Smin Diagn Pathol 2008;25(1): 69–75. 3. Higgins JC, Katzman PJ, Yeager SB, et al: Extraskeletal Ewing’s sarcoma of primary cardiac origin. Pediatr Cardiol 1994;15:207–208. 4. Kim GS, Kim JJ, Kim JB, et al: Fate of atrioventricular valve function of the transplanted heart. Circ J 2014;78 (7):1654–1660. 5. Paul S, Ramanathan T, Cohen DM, et al: Primary Ewing sarcoma invading the heart: Resection and reconstruction. J Thorac Cardiovasc Surg 2007;133(6):1667–1669. 6. Truong PT, Jones SO, Martens B, et al: Treatment and outcomes in adult patients with primary cardiac sarcoma: The British Columbia Cancer Agency experience. Ann Surg Oncol 2009;16(12):3358–3365. 7. Simpson L, Kumar SK, Okuno SH: Malignant primary cardiac tumors: review of a single institution experience. Cancer 2008;112:2440–2446. 8. Lok SI, Schipper ME, De Jonge N, et al: Two young women with soft tissue tumours of the heart. Eur J Cardiothorac Surg 2014;45(1):193–196.
871
Left Ventricular Assist Device (LVAD) as a Bridge to Recovery for Tachycardia-Mediated Cardiomyopathy Michael B. Stokes, F.R.A.C.P.,* Pankaj Saxena, F.R.A.C.S., Ph.D.,y Justin A. Mariani, F.R.A.C.P., Ph.D.,* David M. Kaye, F.R.A.C.P., Ph.D.,* Peter Bergin, F.R.A.C.P.,* and David C. McGiffin, F.R.A.C.S.y *Department of Advanced Heart Failure and Transplantation, The Alfred Hospital and Monash University, Melbourne, Australia; and yDepartment of Cardiothoracic Surgery, The Alfred Hospital and Monash University, Melbourne, Australia ABSTRACT A case is described of cardiogenic shock that occurred following use of sotalol in a patient with severe left ventricular dysfunction. The patient required left ventricular assist device (LVAD) placement with subsequent myocardial recovery to a degree that allowed eventual device removal following 140 days of support. doi: 10.1111/jocs.
12632 (J Card Surg 2015;30:871–873) Myocardial recovery and subsequent removal of an left ventricular assist device (LVAD) is uncommon. We present a case of tachycardia-mediated cardiomyopathy presenting with cardiogenic shock requiring LVAD placement with subsequent recovery to a degree that allowed safe device removal. Our approach to assessment of suitability of myocardial recovery is demonstrated in this case. PATIENT PROFILE A 53-year-old male presented to his local physician with palpitations and dyspnea and was found to be in atrial fibrillation (AF) with rapid ventricular response (RVR). Past medical history included smoking of 15 pack years and remote heavy alcohol consumption. He was started on bisoprolol, digoxin, and warfarin. Transthoracic echocardiogram (TTE) demonstrated a mildly dilated left ventricle with an ejection fraction (LVEF) of 25% and moderate left atrial enlargement. Six weeks later, he presented with poorly controlled AF with RVR with a heart rate (HR) of 150 to 170/min. His bisoprolol and digoxin were discontinued and he
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Michael B. Stokes, F.R.A.C.P., Heart Centre, The Alfred Hospital, Commercial Road, Prahan, Victoria, Australia, 3004. Fax: 61 3 9594 6239; e-mail: [email protected]
872
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
J CARD SURG 2015;30:869–873
resting LVEF estimated at 40% and good augmentation observed in response to dobutamine at 10 mcg/kg/ min with an estimated LVEF of 45% to 50%. Exercise right heart catheterization using a standardized bike exercise protocol with Swan–Ganz catheter placement via the right internal jugular vein demonstrated good exercise tolerance to a workload of 91 W. His cardiac output was measured using the thermodilution method. There was recruitment in cardiac output to a peak estimated at 14.5 L/min (from a resting cardiac output of 5.5 L/min). At peak exercise, his LVAD output remained at 5.5 L/min suggesting recruitment of intrinsic cardiac output of approximately 9 L/min (Table 1). The patient then underwent explantation of his LVAD on cardiopulmonary bypass. The device was disconnected from the sewing cuff and the LV cavity explored to exclude any thrombus. The sewing ring was removed and the defect in the apex of the LV was repaired with a Dacron patch using 2-0 prolene. Using a side biting clamp on the ascending aorta the Dacron graft was removed and the aorta was repaired with 4-0 prolene (Ethicon Inc., Somerville, NJ, USA) in two layers. The explant of the patient’s device occurred following 140 days of LVAD support. He made an excellent recovery with gradual reintroduction of heart failure therapy and remained in sinus rhythm throughout the recovery period. A cardiac magnetic resonance imaging (MRI) scan performed at nine days following device explantation demonstrated a LVEF of 38% and normal RV systolic function. Fibrosis and regional wall motion defects were observed on the cardiac MRI in the area of the explanted LVAD (Fig. 1). At three months following discharge, the patient continued to improve and was functioning at NYHA Class I with repeat TTE demonstrating ongoing improvement in LVEF to 45%.
was started on sotalol 40 mg QD. Four days after his therapy was changed, he represented to a local hospital with cardiogenic shock. Systolic blood pressure was 70 to 80 mmHg and his AF was again associated with RVR at a rate of 160 to 180/min. He complained of nausea, fatigue, and abdominal pain. His lactate level was elevated at 0.04 mg/dL and there was evidence of acute liver injury (ALT 2.36 mg/dL & AST 1.61 mg/dL), as well as acute kidney injury (creatinine 1.90 mg/dL). He was started on intravenous dobutamine and amiodarone. Due to ongoing high inotropic requirement, persistent hypotension, and severe LV dysfunction on TTE, the patient was placed on venous-arterial extracorporeal membrane oxygenation (VA-ECMO) with percutaneous cannula placement into the femoral vein and femoral artery. While on VA-ECMO, the patient was cardioverted into sinus rhythm following a transesophageal echocardiogram (TEE) that excluded the presence of left atrial appendage thrombus. Two attempts were made at weaning the patient off VA-ECMO at days 3 and 5 postcannulation. With reduction in ECMO flow rates to approximately 1 L/min, there was minimal recruitment of his native LV function. His calculated LV stroke volume using echocardiographic data was estimated at 25 mL. The patient then underwent insertion of a HeartWare left ventricular assist device (HVAD) (HeartWare, Framingham, MA, USA) after seven days of ECMO support. Histopathology of the myocardial core demonstrated mild nonspecific changes with no inflammation or myocyte necrosis with mild individual myocyte hypertrophy. In the two to three months following LVAD insertion the patient made an excellent functional recovery improving to NYHA Class I. Improved pulsatility was noted on the HeartWare device monitor. He was started on heart failure therapy including perindopril and bisoprolol which were gradually up-titrated and he remained in sinus rhythm. Improvement in the patient’s LV function was observed on follow-up TTE at three months postLVAD insertion to approximately 40% to 45%. To assess the patient’s suitability for explantation, a TEE with administration of intravenous dobutamine gradually up-titrated from 5 to 20 mcg/kg/min was performed. His LV contractility was assessed with a
DISCUSSION The reported proportion of patients experiencing myocardial recovery to a degree to allow explantation following LVAD placement has ranged from 4.5% to 24.4%. This reflects differences in patient selection for device insertion, differing patient populations, and the aggressiveness of pursuing a recovery strategy.1
TABLE 1 Hemodynamic Data Measured With Right Heart Catheterization Performed With Bike Exercise Exercise Baseline 27 Watts (3 min) 54 Watts (6 min) 91 Watts (9 min)
Estimated LVAD flow (L/min)
Cardiac Ouput (L/min)
Mean PCWP (mmHg)
Pulmonary Artery Pressure
4.4
5.5 –
9 20
23/7 40/18
–
22
50/19
14.5
22
54/20
5.5
LVAD ¼ left ventricular assist device; PCWP ¼ pulmonary capillary wedge pressure.
J CARD SURG 2015;30:869–873
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
873
Figure 1. Cardiac MRI demonstrating areas of fibrosis within the antero-septum and apex and the region of the explantation of the LVAD at the apex of the left ventricle.
A higher incidence of bridge to recovery following LVAD placement occurs in patients under the age of 45 years, particularly with a shorter duration of heart failure. A nonischemic etiology of heart failure is associated with a higher incidence of recovery compared with an ischemic etiology. Acute myocarditis and peripartum cardiomyopathy are diagnoses where the clinical course is more commonly associated with recovery.2 Tachycardia-mediated cardiomyopathy occurs in the setting of persisting uncontrolled ventricular rate from arrhythmias such as atrial fibrillation, atrial flutter, and other supraventricular tachyarrhythmias. Persistent tachycardia results in dilatation of all cardiac chambers, typically accompanied by thinning or preservation of wall thickness without hypertrophy. This occurs from disruption of the extracellular matrix, which can compromise myocyte alignment, with resultant chamber dilatation. Changes in myocyte structure, size, and protein synthesis have also been reported. Myocardial ischemia is also a proposed mechanism given the supra-physiologic heart rates and high ventricular filling pressures.3 Two previously reported cases in the literature have highlighted the role of LVAD placement with eventual recovery allowing device removal in pediatric patients with ectopic atrial tachycardia. Both of these cases highlighted the improvement in LV function following restoration of sinus rhythm using pharmacotherapy that allowed eventual device removal at 28 days and 51 days, respectively, following LVAD placement.4,5 A number of protocols have been published that define criteria to guide clinicians in selection of potential candidacy for LVAD removal. These consist of a number of echocardiographic, clinical, and hemodynamic parameters which include temporary reductions in LVAD speed to assess myocardial reserve and recruitment.6 In the described clinical scenario, we assessed candidacy based upon improvement in the patient’s symptoms to NYHA Class I and improvement in LVEF on serial TTE.
Because of poor endocardial definition and difficulty quantifying LVEF on TTE, TEE was used with dobutamine stress which successfully demonstrated myocardial recruitment and a LVEF of 45% to 50%.
CONCLUSION This case highlights the role of mechanical support in patients with cardiogenic shock and the caution required with sotalol use in patients with significant LV dysfunction. The potential for improvement in LV function in patients with tachycardia-mediated cardiomyopathy is also shown from the case. A successful method assessing recovery of LV function and myocardial reserve is demonstrated by the use of exercise right heart catheterization and dobutamine TEE.
REFERENCES 1. Marcini DM, Beniaminovitz A, Levin H, et al: Low incidence of myocardial recovery after left ventricular assist device implantation in patients with chronic heart failure. Circulation 1998;98:2383–2389. 2. Birks EJ, Tansley PD, Hardy J, et al: Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med 2006;355:1873–1884. 3. Shinbane JS, Wood MA, Jensen DN, et al: Tachycardiainduced cardiomyopathy: A review of animal model and clinical studies. J Am Coll Cardiol 1997;29:709– 715. 4. Cavanaugh JL, Miyamoto SD, da Cruz E, et al: Predicting recovery: Successful explant of a ventricular assist device in a child with dilated cardiomyopathy. J Heart Lung Trasnplant 2010;29:105–108. 5. Tateaki H, Masuda M, Nishida T, et al: Successful treatment of tachycardia-induced cardiomyopathy with LVAD in a 12-year-old boy. Ann Thorac Surgery 2005;80: e5–e7. 6. Guglin M, Miller L: Myocardial recovery with left ventricular assist devices. Curr Treat Options Cardiovasc Med 2012;14 (4):370–383.
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
selected patients.8 Prognosis of cardiac sarcomas underwent transplantation could be better than any surgical methods with good survival range of 48 months more.1,8 However, many patients are not transplanted because of the high risk of tumor recurrence or metastasis and the possible enhancement of tumor growth by immunosuppressive drugs. In this case, heart transplantation was considered as a treatment option because complete surgical resection of the tumor would result in the inability to repair the heart and the patient underwent the same immunosuppression protocol as other usual transplantation patients in our hospital. Resection and reconstruction is rather difficult when the tumor is deeply infiltrated into the left upper pulmonary vein. In such cases, fresh or bovine pericardial angioplasty of the pulmonary veins is an option.5 In many cases, cardiac sarcoma is so widespread that only palliative surgery can be performed. Although a few patients in the current studies underwent cardiac transplantation, this procedure might be described to have a potential to provide disease control for selected patients with primary cardiac sarcoma. REFERENCES 1. Gowdamarajan A, Michler RE: Therapy for primary cardiac tumors: Is there a role for heart transplantation? Curr Opin Cardiol 2000;15:121–125. 2. Catton C: The management of malignant cardiac tumors: Clinical considerations. Smin Diagn Pathol 2008;25(1): 69–75. 3. Higgins JC, Katzman PJ, Yeager SB, et al: Extraskeletal Ewing’s sarcoma of primary cardiac origin. Pediatr Cardiol 1994;15:207–208. 4. Kim GS, Kim JJ, Kim JB, et al: Fate of atrioventricular valve function of the transplanted heart. Circ J 2014;78 (7):1654–1660. 5. Paul S, Ramanathan T, Cohen DM, et al: Primary Ewing sarcoma invading the heart: Resection and reconstruction. J Thorac Cardiovasc Surg 2007;133(6):1667–1669. 6. Truong PT, Jones SO, Martens B, et al: Treatment and outcomes in adult patients with primary cardiac sarcoma: The British Columbia Cancer Agency experience. Ann Surg Oncol 2009;16(12):3358–3365. 7. Simpson L, Kumar SK, Okuno SH: Malignant primary cardiac tumors: review of a single institution experience. Cancer 2008;112:2440–2446. 8. Lok SI, Schipper ME, De Jonge N, et al: Two young women with soft tissue tumours of the heart. Eur J Cardiothorac Surg 2014;45(1):193–196.
871
Left Ventricular Assist Device (LVAD) as a Bridge to Recovery for Tachycardia-Mediated Cardiomyopathy Michael B. Stokes, F.R.A.C.P.,* Pankaj Saxena, F.R.A.C.S., Ph.D.,y Justin A. Mariani, F.R.A.C.P., Ph.D.,* David M. Kaye, F.R.A.C.P., Ph.D.,* Peter Bergin, F.R.A.C.P.,* and David C. McGiffin, F.R.A.C.S.y *Department of Advanced Heart Failure and Transplantation, The Alfred Hospital and Monash University, Melbourne, Australia; and yDepartment of Cardiothoracic Surgery, The Alfred Hospital and Monash University, Melbourne, Australia ABSTRACT A case is described of cardiogenic shock that occurred following use of sotalol in a patient with severe left ventricular dysfunction. The patient required left ventricular assist device (LVAD) placement with subsequent myocardial recovery to a degree that allowed eventual device removal following 140 days of support. doi: 10.1111/jocs.
12632 (J Card Surg 2015;30:871–873) Myocardial recovery and subsequent removal of an left ventricular assist device (LVAD) is uncommon. We present a case of tachycardia-mediated cardiomyopathy presenting with cardiogenic shock requiring LVAD placement with subsequent recovery to a degree that allowed safe device removal. Our approach to assessment of suitability of myocardial recovery is demonstrated in this case. PATIENT PROFILE A 53-year-old male presented to his local physician with palpitations and dyspnea and was found to be in atrial fibrillation (AF) with rapid ventricular response (RVR). Past medical history included smoking of 15 pack years and remote heavy alcohol consumption. He was started on bisoprolol, digoxin, and warfarin. Transthoracic echocardiogram (TTE) demonstrated a mildly dilated left ventricle with an ejection fraction (LVEF) of 25% and moderate left atrial enlargement. Six weeks later, he presented with poorly controlled AF with RVR with a heart rate (HR) of 150 to 170/min. His bisoprolol and digoxin were discontinued and he
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Michael B. Stokes, F.R.A.C.P., Heart Centre, The Alfred Hospital, Commercial Road, Prahan, Victoria, Australia, 3004. Fax: 61 3 9594 6239; e-mail: [email protected]
872
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
J CARD SURG 2015;30:869–873
resting LVEF estimated at 40% and good augmentation observed in response to dobutamine at 10 mcg/kg/ min with an estimated LVEF of 45% to 50%. Exercise right heart catheterization using a standardized bike exercise protocol with Swan–Ganz catheter placement via the right internal jugular vein demonstrated good exercise tolerance to a workload of 91 W. His cardiac output was measured using the thermodilution method. There was recruitment in cardiac output to a peak estimated at 14.5 L/min (from a resting cardiac output of 5.5 L/min). At peak exercise, his LVAD output remained at 5.5 L/min suggesting recruitment of intrinsic cardiac output of approximately 9 L/min (Table 1). The patient then underwent explantation of his LVAD on cardiopulmonary bypass. The device was disconnected from the sewing cuff and the LV cavity explored to exclude any thrombus. The sewing ring was removed and the defect in the apex of the LV was repaired with a Dacron patch using 2-0 prolene. Using a side biting clamp on the ascending aorta the Dacron graft was removed and the aorta was repaired with 4-0 prolene (Ethicon Inc., Somerville, NJ, USA) in two layers. The explant of the patient’s device occurred following 140 days of LVAD support. He made an excellent recovery with gradual reintroduction of heart failure therapy and remained in sinus rhythm throughout the recovery period. A cardiac magnetic resonance imaging (MRI) scan performed at nine days following device explantation demonstrated a LVEF of 38% and normal RV systolic function. Fibrosis and regional wall motion defects were observed on the cardiac MRI in the area of the explanted LVAD (Fig. 1). At three months following discharge, the patient continued to improve and was functioning at NYHA Class I with repeat TTE demonstrating ongoing improvement in LVEF to 45%.
was started on sotalol 40 mg QD. Four days after his therapy was changed, he represented to a local hospital with cardiogenic shock. Systolic blood pressure was 70 to 80 mmHg and his AF was again associated with RVR at a rate of 160 to 180/min. He complained of nausea, fatigue, and abdominal pain. His lactate level was elevated at 0.04 mg/dL and there was evidence of acute liver injury (ALT 2.36 mg/dL & AST 1.61 mg/dL), as well as acute kidney injury (creatinine 1.90 mg/dL). He was started on intravenous dobutamine and amiodarone. Due to ongoing high inotropic requirement, persistent hypotension, and severe LV dysfunction on TTE, the patient was placed on venous-arterial extracorporeal membrane oxygenation (VA-ECMO) with percutaneous cannula placement into the femoral vein and femoral artery. While on VA-ECMO, the patient was cardioverted into sinus rhythm following a transesophageal echocardiogram (TEE) that excluded the presence of left atrial appendage thrombus. Two attempts were made at weaning the patient off VA-ECMO at days 3 and 5 postcannulation. With reduction in ECMO flow rates to approximately 1 L/min, there was minimal recruitment of his native LV function. His calculated LV stroke volume using echocardiographic data was estimated at 25 mL. The patient then underwent insertion of a HeartWare left ventricular assist device (HVAD) (HeartWare, Framingham, MA, USA) after seven days of ECMO support. Histopathology of the myocardial core demonstrated mild nonspecific changes with no inflammation or myocyte necrosis with mild individual myocyte hypertrophy. In the two to three months following LVAD insertion the patient made an excellent functional recovery improving to NYHA Class I. Improved pulsatility was noted on the HeartWare device monitor. He was started on heart failure therapy including perindopril and bisoprolol which were gradually up-titrated and he remained in sinus rhythm. Improvement in the patient’s LV function was observed on follow-up TTE at three months postLVAD insertion to approximately 40% to 45%. To assess the patient’s suitability for explantation, a TEE with administration of intravenous dobutamine gradually up-titrated from 5 to 20 mcg/kg/min was performed. His LV contractility was assessed with a
DISCUSSION The reported proportion of patients experiencing myocardial recovery to a degree to allow explantation following LVAD placement has ranged from 4.5% to 24.4%. This reflects differences in patient selection for device insertion, differing patient populations, and the aggressiveness of pursuing a recovery strategy.1
TABLE 1 Hemodynamic Data Measured With Right Heart Catheterization Performed With Bike Exercise Exercise Baseline 27 Watts (3 min) 54 Watts (6 min) 91 Watts (9 min)
Estimated LVAD flow (L/min)
Cardiac Ouput (L/min)
Mean PCWP (mmHg)
Pulmonary Artery Pressure
4.4
5.5 –
9 20
23/7 40/18
–
22
50/19
14.5
22
54/20
5.5
LVAD ¼ left ventricular assist device; PCWP ¼ pulmonary capillary wedge pressure.
J CARD SURG 2015;30:869–873
STOKES, ET AL. LVAD AS BRIDGE TO RECOVERY
873
Figure 1. Cardiac MRI demonstrating areas of fibrosis within the antero-septum and apex and the region of the explantation of the LVAD at the apex of the left ventricle.
A higher incidence of bridge to recovery following LVAD placement occurs in patients under the age of 45 years, particularly with a shorter duration of heart failure. A nonischemic etiology of heart failure is associated with a higher incidence of recovery compared with an ischemic etiology. Acute myocarditis and peripartum cardiomyopathy are diagnoses where the clinical course is more commonly associated with recovery.2 Tachycardia-mediated cardiomyopathy occurs in the setting of persisting uncontrolled ventricular rate from arrhythmias such as atrial fibrillation, atrial flutter, and other supraventricular tachyarrhythmias. Persistent tachycardia results in dilatation of all cardiac chambers, typically accompanied by thinning or preservation of wall thickness without hypertrophy. This occurs from disruption of the extracellular matrix, which can compromise myocyte alignment, with resultant chamber dilatation. Changes in myocyte structure, size, and protein synthesis have also been reported. Myocardial ischemia is also a proposed mechanism given the supra-physiologic heart rates and high ventricular filling pressures.3 Two previously reported cases in the literature have highlighted the role of LVAD placement with eventual recovery allowing device removal in pediatric patients with ectopic atrial tachycardia. Both of these cases highlighted the improvement in LV function following restoration of sinus rhythm using pharmacotherapy that allowed eventual device removal at 28 days and 51 days, respectively, following LVAD placement.4,5 A number of protocols have been published that define criteria to guide clinicians in selection of potential candidacy for LVAD removal. These consist of a number of echocardiographic, clinical, and hemodynamic parameters which include temporary reductions in LVAD speed to assess myocardial reserve and recruitment.6 In the described clinical scenario, we assessed candidacy based upon improvement in the patient’s symptoms to NYHA Class I and improvement in LVEF on serial TTE.
Because of poor endocardial definition and difficulty quantifying LVEF on TTE, TEE was used with dobutamine stress which successfully demonstrated myocardial recruitment and a LVEF of 45% to 50%.
CONCLUSION This case highlights the role of mechanical support in patients with cardiogenic shock and the caution required with sotalol use in patients with significant LV dysfunction. The potential for improvement in LV function in patients with tachycardia-mediated cardiomyopathy is also shown from the case. A successful method assessing recovery of LV function and myocardial reserve is demonstrated by the use of exercise right heart catheterization and dobutamine TEE.
REFERENCES 1. Marcini DM, Beniaminovitz A, Levin H, et al: Low incidence of myocardial recovery after left ventricular assist device implantation in patients with chronic heart failure. Circulation 1998;98:2383–2389. 2. Birks EJ, Tansley PD, Hardy J, et al: Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med 2006;355:1873–1884. 3. Shinbane JS, Wood MA, Jensen DN, et al: Tachycardiainduced cardiomyopathy: A review of animal model and clinical studies. J Am Coll Cardiol 1997;29:709– 715. 4. Cavanaugh JL, Miyamoto SD, da Cruz E, et al: Predicting recovery: Successful explant of a ventricular assist device in a child with dilated cardiomyopathy. J Heart Lung Trasnplant 2010;29:105–108. 5. Tateaki H, Masuda M, Nishida T, et al: Successful treatment of tachycardia-induced cardiomyopathy with LVAD in a 12-year-old boy. Ann Thorac Surgery 2005;80: e5–e7. 6. Guglin M, Miller L: Myocardial recovery with left ventricular assist devices. Curr Treat Options Cardiovasc Med 2012;14 (4):370–383.
