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Ann Thorac Surg 1998;66:555-557
© 1998 The Society of Thoracic Surgeons

Case Reports

Recovery from end-stage ischemic cardiomyopathy during long-term LVAD support

Lars Pietsch, MDa, Horst Laube, MDa, Gerd Baumann, MD, PhDb, Wolfgang Konertz, MD, PhDa

a Department of Cardiac Surgery, Charité, Humboldt University, Berlin, Germany
b Department of Cardiology, Charité, Humboldt University, Berlin, Germany

Accepted for publication February 25, 1998.

Address reprint requests to Dr Pietsch, Universitätsklinikum Charite, Klinik für Herzchirurgie, Schumannstr 20-21, 10717 Berlin, Germany
e-mail: (cardiac&rz.charite.hu-berlin.de)


   Abstract
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 Abstract
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A patient with ischemic cardiomyopathy and extremely reduced left ventricular function (left ventricular ejection fraction = 0.10) presented to our institution for cardiac transplantation. Because of his worsening condition he was placed on the Novacor left ventricular assist device. During 3 months of support his left ventricular function recovered and he successfully underwent percutaneous transluminal coronary angioplasty and minimally invasive direct coronary artery bypass grafting procedures; subsequently he could be weaned from the left ventricular assist device and discharged. The patient is no longer considered for cardiac transplantation.


   Introduction
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There is increasing evidence that some patients’ hearts recover during long-term left ventricular (LV) assist [1]. This has been observed with patients after heterotopic heart transplantation [2], as well as after mechanical circulatory assist.

Successful coronary revascularization is highly dependent on the presence of viable myocardium. Tools for discriminating hibernating myocardium from scar and nonviable tissue are not perfect. Currently no technique shows 100% accuracy, especially in extremely dysfunctional hearts [3].

A 54-year-old patient was transferred to our institution with cardiac failure. An intensified medical regimen including diuretics, ß-blockers, digitalis, and angiotensin-converting enzyme inhibitors failed to improve his situation. Cardiac catheterization showed two-vessel disease with occlusion of the proximal left anterior descending artery and a 75% stenosis of the circumflex artery. Left ventricular function was extremely reduced, with an LV ejection fraction of 0.10. The LV end-diastolic volume was 287 mL, and the end-systolic volume was 258 mL (Fig 1). Cardiac index was calculated as 1.3 L · min-1 · m-2 by the Fick method. Pulmonary hypertension with a mean pressure of 45 mm Hg, a wedge pressure of 24 mm Hg, and a pulmonary vascular resistance of 8 Wood units were present. Scintigraphy showed no viable myocardium.



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  		Fig 1. Left ventriculogram at admission showing severe left ventricular dysfunction and increased left ventricular volumes (EF = ejection fraction.)

 
Because of the elevated pulmonary vascular resistance, cardiac transplantation seemed to be contraindicated and the patient was placed on the wearable Novacor LV assist device (Baxter Healthcare Corporation, Irvine, CA) for improvement of the peripheral circulation and to see whether his pulmonary hypertension was reversible with long-term unloading of the left ventricle. Implantation and postoperative course were uneventful, and the patient could be transferred to a partial outpatient status after 6 weeks. Two months later cardiac recatheterization, which is our routine institutional protocol for patients on long-term chronic LV assist devices, showed an unforeseen recovery of the myocardium. The LV ejection fraction was 0.46 with the device on and fell to 0.36 after the Novacor device was switched off (Fig 2). Left ventricular volumes had returned to near normal. Pulmonary artery pressure had dropped to normal on the device and showed no increase when the LV assist device was switched off. This, the increase in contractility, and the improved LV function made treatment of the underlying coronary artery disease possible. The patient underwent a successful percutaneous transluminal coronary angioplasty of the circumflex artery, and the next day minimally invasive direct coronary artery bypass grafting of the left internal mammary artery to the left anterior descending artery on the beating heart was performed.



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  		Fig 2. Left ventriculogram after recovery with the left ventricular assist device switched off showed remarkable recovery of left ventricular function and dimensions.

 
After recovery from the operation, the Novacor LV assist device was set on the fixed-rate mode at 60 beats/min, and slowly during three subsequent weeks the rate was slowed down to 40 beats/min. As the patient tolerated this gradual decrease of support well, he underwent elective removal of the device 4 weeks after revascularization. Six weeks later the patient was discharged home. The LV ejection fraction at this time had increased to 0.50. Six months later the patient is doing well with medication of digitalis, angiotensin-converting enzyme inhibitor, ß-blocker, and aspirin. Echocardiographic estimation of LV function in the outpatient clinic showed an unchanged LV ejection fraction of 0.50.


   Comment
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Several points in this report seem noteworthy. First is the inability of nuclear scan to detect viable myocardium in this patient. This could be caused by two mechanisms: (1) the metabolic status of hibernating myocardium and (2) high wall tension and stretch on the epicardial vessels making perfusion indetectable. There is evidence that myocardial perfusion is limited not only by hypertrophy but also by dilatation of the left ventricle [3].

Chronic LV unloading leads to a decrease in LV size, wall tension, and intramyocardial pressurizing force, which subsequently improves perfusion and function, a pathophysiologic pathway that is currently being thoroughly investigated for the LV size reduction operation [4]. Recovery of LV function in our patient made possible treatment of the underlying coronary artery disease, which could be performed rather atraumatically by a so-called hybrid procedure, which means a combination of percutaneous catheter techniques and a minimally invasive cardiac operation. Surgical revascularization of the posterior wall with the Novacor device in situ would have been extremely technically demanding. Cardiopulmonary bypass, cardioplegic arrest, and extensive dissection of the heart were avoided by use of the hybrid procedure.

Recovery of the heart after chronic LV assist has been observed in the setting of myocarditis [5] and occasionally in idiopathic dilative cardiomyopathy. Also, we and others found reversal of LV dysfunction in patients with ischemic dilative cardiomyopathy after heterotopic cardiac transplantation and concomitant repair of the recipient’s heart [2, 6]. In 1 pediatric patient with a large anterior myocardial infarction caused by an anomalous left coronary artery from the pulmonary artery, it was possible to explant the donor heart after near-complete recovery of the native heart had occurred 3 years after revascularization and simultaneous heterotopic cardiac transplantation [6].

This case report indicates that some high-risk patients may benefit from LV assist device implantation as a "bridge to repair" rather than a "bridge to transplantation," which has been shown to work well recently for other surgical procedures, for example, partial left ventriculectomy [7].


   References
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  1. Levin H.R., Oz M.C., Chen J.M., Packer M., Rose E.A., Burkhoff D. Reversal of chronic ventricular dilation in patients with end stage cardiomyopathy by prolonged mechanical unloading. Circulation 1995;91:2717-2720.[Abstract/Free Full Text]
  2. Konertz W., Sheikzadeh A., Weigand M., Friedl A., Bernhard A. Heterotopic heart transplantation—current indications for the procedure with results in 10 patients. Tex Heart Inst J 1988;15:159-162.
  3. Soha G.B., Macintyre J., Brunken R., et al. Present assessment of myocardial viability by nuclear imaging. Semin Nucl Med 1996;26:315-335.[Medline]
  4. Lunkenheimer P.P., Redmann K., Dietl L.H., et al. The assessment of intramural stress alignment on the beating heart in situ using microergometry: functional implications. Technol Healthcare 1997;5:115-122.
  5. Martin G., Kogpani S., Schindler M., van de Loo A., Yoshitoke M., Beyersdorf F. MEDOS HIA-VAD biventricular assist device for bridge to recovery in fulminant myocarditis. Ann Thorac Surg 1997;63:1145-1146.[Abstract/Free Full Text]
  6. Schmid C., Kececioglu D., Konertz W., Möllhoff T., Scheld H. Biological bridging after repair of an anomolous origin of a left coronary artery. Ann Thorac Surg 1996;62:1839-1841.[Abstract/Free Full Text]
  7. Frazier O.H., Radovancevic B., Odegaard P., Hernandez P., Wilansky S., Cook P. Left ventricular reduction in patients with idiopathic cardiomyopathy awaiting heart transplantation—preliminary results [Abstract]. J Heart Lung Transplant 1997;16:80.



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This Article
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