Midterm follow-up of patients who underwent removal of a left ventricular assist device after cardiac recovery from end-stage dilated cardiomyopathy

Hetzer, Roland; Müller, Johannes; Weng, Y.; Loebe, Matthias; Wallukat, G.

doi:10.1067/mtc.2000.108931

Cited by 89 publications

(43 citation statements)

References 14 publications

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“…As described previously, not all patients may recover sufficient ventricular strength to allow weaning from their LVAD 8 -12 and prolonged recovery of their myocardial contractile function. 21 In the present study, failing hearts required 1 month of unloading after a large LV infarction before we were able to measure functional improvement. In contrast, failing hearts that received intracoronary Adv-␤ 2 AR demonstrated significant LV functional improvement within the first week of ventricular unloading.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

et al. 2002

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Background-Mechanical assistance of the failing left ventricle (LV) can lead to functional recovery after a period of unloading, including restoration of ␤-adrenergic receptor (␤AR) inotropic reserve. We tested whether prolonged LV unloading of failing rabbit hearts by use of a heterotopic transplantation technique could lead to recovery and whether adenoviral gene transfer of a ␤ 2 AR transgene (Adv-␤ 2 AR) could alter this process. Methods and Results-Heart failure was induced by coronary artery ligation in adult New Zealand White rabbits. After 4 weeks, failing hearts were heterotopically transplanted into recipient rabbits, allowing normal coronary perfusion but complete LV unloading. We also placed an LV latex balloon for remote access and in vivo physiological analysis. We found that there was reversal of signaling and functional abnormalities after 30 days of unloading. In another set of failing hearts, we randomly delivered, at the time of transplantation, either 2ϫ10 11 viral particles of Adv-␤ 2 AR or saline via the coronary arteries. Sham-operated animals with nonfailing hearts served as controls. After 5 days of unloading, in vivo LV contractility (LV dP/dt max ) and relaxation (LV dP/dt min ) were significantly decreased in saline-treated failing hearts compared with control nonfailing hearts (PϽ0.05). In failing hearts treated with Adv-␤ 2 AR, however, LV dP/dt max and LV dP/dt min were improved in response to higher preloads (PϽ0.05) and ␤AR stimulation (PϽ0.01). Conclusions-Heterotopic transplantation in the rabbit does allow recovery of the failing heart, and ␤ 2 AR overexpression acutely enhances this functional improvement. Accordingly, genetic manipulation of ␤AR signaling may represent a novel molecular adjunct to mechanical assistance to facilitate functional myocardial recovery.

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Section: Discussionmentioning

confidence: 99%

Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

et al. 2002

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“…In prior retrospective clinical studies, the frequency of cardiac recovery and device explantation has varied. 9,12,22 Recent reports from the Harefield Hospital (UK) describe the use of clenbuterol, an oral ␤ 2 agonist, in combination with an aggressive pharmacological regimen consisting of lisinopril, carvediol, spironolactone, and losartan in LVAD patients to enhance myocardial recovery. 23 With this approach, 11 of 15 dilated cardiomyopathy patients (73%) demonstrated cardiac recovery sufficient to undergo successful device explantation, with 100% and 89% cumulative rates of freedom from recurrent HF at 1 and 4 years, respectively.…”

Section: Recoverymentioning

confidence: 99%

Cardiac Improvement During Mechanical Circulatory Support

et al. 2007

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Background-Myocardial recovery after left ventricular assist device (LVAD) support has been reported. The LVAD Working Group Recovery Study was a prospective multicenter trial to assess the incidence of myocardial recovery in patients bridged to cardiac transplantation. Methods and Results-After LVAD implantation, patients were evaluated with the use of rest echocardiograms with partial LVAD support and cardiopulmonary exercise testing. Dobutamine echocardiography with hemodynamic measurements was performed in those patients with left ventricular ejection fraction Ͼ40% during resting studies.Histological analysis was performed on myocardial samples taken at LVAD implantation and explantation. Sixty-seven LVAD patients with heart failure participated in the study. 001).Tissue analysis revealed significant reductions in myocyte size, collagen content, and cardiac tumor necrosis factor-␣. Six subjects (9%) underwent LVAD explantation for recovery. Conclusions-Cardiac function improves significantly after device implantation. Although cellular recovery and improvement in ventricular function are observed, the degree of clinical recovery is insufficient for device explantation in most patients with chronic heart failure.

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“…Unloading of failing rodent hearts by heterotopic transplantation 29 and failing human hearts by LVAD has the potential to contribute to functional recovery. 3,4 Mechanical LVAD unloading in a subset of patients with heart failure can improve dysregulated cardiac gene expression 3,4,30,31 as well as contractile properties and [Ca 2ϩ ] i handling. 32,33 It is speculated that cardiac unloading by LVAD for a very long duration in heart failure patients may result in partial cardiac atrophy and depressed contractile performance.…”

Section: Implications For Humans With Excess Cardiac Unloadingmentioning

confidence: 99%

“…1,2 Mechanical unloading of failing human hearts with LV-assist devices (LVADs) reduces excess LV load and mass and improves cardiac performance in some patients. 3,4 However, the effect of severe and chronic unloading of the normal heart on myocyte contractile function is unclear.…”

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confidence: 99%

Contractile Reserve and Calcium Regulation Are Depressed in Myocytes From Chronically Unloaded Hearts

et al. 2003

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Background-Chronic cardiac unloading of the normal heart results in the reduction of left ventricular (LV) mass, but effects on myocyte contractile function are not known. Methods and Results-Cardiac unloading and reduction in LV mass were induced by heterotopic heart transplantation to the abdominal aorta in isogenic rats. Contractility and [Ca 2ϩ ] i regulation in LV myocytes were studied at both 2 and 5 weeks after transplantation. Native in situ hearts from recipient animals were used as the controls for all experiments. Contractile function indices in myocytes from 2-week unloaded and native (control) hearts were similar under baseline conditions (0.5 Hz, 1.2 mmol/L [Ca 2ϩ ] o , and 36°C) and in response to stimulation with high [Ca 2ϩ ] o (range 2.5 to 4.0 mmol/L). In myocytes from 5-week unloaded hearts, there were no differences in fractional cell shortening and peak-systolic [Ca 2ϩ ] i at baseline; however, time to 50% relengthening and time to 50% decline in [Ca 2ϩ ] i were prolonged compared with controls. Severe defects in fractional cell shortening and peak-systolic [Ca 2ϩ ] i were elicited in myocytes from 5-week unloaded hearts in response to high [Ca 2ϩ ] o . However, there were no differences in the contractile response to isoproterenol between myocytes from unloaded and native hearts. In 5-week unloaded hearts, but not in 2-week unloaded hearts, LV protein levels of phospholamban were increased (345% of native heart values). Protein levels of sarcoplasmic reticulum Ca 2ϩ ATPase and the Na ϩ /Ca 2ϩ exchanger were not changed. Conclusions-Chronic unloading of the normal heart caused a time-dependent depression of myocyte contractile function, suggesting the potential for impaired performance in states associated with prolonged cardiac atrophy. (Circulation.

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Midterm follow-up of patients who underwent removal of a left ventricular assist device after cardiac recovery from end-stage dilated cardiomyopathy

Abstract: In selected patients with idiopathic dilated cardiomyopathy, lasting recovery can be achieved after unloading with a left ventricular assist device. Lasting cardiac recovery seems to be related to functional normalization and a more rapid recovery during the unloading period.

Cited by 89 publications

References 14 publications

Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

Cardiac Improvement During Mechanical Circulatory Support

Contractile Reserve and Calcium Regulation Are Depressed in Myocytes From Chronically Unloaded Hearts

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Midterm follow-up of patients who underwent removal of a left ventricular assist device after cardiac recovery from end-stage dilated cardiomyopathy

Abstract: In selected patients with idiopathic dilated cardiomyopathy, lasting recovery can be achieved after unloading with a left ventricular assist device. Lasting cardiac recovery seems to be related to functional normalization and a more rapid recovery during the unloading period.

Cited by 89 publications

References 14 publications

Myocardial Gene Transfer and Overexpression of β 2 -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

Myocardial Gene Transfer and Overexpression of β 2 -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

Cardiac Improvement During Mechanical Circulatory Support

Contractile Reserve and Calcium Regulation Are Depressed in Myocytes From Chronically Unloaded Hearts

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Product

Resources

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Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts

Myocardial Gene Transfer and Overexpression of β ₂ -Adrenergic Receptors Potentiates the Functional Recovery of Unloaded Failing Hearts