Degree of cardiac fibrosis and hypertrophy at time of implantation predicts myocardial improvement during left ventricular assist device support

Bruckner, Brian A.; Razeghi, Peter; Stetson, Sonny J.; Thompson, Larry O.; Lafuente, Javier; Entman, Mark L.; Loebe, Matthias; Noon, George P.; Taegtmeyer, Heinrich; Frazier, O.H.; Youker, Keith A.

doi:10.1016/s1053-2498(03)00103-7

Cited by 74 publications

(45 citation statements)

References 20 publications

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“…4,11,20 Many studies were performed in the absence of clinical correlation, but in the few studies in which clinical parameters were analyzed, the cellular improvement was more impressive than the clinical impact. 11,21 In this study, paired myocardial tissue analysis revealed reduction in myocyte size, collagen deposition, and myocardial TNF-␣ expression consistent with some previous reports. The improvement in the tissue parameters appears greater than the modest changes observed in cardiac function.…”

Section: Recoverysupporting

confidence: 92%

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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Section: Recoverysupporting

confidence: 92%

Cardiac Improvement During Mechanical Circulatory Support

et al. 2007

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“…Less fibrosis may therefore predict patients with a higher probability of LVAD removal and myocardial recovery after LVAD support. Another study 56 has shown that patients BTT who gain the maximum improvement in LV ejection fraction (LVEF) during LVAD support had less fibrosis at the time of device implantation. Furthermore, Yamada et al 57 found a correlation between the amount of fibrosis and brain natriuretic peptide change after LVAD implantation, such that patients with less fibrosis had significantly improved brain natriuretic peptide levels.…”

Section: Circulation Research August 30 2013mentioning

confidence: 99%

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Birks

2013

Circulation Research

106

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Abstract-Heart failure is associated with remodeling that consists of adverse cellular, structural, and functional changes in the myocardium. Until recently, this was thought to be unidirectional, progressive, and irreversible. However, irreversibility has been shown to be incorrect because complete or partial reversal can occur that can be marked after myocardial unloading with a left ventricular assist device (LVAD). Patients with chronic advanced heart failure can show near-normalization of nearly all structural abnormalities of the myocardium or reverse remodeling after LVAD support. However, reverse remodeling does not always equate with clinical recovery. The molecular changes occurring after LVAD support are reviewed, both those demonstrated with LVAD unloading alone in patients bridged to transplantation and those occurring in the myocardium of patients who have recovered enough myocardial function to have the device removed. Reverse remodeling may be attributable to a reversal of the pathological mechanisms that occur in remodeling or the generation of new pathways. A reduction in cell size occurs after LVAD unloading, which does not necessarily correlate with improved cardiac function. However, some of the changes in both the cardiac myocyte and the matrix after LVAD support are specific to myocardial recovery. In the myocyte, increases in the cytoskeletal proteins and improvements in the Ca 2+ handling pathway seem to be specifically associated with myocardial recovery. Changes in the matrix are complex, but excessive scarring appears to limit the ability for recovery, and the degree of fibrosis in the myocardium at the time of implantation may predict the ability to recover. (Circ Res. 2013;113:777-791.)

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“…Bruckner et al 13 have reported that patients with a higher degree of fibrosis at the time of LVAD implantation had less recovery of LV systolic function during LVAD unloading. It is well described that HF is associated with defects in calcium homeostasis.…”

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confidence: 99%

Heart Failure—A New Phenotype Emerges

Wilcox

Yancy

2016

JAMA Cardiol

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The generation of clinical practice guidelines accomplishes several aims. First, it reviews available evidence that when placed in a graded hierarchal framework informs clinical practice statements. Second, it identifies gaps in evidence intended to spur future research. Third, it introduces new concepts that orient the discipline toward new models of understanding. Therefore, with regard to the latter aim, the American College of Cardiology/American Heart Association 2013 heart failure (HF) guidelines for the first time articulated a theoretical categorization of HF based on ejection fraction (EF) measurements that differed from prior schemes. 1 Rather than wrestle with the demarcation of HF with reduced EF (HFrEF) vs HF with preserved EF (HFpEF) at a single cut point, the writing group recognized that no evidence base existed to accommodate such precision and that, indeed, the experiential observations captured the theme of a "gray zone" with borderline EF (ie, left ventricular ejection fraction [LVEF] >0.40 and <0.50). Moreover, clinical empiricism led the committee to opine that the pathway to this borderline zone was either de novo discovery or recovery from prior documented HFrEF. Such a categorization raised several important questions. Are those patients still candidates for class of recommendation I evidence-based medical and device therapy as indicated by the guidelines for HFrEF? What is the natural history of HF with improved EF? How large is this cohort? What are the patient experiences of those who have experienced recovery? Most important, is there a science to recovery that creates insight regarding new mechanisms and treatments of left ventricular (LV) dysfunction?In this issue of JAMA Cardiology, Kalogeropoulos et al 2 add nicely to this emerging phenotype with a careful singlecenter analysis of all patients with HF, including detailed phenotyping and longitudinal follow-up with the best evidence to date to endorse the original effort of the American College of Cardiology/American Heart Association HF guideline writing committee to identify this new and potentially important category of HF. 1 The work by Kalogeropoulos et al 2 establishes several new insights: (1) 16.2% (350 of 2166) of those with an LVEF exceeding 0.40 potentially represented improved or "recovered" HF (ie, HFrecEF), (2) 3-year mortality was lowest for HFrecEF compared with HFrEF and HFpEF, and (3) hospitalization burden was significantly lower for HFrecEF compared with the other phenotypes. These data seemingly confirmatory of this new HF phenotype are supportive but not definitive. As pointed out by the authors, the limitations are important and merit emphasis, including it being a singlecenter study, academic referral bias, the absence of anteced-

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Degree of cardiac fibrosis and hypertrophy at time of implantation predicts myocardial improvement during left ventricular assist device support

Cited by 74 publications

References 20 publications

Cardiac Improvement During Mechanical Circulatory Support

Cardiac Improvement During Mechanical Circulatory Support

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Heart Failure—A New Phenotype Emerges

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