Left ventricular assist device unloading effects on myocardial structure and function: current status of the field and call for action

Drakos, Stavros G.; Kfoury, Abdallah G.; Selzman, Craig H.; Verma, Divya Ratan; Nanas, John N.; Li, Dean Y.; Stehlik, Josef

doi:10.1097/hco.0b013e328345af13

Cited by 82 publications

(80 citation statements)

References 114 publications

(105 reference statements)

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“…Bruggink et al 43 demonstrated a biphasic response with an initial increase in fibrosis, followed by a subsequent regression with prolonged LVAD therapy (after 200 days of support). Drakos et al 7,46 with advanced image analysis found higher interstitial and total fibrosis in failing hearts and that the collagen content increased further after LVAD unloading.…”

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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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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“…Continuous flow LVADs (CF‐LVADs) have been shown to improve mortality, morbidity, functional status, and quality of life in patients with advanced HF 2, 3, 4. Ventricular arrhythmias, however, are commonly seen in patients with LVAD,5, 6, 7 and the vast majority of LVAD recipients who had implantable cardioverter defibrillators (ICDs) continue to receive ICD therapies post‐LVAD implant 8.…”

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confidence: 99%

Cardiac Resynchronization Therapy and Clinical Outcomes in Continuous Flow Left Ventricular Assist Device Recipients

Gopinathannair

Roukoz

Bhan

et al. 2018

JAHA

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BackgroundMany patients with heart failure continue cardiac resynchronization therapy (CRT) after continuous flow left ventricular assist device (CF‐LVAD) implant. We report the first multicenter study to assess the impact of CRT on clinical outcomes in CF‐LVAD patients.Methods and ResultsAnalysis was performed on 488 patients (58±13 years, 81% male) with an implantable cardioverter defibrillator (ICD) (n=223) or CRT‐D (n=265) who underwent CF‐LVAD implantation at 5 centers from 2007 to 2015. Effects of CRT on mortality, hospitalizations, and ventricular arrhythmia incidence were compared against CF‐LVAD patients with an ICD alone. Baseline differences were noted between the 2 groups in age (60±12 versus 55±14, P<0.001) and QRS duration (159±29 versus 126±34, P=0.001). Median biventricular pacing in the CRT group was 96%. During a median follow‐up of 478 days, Kaplan–Meier analysis showed no difference in survival between groups (log rank P=0.28). Multivariate Cox regression demonstrated no survival benefit with type of device (ICD versus CRT‐D; P=0.16), whereas use of amiodarone was associated with increased mortality (hazard ratio 1.77, 95% confidence interval 1.1–2.8, P=0.01). No differences were noted between CRT and ICD groups in all‐cause (P=0.06) and heart failure (P=0.9) hospitalizations, ventricular arrhythmia incidence (43% versus 39%, P=0.3), or ICD shocks (35% versus 29%, P=0.2). During follow‐up, 69 (26%) patients underwent pulse generator replacement in the CRT‐D group compared with 36 (15.5%) in the ICD group (P=0.003).ConclusionsIn this large, multicenter CF‐LVAD cohort, continued CRT was not associated with improved survival, hospitalizations, incidence of ventricular arrhythmia and ICD therapies, and was related to a significantly higher number of pulse generator changes.

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“…the left ventricle relieved by this pump system. Although histopathological evaluation of cardiac apex in these circumstances might represent a useful adjunct for further assessment of prognosis and planning of treatment strategies for patients on an individual base, there are only very limited data on this aspect in the clinical and pathological cardiology literature [7,8]. To our knowledge, only two studies have analysed this in more details [9,10].…”

Section: Introductionmentioning

confidence: 99%

Pathological Findings in Cardiac Apex Removed during Implantation of Left Ventricular Assist Devices (LVAD) are Non-Specific. A 13-Year-Experience at a German Heart Center

Strecker

Agaimy

Roesch

et al. 2015

Thorac cardiovasc Surg

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Background and aim: Ventricular assist devices (VAD) have become an established therapy for patients with end-stage heart failure. The two main reasons for this development are the shortage of appropriate donor organs and the increasing number of patients waiting for heart transplantation (HTX). Furthermore, the enormous advances in the technical equipment and the rising clinical experience have improved the implantation technique, the durability and the long-term patient outcomes. Methods: We reviewed all cases of left ventricular assist device (LVAD) implantation at our Erlangen Heart Center during January 2000-July 2013. The main aim of this study was to analyze the underlying pathology from the cardiac apex removed during the implantation. From all patients, we created a follow-up, analyzed the pathological features with the clinical diagnoses and described the overall outcome. Results: VAD implantation was performed in 266 cases at our center in the last 13 years (2.2% of the total of 12254 cardiac surgical operations in that period). From these patients, 223 underwent LVAD or biventricular (BVAD) implantation; the remaining received a right (RVAD) implantation. The most frequent underlying clinical diagnoses were dilated (n = 84, 37.7%, DCM) or ischemic (n = 61, 27.4%, ICM) cardiomyopathy. The pathological findings in the apex biopsy were generally non-specific and showed variable interstitial myocardial fibrosis with evidence of fibre loss, fatty degeneration and variable irregular atrophy of muscle fibres, consistent with dilated and ischemic cardiomyopathies as the most frequent causes of heart failure in these patients. Only a few cases showed other specific features such as myocarditis and AL-amyloidosis. Conclusions: Pathological findings in cardiac apex removed during LVAD implantation are rather non-specific and they generally reflect the late stage or consequences of chronic myocardial damage in cases of dilated or ischemic cardiomyopathies. Variable patchy chronic inflammatory changes may be observed in cardiomyopathies as a non-specific reaction caused by myocardial fiber damage and should not lead to misinterpretation as evidence of myocarditis or revision of original diagnosis.

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Left ventricular assist device unloading effects on myocardial structure and function: current status of the field and call for action

Cited by 82 publications

References 114 publications

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Cardiac Resynchronization Therapy and Clinical Outcomes in Continuous Flow Left Ventricular Assist Device Recipients

Pathological Findings in Cardiac Apex Removed during Implantation of Left Ventricular Assist Devices (LVAD) are Non-Specific. A 13-Year-Experience at a German Heart Center

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