Recovery of failing hearts by mechanical unloading: Pathophysiologic insights and clinical relevance
- PMID: 30300847
- DOI: 10.1016/j.ahj.2018.09.004
Recovery of failing hearts by mechanical unloading: Pathophysiologic insights and clinical relevance
Abstract
By reduction of ventricular wall-tension and improving the blood supply to vital organs, ventricular assist devices (VADs) can eliminate the major pathophysiological stimuli for cardiac remodeling and even induce reverse remodeling occasionally accompanied by clinically relevant reversal of cardiac structural and functional alterations allowing VAD explantation, even if the underlying cause for the heart failure (HF) was dilated cardiomyopathy. Accordingly, a tempting potential indication for VADs in the future might be their elective implantation as a therapeutic strategy to promote cardiac recovery in earlier stages of HF, when the reversibility of morphological and functional alterations is higher. However, the low probability of clinically relevant cardiac improvement after VAD implantation and the lack of criteria which can predict recovery already before VAD implantation do not allow so far VAD implantations primarily designed as a bridge to cardiac recovery. The few investigations regarding myocardial reverse remodeling at cellular and sub-cellular level in recovered patients who underwent VAD explantation, the differences in HF etiology and pre-implant duration of HF in recovered patients and also the differences in medical therapy used by different institutions during VAD support make it currently impossible to understand sufficiently all the biological processes and mechanisms involved in cardiac improvement which allows even VAD explantation in some patients. This article aims to provide an overview of the existing knowledge about VAD-promoted cardiac improvement focusing on the importance of bench-to-bedside research which is mandatory for attaining the future goal to use long-term VADs also as therapy-devices for reversal of chronic HF.
Copyright © 2018 Elsevier Inc. All rights reserved.
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