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Continuous internal counterpulsation as a bridge to recovery in acute and chronic heart failure.

ABSTRACT: Cardiac recovery from cardiogenic shock (CS) and end-stage chronic heart failure (HF) remains an often insurmountable therapeutic challenge. The counterpulsation technique exerts numerous beneficial effects on systemic hemodynamics and left ventricular mechanoenergetics, rendering it attractive for promoting myocardial recovery in both acute and chronic HF. Although a recent clinical trial has questioned the clinical effectiveness of short-term hemodynamic support with intra-aortic balloon pump (IABP, the main representative of the counterpulsation technique) in CS complicating myocardial infarction, the issue remains open to further investigation. Moreover, preliminary data suggest that long-term IABP support in patients with end-stage HF is safe and may mediate recovery of left- or/and right-sided cardiac function, facilitating long-term weaning from mechanical support or enabling the application of other permanent, life-saving solutions. The potential of long-term counterpulsation could possibly be enhanced by implementation of novel, fully implantable counterpulsation devices.

SUBMITTER: Kontogiannis CD

PROVIDER: S-EPMC4801787 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Continuous internal counterpulsation as a bridge to recovery in acute and chronic heart failure.

Kontogiannis Christos D CD Malliaras Konstantinos K Kapelios Chris J CJ Mason Jay W JW Nanas John N JN

World journal of transplantation 20160301 1

Cardiac recovery from cardiogenic shock (CS) and end-stage chronic heart failure (HF) remains an often insurmountable therapeutic challenge. The counterpulsation technique exerts numerous beneficial effects on systemic hemodynamics and left ventricular mechanoenergetics, rendering it attractive for promoting myocardial recovery in both acute and chronic HF. Although a recent clinical trial has questioned the clinical effectiveness of short-term hemodynamic support with intra-aortic balloon pump ...[more]

PMID: 27011909

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Project description:Background: Heart failure (HF) is a significant global health problem. Left-ventricular assist device (LVAD) implantation serves as a bridge for patients awaiting heart transplantation. Intriguingly, LVAD support often improves cardiac histology and function, sometimes enough to avoid transplantation after LVAD removal. However, the cellular programs underlying this recovery remain unclear. Methods: Myocardial tissues were obtained from patients with HF at the time of LVAD implantation (pre-LVAD) and explantation (post-LVAD) for histological analysis and single-nucleus RNA sequencing (snRNA-seq). A murine model of HF recovery, combined with lineage tracing studies, was employed to define cellular sources of vascular repair. Cardiac function, fibrosis, and vascular density were assessed using echocardiography, histology, and fluorescent microsphere perfusion. A patient-derived cardiac non-myocyte culture system was established to interrogate mechanisms of cell-fate regulation. Results: Post-LVAD myocardial tissues exhibited reduced fibrosis and increased capillary density compared to pre-LVAD samples. Across samples, fibroblast abundance inversely correlated with endothelial cell abundance, consistent with enhanced angiogenesis during recovery. SnRNA-seq identified a fibroblast subset predisposed to undergo mesenchymal-to-endothelial transition, acquiring an endothelial cell identity. Additionally, non-myocytes from pre-LVAD hearts proliferated poorly and failed to form vascular structures, whereas non-myocytes from post-LVAD hearts displayed greater proliferative and angiogenic capacity, forming vessel-like structures, reinforcing the association of HF recovery with angiogenic reprogramming. Mechanistically, knockdown of c-Myc by siRNA shifted post-LVAD non-myocytes to a pre-LVAD-like state, while c-Myc overexpression by mRNA in pre-LVAD cells induced a post-LVAD-like phenotype, implicating c-Myc as one contributor to this fate switch. A model of heart failure recovery in mice mimicked the histological and functional changes in patients, with physiological evidence of increased microvascular perfusion, associated with a fibroblast-to-endothelial transition documented by lineage tracing. Conclusions: HF recovery involves reduced fibrosis and enhanced microvascularization, partly driven by fibroblast-to-endothelial cell fate transition. c-Myc functions as one regulator of this transition, offering a mechanistic entry point to develop regenerative therapies in HF.

Dataset Information

Continuous internal counterpulsation as a bridge to recovery in acute and chronic heart failure.

Publications

Continuous internal counterpulsation as a bridge to recovery in acute and chronic heart failure.

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