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Related Experiment Video

Updated: May 8, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

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Molecular changes after left ventricular assist device support for heart failure.

¹Department of Cardiovascular Medicine, University of Louisville, Louisville, KY, USA. emma.birks@louisville.edu

Circulation Research

|August 31, 2013

Summary

Heart failure reverse remodeling is possible with left ventricular assist device (LVAD) support, leading to near-normalization of heart structure. However, reverse remodeling does not always guarantee full clinical recovery.

Keywords:

heart failure left ventricular assist device remodeling reverse remodeling

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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction

Published on: February 13, 2021

Area of Science:

Cardiology
Biomedical Engineering
Molecular Biology

Background:

Heart failure involves adverse myocardial remodeling, previously considered irreversible.
Left ventricular assist devices (LVADs) can induce significant reverse remodeling in advanced heart failure patients.

Purpose of the Study:

To review molecular changes in the myocardium following LVAD support.
To explore factors influencing myocardial recovery and clinical outcomes after LVAD implantation.

Main Methods:

Analysis of molecular and cellular changes in myocardial tissue from heart failure patients with LVADs.
Comparison of changes in patients bridged to transplantation versus those who recovered device explantation.

Main Results:

LVAD support can lead to near-normalization of myocardial structure and reverse remodeling.
Cell size reduction post-LVAD does not always correlate with improved function.
Specific myocyte changes (cytoskeletal proteins, Ca²⁺ handling) and matrix alterations are linked to recovery.
Myocardial fibrosis at implantation may limit recovery potential.

Conclusions:

Reverse remodeling after LVADs is possible but does not always equate to clinical recovery.
Specific molecular pathways in myocytes and the extracellular matrix are crucial for myocardial recovery.
Fibrosis extent is a key predictor of recovery after LVAD support.