title: Depressed Myocardial Contractility: Can It Be Rescued?
abstract: Current dogma suggests patients with advanced systolic heart failure have an irreversible depression in myocardial contractility. Recent experience with improved ventricular function during continuous flow ventricular assist devices used as destination therapy would suggest otherwise. Herein, cellular and molecular signaling involved in reversing depressed myocardial contractility would be addressed. This includes cardiomyocyte thyroid hormone signaling responsible for the reexpression of fetal gene program that preserves cell efficiency (work and energy consumed) and the rescue of an endogenous population of atrophic myocytes bordering on microdomains of fibrosis to improve contractile mass.
authors: Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, TN. Electronic address: KTWeber@uthsc.edu.
authors: Karl T
authors: KT
authors: Weber
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism*; D018384:Oxidative Stress; D013963:Thyroid Hormones / Q000378:metabolism
chemical_list: D013963:Thyroid Hormones
keywords: Fetal gene program; Heart failure; Myocardial contractility; Rescue atrophic myocytes; Thyroid hormone signaling