Depressed Myocardial Contractility

Can It Be Rescued?

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)428-432
Number of pages5
JournalAmerican Journal of the Medical Sciences
Volume352
Issue number4
DOIs
StatePublished - Oct 1 2016

Fingerprint

Systolic Heart Failure
Heart-Assist Devices
Ventricular Function
Thyroid Hormones
Cardiac Myocytes
Muscle Cells
Fibrosis
Population
Genes
Therapeutics

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Depressed Myocardial Contractility : Can It Be Rescued? / Weber, Karl.

In: American Journal of the Medical Sciences, Vol. 352, No. 4, 01.10.2016, p. 428-432.

Research output: Contribution to journalArticle

@article{36611dd1fe14476088dfc9887cd1ab31,
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.",
author = "Karl Weber",
year = "2016",
month = "10",
day = "1",
doi = "10.1016/j.amjms.2016.05.026",
language = "English (US)",
volume = "352",
pages = "428--432",
journal = "American Journal of the Medical Sciences",
issn = "0002-9629",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Depressed Myocardial Contractility

T2 - Can It Be Rescued?

AU - Weber, Karl

PY - 2016/10/1

Y1 - 2016/10/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84994750358&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84994750358&partnerID=8YFLogxK

U2 - 10.1016/j.amjms.2016.05.026

DO - 10.1016/j.amjms.2016.05.026

M3 - Article

VL - 352

SP - 428

EP - 432

JO - American Journal of the Medical Sciences

JF - American Journal of the Medical Sciences

SN - 0002-9629

IS - 4

ER -