Cited by 205Cardiac electrophysiology and arrhythmiasCardiac Ischemia and ReperfusionCardiac Fibrosis and Remodeling

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Heart Failure After Myocardial Infarction: Altered Excitation-Contraction Coupling

Gómez, A.M., Guatimosim, S., Dilly, K.W., Vassort, G., Lederer, W.J.·2001·Circulation

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Abstract

Background — Heart failure (HF) frequently follows the occurrence of myocardial infarction (MI). Questions about how HF develops and what cellular defects contribute to this dysfunction led to this study. Methods and Results — MI was induced in rats by coronary artery ligation. Clinical examination of the post-MI (PMI) surviving animals indicated that they were in overt HF by all measures. Cellular examination of the cardiomyocytes by patch-clamp and confocal [Ca 2+ ] i imaging methods indicated that cellular function was significantly compromised. At the single-cell level, [Ca 2+ ] i transient amplitudes were reduced and contractions were decreased and slowed, although Ca 2+ current ( I Ca ) remained unchanged. The excitation-contraction coupling (ECC) gain function measured as Δ[Ca 2+ ] i / I Ca was significantly decreased. Ouabain, a cardiotonic steroid that blocks the Na + ,K + -ATPase and activates Ca 2+ entry via cardiac Na + channels, largely alleviated this defect. Conclusions — After MI, I Ca becomes less able to trigger release of Ca 2+ from the sarcoplasmic reticulum. This failure of ECC is a major factor contributing to the development of contractile dysfunction and HF in PMI animals. The improved ECC gain, enhanced Ca 2+ entry, and augmented Ca 2+ signaling due to cardiotonic steroids contribute to the beneficial effects of these agents.

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Authors: Gómez, A. M., Guatimosim, S., Dilly, K. W., Vassort, G., & Lederer, W. J.
Affiliations: From INSERM-U.390, IFR-3, Montpellier, France (A.M.G., G.V.), and Medical Biotechnology Center and School of Medicine, University of Maryland Biotechnology Institute, Baltimore (A.M.G., S.G., K.W.D., W.J.L.).
Inserm (FR)
ORCID: Guatimosim, S.
Dilly, K.W.
Lederer, W.J.
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2001-08-07
Volume: 104
Issue: 6
Pages: 688-693
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/hc3201.092285
OpenAlex: W2096667649
Cited by: 205
References: 29
Citations by year: 2026: 3 · 2025: 4 · 2024: 8 · 2023: 4 · 2022: 6 · 2021: 6 · 2020: 8 · 2019: 2 · 2018: 3 · 2017: 5 · 2016: 9 · 2015: 6 · 2014: 6 · 2013: 15 · 2012: 9
FWCI: 9.99
Type: journal article
Language: en
Open access: closed
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
Funders: Institut National de la Santé et de la Recherche Médicale
Centre National de la Recherche Scientifique
National Institutes of Health
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords: heart failure, myocardial infarction, excitation-contraction coupling, calcium transients, sarcoplasmic reticulum calcium release, calcium current, cardiomyocyte contractile dysfunction, ouabain, cardiac glycosides, Na+/K+-ATPase, cardiac sodium channel, coronary artery ligation, rat model
MeSH terms: Animals, Calcium, Cardiotonic Agents, Heart Failure, Hypertrophy, Male, Membrane Potentials, Myocardial Contraction, Myocardial Infarction, Myocardium, Ouabain, Sarcoplasmic Reticulum, Tetrodotoxin, Calcium Channels, Survival Rate, Rats, Wistar, Calcium Signaling, Cell Size, Rats

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Heart Failure After Myocardial Infarction: Altered Excitation-Contraction Coupling

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