Heart Failure After Myocardial Infarction: Altered Excitation-Contraction Coupling
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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MI and ischemic cardiomyopathy are among the leading causes of heart failure, associated morbidity, and death worldwide and continue to impose staggering financial burden on healthcare systems.
“Despite advancements in clinical management, MI and ischemic cardiomyopathy are among the leading causes of heart failure, associated morbidity, and death worldwide 3,4 and continue to impose staggering financial burden on healthcare systems 3,5-8 .”
From Targeting the Immune-Fibrosis Axis in Myocardial Infarction and Heart Failure (2022) · cites this paper as [4]
The introductory passage in our copy (page not provided) calls MI a leading cause of cardiac mortality, morbidity, and dysfunction and says heart failure frequently follows it. The paper does not establish the same claim for ischemic cardiomyopathy, a worldwide ranking, or a financial burden on healthcare systems. (LLM, conf=0.88)
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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)
- Venue
- Circulation
- Published
- 2001-08-07
- Volume
- 104
- Issue
- 6
- Pages
- 688-693
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- 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 › Pathology and Forensic 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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