Cited by 135Cardiomyopathy and Myosin StudiesCardiac Fibrosis and RemodelingCardiovascular Function and Risk Factors

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Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency.

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Pagani, E D, Alousi, A A, Grant, A M, Older, T M, Dziuban, S W, Allen, P D·1988·Circulation Research

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Abstract

Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.

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Self-citation

Authors: Pagani, E. D., Alousi, A. A., Grant, A. M., Older, T. M., Dziuban, S. W., & Allen, P. D.
Affiliations: Molecular Cardiology Unit, Sterling-Winthrop Research Institute, Rensselaer, New York 12144.
ORCID: Allen, P D
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1988-08
Volume: 63
Issue: 2
Pages: 380-385
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/01.res.63.2.380
OpenAlex: W2110787501
Cited by: 135
References: 27
Citations by year: 2024: 1 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 1 · 2017: 1 · 2014: 2
FWCI: 4.99
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords: heart failure, Mg2+-ATPase activity, ventricular myocardium, coronary artery disease, cardiomyopathy, mitral regurgitation, end-stage heart failure, actin-myosin interaction
MeSH terms: Coronary Disease, Cardiac Catheterization, Heart Failure, Humans, Mitral Valve Insufficiency, Muscle Proteins, Cardiomyopathies, Myocardium, Myofibrils, Reference Values, Ca(2+) Mg(2+)-ATPase

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Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency.

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