Journal
PHARMACOLOGICAL REPORTS
Volume 61, Issue 1, Pages 139-145Publisher
POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/S1734-1140(09)70016-7
Keywords
heart failure; diastolic function; cardiomyocytes; myofilamentary proteins; fibrosis; diabetes mellitus
Categories
Funding
- UDMHSC, Hungary [Mec-4/2008]
- Heart Failure Association of the European Society of Cardiology, Nice, France
- Hungarian Academy of Sciences
- [ETT 449/2006]
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In population-based studies, heart failure with normal left ventricular (LV) ejection fraction (HFNEF) is now increasingly recognized and referred to as diastolic heart failure. However, the pathogenic. mechanisms underlying HFNEF are incompletely understood, mainly because of limited availability of human myocardial biopsy material. Nevertheless, recent studies have examined in vivo hemodynamics, in vitro cardiomyocyte function, myofilamentary protein composition, collagen content and deposition of advanced glycation end products from LV endomyocardial biopsies. These measures were compared between HFNEF patients, subjects without symptoms of heart failure (controls), patients with heart failure and reduced ejection function (HFREF), and patients with HFNEF and HFREF with diabetes mellitus. This article summarizes the various findings of these studies and focuses on the possible correlations among altered LV myocardial structure, cardiomyocyte function, myofilamentary proteins, and extracellular matrices. These findings revealed novel mechanisms responsible for diastolic LV dysfunction, and they have important therapeutic implications, particularly HFNEF, for which a specific heart failure treatment strategy is largely lacking.
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