Cellular Mechanisms for Diastolic Dysfunction in the Human Heart

Author(s): Daniel Czuriga, Walter J. Paulus, Istvan Czuriga, Istvan Edes, Zoltan Papp, Attila Borbely

Journal Name: Current Pharmaceutical Biotechnology

Volume 13 , Issue 13 , 2012

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Left ventricular (LV) diastolic dysfunction is an important contributor to many different cardiovascular diseases. LV diastolic dysfunction can manifest itself as slow LV relaxation, slow LV filling or high diastolic LV stiffness. Diastolic abnormalities have been described in the senescent heart, in heart failure with preserved ejection fraction (HFPEF), in diabetic cardiomyopathy, in aortic valve stenosis (AVS), in hypertrophic cardiomyopathy (HCM), as well as in Fabry disease (FD), however, exact cellular and molecular alterations behind the diastolic deterioration in these diseases are not yet completely characterized. Several studies thoroughly investigated altered cardiomyocyte function, changes of contractile myofilaments, extracellular collagen deposition and advanced glycation end products (AGEs) cross-linking in the background of diastolic dysfunction. These clinical and experimental data suggest that underlying mechanisms of LV diastolic dysfunction are divergent in different cardiac pathologies, therefore the present review aims to summarize mechanisms at the cellular level of diastolic abnormalities in various cardiovascular diseases.

Keywords: Cardiomyocytes, contractile dysfunction, diabetes mellitus, diastole, fibrosis, human heart

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Article Details

Year: 2012
Page: [2532 - 2538]
Pages: 7
DOI: 10.2174/1389201011208062532
Price: $65

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