Work

Myocyte reorganization in hypertrophied and failing hearts

Year: 1995

Type: article

Abstract: In hypertrophied and failing hearts there are major changes in the overall contractile performance. We present a review of our previous work relating the alterations in myocardial force, work, power and relaxation, that lead to changes in overall ventricular performance, to changes in the actin-myosin cross-bridge cycle characteristics along with the degree of activation and inactivation (calcium cycling). Tissues from hypertrophied rabbit and failing human (volume overload, dilated car-diomyopathy) heart were used in these studies. Myocardial peak twitch tension (mN.mm−2) was reduced in dilated car-diomyopathy (human) (25.9 ± 3.9 vs 13.9 ± 2.0, 37°C), volume overload (human) (44.0 ±11.7 vs 19.9 ± 3.7, 21°C) and pressure overload (rabbit) (461 ± 2.6 vs 41.7 ± 50, 21°C). We used myothermal and mechanical data to analyse the average cross-bridge force time integral and the amount of calcium cycled per gram per beat. Tension-dependent heat (mJ.g−1) (TDH) (cross-bridge cycling) and tension-independent heat (mJ.g”) (T1H) were reduced in all of the experimental preparations (dilatedcardiomyopathy, human, 377°C: TDH, 3.39 ± 0.59 vs 1.34 ± 0.22; TIH, 0.51 ± 0.02 vs 0.16 ± 0.03) (volume overload, human 21“C: TDH, 7.23 ± 2.22 vs 1.92 ± 0.25; TIH, 0.75 ± 0.19 vs 0.39 ± 0.04) (pressure overload, rabbit, 21“C: TDH, 6.60 ± 0.75 vs 305 ± 0.46; TIH, 1.00 ± 0.17 vs 0.41 ± 0.08). The cross-bridge force-time integral (pNs, pico Newton seconds) was increased in all experimental preparations (dilated cardiomyopathy, 138%; volume overload, 175%; pressure overload, 253%), while in each of the experimental preparations, the amount of calcium cycled (nmoles.beat-g) is reduced (expressed as % control) (dilated cardiomyopathy, 36%; volume overload, 53%; pressure overload, 46%). The decrease in power observed in these hearts and the inadequate cardiac output in the failing hearts are attributed to these documented changes in the contractile and excitation contraction coupling systems

Source: European Heart Journal

DOI: 10.1093/eurheartj/16.suppl_c.2

Authors: N. R. Alpert, L. A. Mulieri, G. Hasenfuss, C. Holubarsch

Institutions: University of Vermont, University of Freiburg

Language: English

Topic: Cardiomyopathy and Myosin Studies

Subfield: Cardiology and Cardiovascular Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funders: National Institutes of Health, National Heart, Lung, and Blood Institute