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European Heart Journal 2004 25(2):136-143; doi:10.1016/j.ehj.2003.09.027
Copyright © 2004 by the European Society of Cardiology.
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Clinical research

Beneficial effects of chronic low-frequency stimulation of thigh muscles in patients with advanced chronic heart failure

Martin J. Nuhra, Dirk Petted, Rudolf Bergerb, Michael Quittana,*, Richard Crevennaa, Martin Huelsmanb, Guenther F. Wiesingera, Petra Moserc, Veronika Fialka-Mosera and Richard Pacherb,c

a Department of Physical Medicine and Rehabilitation, General Hospital Vienna, University of Vienna, Vienna, Austria
b Department of Internal Medicine II—Cardiology, General Hospital Vienna, University of Vienna, Vienna, Austria
c Ludwig Boltzmann Institut für Herz-Kreislaufforschung, General Hospital Vienna, University of Vienna, Vienna, Austria
d Department of Biology, University of Konstanz, Konstanz, Germany

* Corresponding author. Michael Quittan, M.D. Department of Physical Medicine and Rehabilitation, General Hospital Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria. Tel.: +43-1-40400-4333; fax: +43-1-40400-5281
E-mail address: michael.quittan{at}univie.ac.at

Received 31 May 2003; revised 20 August 2003; accepted 25 September 2003

Abstract

Aims Patients with chronic heart failure (CHF) exhibit detrimental changes in skeletal muscle that contribute to their impaired physical performance. This study investigates the possibility of counteracting these changes by chronic low-frequency electrical stimulation (CLFS) of left and right thigh muscles.

Methods and results (mean±SD) 32 CHF patients (53±10 years) with an LVEF of 22±5%, NYHA II-IV, undergoing optimized drug therapy, were randomized in a CLFS group (CLFSG) or a control group (controls). The groups differed in terms of the intensity of stimulation, which elicited strong muscle contractions only in the CLFSG, whereas the controls received current input up to the sensory threshold without muscle contractions. Functional capacity was assessed by peak VO2, work capacity, and a 6-min-walk (6-MW). Muscle biopsies were analyzed for myosin heavy chain (MHC) isoforms, citrate synthase (CS) and glyceraldehydephosphate dehydrogenase (GAPDH) activities. Peak VO2(mlmin-1kg –1) increased from 9.6±3.5 to 11.6±2.8 (P<0.001) in the CLFSG, and decreased from 10.6±2.8 to 9.4±3.2 (P<0.05) in the controls. The increase in the CLFSG was paralleled by increases in maximal workload (P<0.05) and oxygen uptake at the anaerobic threshold (P<0.01). The corresponding values of the controls were unchanged, as also the 6-MW values, the MHC isoform distribution, and both CS and GAPDH activities. In the CLFSG, the 6-MW values increased (P<0.001), CS activity was elevated (P<0.05), GAPDH activity decreased (P<0.01), and the MHC isoforms were shifted in the slow direction with increases in MHCI at the expense of MHCIId/x (P<0.01).

Conclusion Our results suggest that CLFS is a suitable treatment to counteract detrimental changes in skeletal muscle and to increase exercise capacity in patients with severe CHF.

Key Words: Electrical stimulation • Exercise • Muscle • Heart failure


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