Circulation Research, Vol 73, 379-385, Copyright © 1993 by American Heart Association

ARTICLES

Alterations of K+ currents in isolated human ventricular myocytes from patients with terminal heart failure

DJ Beuckelmann, M Nabauer and E Erdmann
Department of Medicine I, University of Munich, Germany.

Prolongation of the action potential has been postulated to be a major reason for the altered diastolic relaxation of the heart in patients with severe heart failure. To investigate the electrophysiological basis for this action potential prolongation in terminal heart failure, K+ currents were recorded in single ventricular myocytes isolated from 16 explanted hearts of patients undergoing transplantation. Results from diseased hearts were compared with ventricular cells isolated from six undiseased donor hearts. Action potential duration was significantly prolonged in cells from patients with heart failure. A delayed rectifier K+ current was hardly detectable in most cells, and if it could be recorded, it was very small in both diseased and undiseased cells. When currents were normalized for cell surface area, the average current density of the inward rectifier K+ current was significantly reduced in diseased cells when compared with normal control cells (hyperpolarization at -100 mV, -15.9 +/- 2.2 vs -9.0 +/- 1.2 microA/cm2; P < .01). In addition, a large transient outward K+ current could be recorded in human myocytes. The average current density of the time-dependent component of this transient outward K+ current was significantly reduced in heart failure (depolarization at +40 mV, 9.1 +/- 1.0 vs 5.8 +/- 0.64 microA/cm2; P < .01). Action potential prolongation in severe heart failure may partially be explained by a reduction in current densities of the inward rectifier K+ current and of the transient outward K+ current. These alterations may thereby have a significant effect on cardiac relaxation.

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				J. A. Wasserstrom, E. Holt, I. Sjaastad, P. K. Lunde, A. Odegaard, and O. M. Sejersted Altered E-C coupling in rat ventricular myocytes from failing hearts 6 wk after MI Am J Physiol Heart Circ Physiol, August 1, 2000; 279(2): H798 - H807. [Abstract] [Full Text] [PDF]

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				S. Mitarai, T. D. Reed, and A. Yatani Changes in ionic currents and beta -adrenergic receptor signaling in hypertrophied myocytes overexpressing Galpha q Am J Physiol Heart Circ Physiol, July 1, 2000; 279(1): H139 - H148. [Abstract] [Full Text] [PDF]

				A. O. Verkerk, M. W. Veldkamp, N. de Jonge, R. Wilders, and A. C.G. van Ginneken Injury current modulates afterdepolarizations in single human ventricular cells Cardiovasc Res, July 1, 2000; 47(1): 124 - 132. [Abstract] [Full Text] [PDF]

				D. Li, P. Melnyk, J. Feng, Z. Wang, K. Petrecca, A. Shrier, and S. Nattel Effects of Experimental Heart Failure on Atrial Cellular and Ionic Electrophysiology Circulation, June 6, 2000; 101(22): 2631 - 2638. [Abstract] [Full Text] [PDF]

				S.H. Hohnloser Electrocardiographic risk stratification in dilative cardiomyopathy: an unfulfilled promise Eur. Heart J., June 2, 2000; 21(12): 953 - 954. [PDF]

				B. C Knollmann, B. E C Knollmann-Ritschel, N. J Weissman, L. R Jones, and M. Morad Remodelling of ionic currents in hypertrophied and failing hearts of transgenic mice overexpressing calsequestrin J. Physiol., June 1, 2000; 525(2): 483 - 498. [Abstract] [Full Text] [PDF]

				P. G.A. Volders, M. A. Vos, B. Szabo, K. R. Sipido, S.H.M. de Groot, A. P.M. Gorgels, H. J.J. Wellens, and R. Lazzara Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts Cardiovasc Res, June 1, 2000; 46(3): 376 - 392. [Full Text] [PDF]

				G. U. Ahmmed, P. H. Dong, G. Song, N. A. Ball, Y. Xu, R. A. Walsh, and N. Chiamvimonvat Changes in Ca2+ Cycling Proteins Underlie Cardiac Action Potential Prolongation in a Pressure-Overloaded Guinea Pig Model With Cardiac Hypertrophy and Failure Circ. Res., March 17, 2000; 86(5): 558 - 570. [Abstract] [Full Text] [PDF]

				R. G Matteo and C. S. Moravec Immunolocalization of annexins IV, V and VI in the failing and non-failing human heart Cardiovasc Res, March 1, 2000; 45(4): 961 - 970. [Abstract] [Full Text] [PDF]