Alternans resonance and propagation block during supernormal conduction in cardiac tissue with decreased [K(+)](o).
Cardiac restitution is an important factor in arrhythmogenesis. Steep positive action potential duration and conduction velocity (CV) restitution slopes promote alternans and reentrant arrhythmias. We examined the consequences of supernormal conduction (characterized by a negative CV restitution slope) on patterns of conduction and alternans in strands of Luo-Rudy model cells and in cultured cardiac cell strands. Interbeat intervals (IBIs) were analyzed as a function of distance during S1S2 protocols and during pacing at alternating cycle lengths. Supernormal conduction was induced by decreasing [K(+)](o). In control [K(+)](o) simulations, S1S2 intervals converged toward basic cycle length with a length constant determined by both CV and the CV restitution slope. During alternant pacing, the amplitude of IBI alternans converged with a shorter length constant, determined also by the action potential duration restitution slope. In contrast, during supernormal conduction, S1S2 intervals and the amplitude of alternans diverged. This amplification (resonance) led to phase-locked or more complex alternans patterns, and then to distal conduction block. The convergence/divergence of IBIs was verified in the cultured strands, in which naturally occurring tissue heterogeneities resulted in prominent discontinuities of the spatial IBI profiles. We conclude that supernormal conduction potentiates alternans and spatial analysis of IBIs represents a powerful method to locate tissue heterogeneities.
de Lange
Enno
E
Department of Physiology, University of Bern, Bern, Switzerland.
Kucera
Jan P
JP
D000200:Action Potentials / Q000502:physiology*; D000465:Algorithms; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001703:Biophysics / Q000379:methods*; D003198:Computer Simulation; D004566:Electrodes; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000502:physiology / Q000503:physiopathology; D006352:Heart Ventricles / Q000473:pathology; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac / Q000502:physiology; D011191:Potassium Deficiency / Q000378:metabolism*; D051381:Rats