Coupling between cardiac cells—An important determinant of electrical impulse propagation and arrhythmogenesis

2021 ◽  
Vol 2 (3) ◽  
pp. 031301
Author(s):  
André G. Kléber ◽  
Qianru Jin
Physiology ◽  
1997 ◽  
Vol 12 (4) ◽  
pp. 171-177 ◽  
Author(s):  
S Rohr ◽  
JP Kucera ◽  
AG Kleber

The architecture of the cellular network forming the myocardium is an important determinant of the characteristics of impulse propagation. This article describes an experimental approach permitting the systematic study of this structure-function relationship, which is based on optical micromapping of electrical activity in cardiac cell cultures with a defined two-dimensional geometry.


2004 ◽  
Vol 84 (2) ◽  
pp. 431-488 ◽  
Author(s):  
ANDRÉ G. KLÉBER ◽  
YORAM RUDY

Kléber, André G., and Yoram Rudy. Basic Mechanisms of Cardiac Impulse Propagation and Associated Arrhythmias. Physiol Rev 84: 431–488, 2004; 10.1152/physrev.00025.2003.—Propagation of excitation in the heart involves action potential (AP) generation by cardiac cells and its propagation in the multicellular tissue. AP conduction is the outcome of complex interactions between cellular electrical activity, electrical cell-to-cell communication, and the cardiac tissue structure. As shown in this review, strong interactions occur among these determinants of electrical impulse propagation. A special form of conduction that underlies many cardiac arrhythmias involves circulating excitation. In this situation, the curvature of the propagating excitation wavefront and the interaction of the wavefront with the repolarization tail of the preceding wave are additional important determinants of impulse propagation. This review attempts to synthesize results from computer simulations and experimental preparations to define mechanisms and biophysical principles that govern normal and abnormal conduction in the heart.


2008 ◽  
Vol 294 (5) ◽  
pp. H2040-H2052 ◽  
Author(s):  
Vincent Jacquemet ◽  
Craig S. Henriquez

The numerous nonmyocytes present within the myocardium may establish electrical connections with myocytes through gap junctions, formed naturally or as a result of a cell therapy. The strength of the coupling and its potential impact on action potential characteristics and conduction are not well understood. This study used computer simulation to investigate the load-induced electrophysiological consequences of the coupling of myocytes with fibroblasts, where the fibroblast resting potential, density, distribution, and coupling strength were varied. Conduction velocity (CV), upstroke velocity, and action potential duration (APD) were analyzed for longitudinal and transverse impulse propagation in a two-dimensional microstructure tissue model, developed to represent a monolayer culture of cardiac cells covered by a layer of fibroblasts. The results show that 1) at weak coupling (<0.25 nS), the myocyte resting potential was elevated, leading to CV up to 5% faster than control; 2) at intermediate coupling, the myocyte resting potential elevation saturated, whereas the current flowing from the myocyte to the fibroblast progressively slowed down both CV and upstroke velocity; 3) at strong couplings (>8 nS), all of the effects saturated; and 4) APD at 90% repolarization was usually prolonged by 0–20 ms (up to 60–80 ms for high fibroblast density and coupling) by the coupling to fibroblasts. The changes in APD depended on the fibroblast resting potential. This complex, coupling-dependent interaction of fibroblast and myocytes also has relevance to the integration of other nonmyocytes in the heart, such as those used in cellular therapies.


Theranostics ◽  
2018 ◽  
Vol 8 (10) ◽  
pp. 2752-2764 ◽  
Author(s):  
Zhi Cui ◽  
Nathan C. Ni ◽  
Jun Wu ◽  
Guo-Qing Du ◽  
Sheng He ◽  
...  

Author(s):  
W.G. Wier

A fundamentally new understanding of cardiac excitation-contraction (E-C) coupling is being developed from recent experimental work using confocal microscopy of single isolated heart cells. In particular, the transient change in intracellular free calcium ion concentration ([Ca2+]i transient) that activates muscle contraction is now viewed as resulting from the spatial and temporal summation of small (∼ 8 μm3), subcellular, stereotyped ‘local [Ca2+]i-transients' or, as they have been called, ‘calcium sparks'. This new understanding may be called ‘local control of E-C coupling'. The relevance to normal heart cell function of ‘local control, theory and the recent confocal data on spontaneous Ca2+ ‘sparks', and on electrically evoked local [Ca2+]i-transients has been unknown however, because the previous studies were all conducted on slack, internally perfused, single, enzymatically dissociated cardiac cells, at room temperature, usually with Cs+ replacing K+, and often in the presence of Ca2-channel blockers. The present work was undertaken to establish whether or not the concepts derived from these studies are in fact relevant to normal cardiac tissue under physiological conditions, by attempting to record local [Ca2+]i-transients, sparks (and Ca2+ waves) in intact, multi-cellular cardiac tissue.


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