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Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback

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Abstract

The macroscopic hallmarks of the normal heartbeat are rapid onset of contraction and rapid relaxation and an inotropic response to both increased end diastolic volume and increased heart rate. At the microscopic level, the calcium ion (Ca2+) plays a crucial role in normal cardiac contraction. This paper reviews the cycle of Ca2+ fluxes during the normal heartbeat, which underlie the coupling between excitation and contraction (ECC) and permit a highly synchronized action of cardiac sarcomeres. Length dependence of the response of the regulatory sarcomeric proteins mediates the Frank–Starling Law of the heart. However, Ca2+ transport may go astray in heart disease and both jeopardize the exquisite mechanism of systole and diastole and triggering arrhythmias. The interplay between weakened and strong segments in nonuniform cardiac muscle may further lead to mechanoelectric feedback—or reverse excitation contraction coupling (RECC) mediating an early diastolic Ca2+ transient caused by the rapid force decrease during the relaxation phase. These rapid force changes in nonuniform muscle may cause arrhythmogenic Ca2+ waves to propagate by activation of neighbouring SR by diffusing Ca2+ ions.

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Acknowledgements

This work was supported by grants HL-58860-O6A2 and HL-66140 from the National Heart and Lung Institute of the NIH, by the Canadian Institutes for Health Research and the Heart and Stroke Foundation of Alberta the North West Territories and Nunavut. H.E.D.J. ter Keurs is Senior Investigator of the Alberta Heritage Foundation for Medical Research.

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  1. Department of Physiology and Biophysics, University of Calgary, 3280 Hospital Drive, NW, Calgary, AB, T2N 4Z6, Canada

    Henk E. D. J. ter Keurs

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ter Keurs, H.E.D.J. Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback. Pflugers Arch - Eur J Physiol 462, 165–175 (2011). https://doi.org/10.1007/s00424-011-0944-3

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