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Calcium homeostasis, myocardial ischemia and arrhythmogenic impact

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Myocardial Ischemia and Arrhythmia

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Summary

Ventricular tachyarrhythmias can originate from disturbed impulse conduction (reentry) or from abnormal impulse generation, i.e., focal activation by normal or abnormal automaticity or by triggered activity due to early or late afterdepolarisations. Although reentry is traditionally considered as the predominant mechanism of tachyarrhythmias in ischaemic heart disease, the coexistence of reentry, intramural reentry and focal nonreentrant mechanisms as initiating causes has been demonstrated. Presently, the quantitative assessment of the relative impact of these various mechanisms appears impossible. Theoretically, all these arrhythmogenic mechanisms may be sensitive to cytosolic Ca++ overload: cytosolic Ca++ and acidosis can reduce intercellular conduction by altering gating kinetics of intercellular gap junctions, thereby facilitating reentry; late after depolarisations result from Ca++-induced Ca++ release and subsequent activation of the rheogenic Na+-Ca++-exchanger (and probably of Ca++-dependent cation channels); other arrhythmogenic mechanisms are not directly elicitated by cytosolic Ca -overload, but a reduced intercellular conductivity (due to Ca overload-induced alteration in gating of gap junctions) will reduce the stability of the cellular network against any local depolarizing stimulus. In hemodynamically overloaded ventricular myocardium, the myocyte phenotype of the hypertrophied cardiocytes is shifted towards a more “neonatal-like” phenotype. In human myocardium, this phenotype shift includes downregulation of the sarcoplasmatic reticulum Ca++-ATPase and an upregulation of the sarcolemmal Na+-Ca ++-exchanger, together with a rather normal depolarisation-induced Ca++-influx and a reduced density of intercellular gap junctions. This phenotype can be considered as “fragile Ca + + homeostasis”, prone to cytosoloic Ca++ overload and associated with the enhanced susceptibility of overloaded myocardium to arrhythmogenesis. The augmentation of the cytosolic Ca++ rather early during ischemia is demonstrable in many experimental models, but the mechanisms contributing to this cytosolic Ca++-overload are only partially understood. Indirect arguments indicate that ischemia causes more disturbance of the cytosolic Ca++-homeostasis in myocardium with overload induced hypertrophy than in normal hearts. The available evidence indicates that hemodynamically overloaded, hypertrophied myocardium has a greater susceptibility for Ca++-overload-induced arrhythmogenesis.

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  1. Institut für Pathophysiologie, Martin-Luther-Universtät, Magdeburger Str. 18, 06097, Halle, Germany

    Prof. Dr. med. J. Holtz

  2. Institut für Pathophysiologie, Martin-Luther-Universität, Halle-Wittenberg, Germany

    M. Koban

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Holtz, J., Koban, M. (1994). Calcium homeostasis, myocardial ischemia and arrhythmogenic impact. In: Zehender, M., Meinertz, T., Just, H. (eds) Myocardial Ischemia and Arrhythmia. Steinkopff. https://doi.org/10.1007/978-3-642-72505-0_1

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