Key result
Acute proarrhythmogenic conditions inducing Ca2+ overload resulted in nonuniform sarcomere shortening, gap junction internalization, and myofilament disruption that preceded malignant arrhythmias.
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Acute disturbances in calcium handling and intercellular coupling cause ultrastructural cardiomyocyte damage that precedes and sustains malignant arrhythmias and contractile dysfunction.
bACKgRoUND: It has been previously reported that various acute interventions causing myocardial abnormalities in Ca 2+ handling and defects in intercellular coupling facilitate the occurrence of malignant arrhythmias. objECTIVES: To comprehensively determine the impact of such Ca 2+related disorders induced in intact animal hearts on the ultrastructure of the cardiomyocytes before occurrence and during sustaining of severe arrhythmias. METhoDS: Three types of acute experiments known to be accompanied by disturbances in Ca 2+ handling were performed. Langendorff-perfused rat and guinea pig hearts were subjected to K + -deficient perfusion to induce ventricular fibrillation; Langendorff-perfused guinea pig heart underwent burst atrial pacing to induce atrial fibrillation; and open chest pig heart was used for intramyocardial noradrenaline infusion to induce ventricular tachycardia. Tissue samples for electron microscopy examination were obtained during basal conditions, previous occurrence and during sustaining of malignant arrhythmias.
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Tribulová et al. (2015) studied Malignant arrhythmias and acute heart failure (n=72). Acute proarrhythmogenic conditions (low K+ perfusion, burst atrial pacing, intramyocardial noradrenaline) vs. Basal conditions was evaluated on Ultrastructural alterations of cardiomyocytes and intercellular junctions. Acute proarrhythmogenic conditions inducing Ca2+ overload resulted in nonuniform sarcomere shortening, gap junction internalization, and myofilament disruption that preceded malignant arrhythmias.
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