Effect of dephosphorylation of troponin I on arrhythmogenesis in failing hearts

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An increase in the affinity of the myofilaments for Ca^<2+> by lengthening the muscle or applying a Ca^<2+> sensitizer for myofilaments sustained triggered arrhythmias and increased their frequency in intact cardiac muscle. In failing hearts, dephosphorylation of troponin-I and an increase in Ca^<2+> sensitivity of the sarcoplasmic reticulum Ca^<2+> release channel increased the velocity of Ca^<2+> 2+ waves and the amplitude of delayed afterdepolarizations, thereby causing arrhythmogenesis. The affinity of the myofilaments for Ca^<2+> plays an important role in the occurrence of arrhythmias.