Infarcted canine ventricular myocytes exhibit reduced amplitudes and altered kinetics of delayed rectifier K currents, which may impact repolarization dynamics.
No immediate clinical implications; leaves open translation of altered repolarization to human post-MI arrhythmias.
The decrease in I(Kr) and I(Ks) amplitudes and changes in their kinetics in infarcted tissue might be due to a decrease in functional channels and/or changes in their subunit composition. Heterogeneous changes in I(Kr) and I(Ks) in infarcted hearts may impact on the effects of varying heart rate or neurohumoral modulation on repolarization.
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Min Jiang (2000) studied this question.
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