Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability.

ABSTRACT:

Background

Late Na(+) current (I(NaL)) in human and dog hearts has been implicated in abnormal repolarization associated with heart failure (HF). HF slows inactivation gating of late Na(+) channels, which could contribute to these abnormalities.

Aims

To test how altered gating affects I(NaL) time course, Na(+) influx, and action potential (AP) repolarization.

Methods

I(NaL) and AP were measured by patch clamp in left ventricular cardiomyocytes from normal and failing hearts of humans and dogs. Canine HF was induced by coronary microembolization.

Results

I(NaL) decay was slower and I(NaL) density was greater in failing hearts than in normal hearts at 24 degrees C (human hearts: tau=659+/-16 vs. 529+/-21 ms; n=16 and 4 hearts, respectively; mean+/-SEM; p<0.002; d

SUBMITTER: Maltsev VA 

PROVIDER: S-EPMC1847560 | biostudies-literature | 2007 Mar

REPOSITORIES: biostudies-literature