Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activity.

ABSTRACT:

Rationale

Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome.

Objective

We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (V(m)) to elevated intracellular calcium (Ca(i)) (high diastolic Ca(i)-voltage coupling gains).

Methods and results

We simultaneously mapped Ca(i) and V(m) on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Ca(i) elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81%

SUBMITTER: Maruyama M 

PROVIDER: S-EPMC2818796 | biostudies-literature | 2010 Feb

REPOSITORIES: biostudies-literature