Altered ventricular stretch contributes to initiation of cardiac memory.

BACKGROUND

Cardiac memory is a change in T-wave morphology induced by ventricular pacing or arrhythmias that persist after resumption of normal AV conduction. Changing the pacemaker site from atrium to ventricle alters ventricular activation and the mechanical pattern of ventricular contraction. Either or both alterations affect T-wave configuration.

OBJECTIVE

The purpose of this study was to study the role of altered contractile patterns on initiation of cardiac memory.

METHODS

Isolated rabbit hearts were immersed in Tyrode's solution (37 degrees C) and aortically perfused at a constant pressure of 70 mmHg. Three orthogonal quasi-ECG leads were recorded via six Ag-AgCl electrodes located on the walls of the bath. Hearts were paced at a constant cycle length from either the right atrial appendage or left ventricle lateral wall. The pulmonary artery was sealed, and both ventricles contracted isovolumetrically. Cardiac memory was quantified as T-wave vector displacement expressed as distance between T-wave vector peaks during atrial pacing before and after ventricular pacing.

RESULTS

Five minutes of ventricular pacing induced significant T-wave vector displacement that returned to control in 5 to 10 minutes. No significant changes in intraventricular pressure occurred during and after ventricular pacing. Interventions that decreased ventricular load (shunting both ventricles to the bath) or contractility (excitation-contraction uncoupler blebbistatin) significantly decreased developed pressure and eliminated T-wave vector displacement. Neither intervention affected ventricular activation during ventricular pacing. Locally applied left ventricular epicardial stretch induced T-wave vector displacement similar to that induced by ventricular pacing.

CONCLUSION

Altered ventricular activation during ventricular pacing initiates cardiac memory via induction of altered contractile patterns and altered stretch.