Atrial bigeminy results in decreased left ventricular function: an insight into the mechanism of PVC-induced cardiomyopathy.

BACKGROUND

Premature ventricular complexes have been recently recognized as a reversible cause of cardiomyopathy. The purpose of this study was to determine if premature complexes independent of "dyssynchrony" resulted in increased left ventricular (LV) dimensions and decreased LV function.

METHODS

Ten mongrel dogs underwent the implantation of a pacemaker and were randomized to a control group (n = 5) or a paced group (n = 5). In the paced group, the pacemaker was connected to two endocardial atrial leads, one inserted into the atrial port and the other one into the ventricular port with an atrioventricular delay adjusted to ensure the presence of coupled pacing simulating atrial bigeminy with conducted beats in the absence of aberrancy. Echocardiographic parameters of LV size (LV end-diastolic diameter [LV-EDD], LV end-systolic diameter [LV-ESD]), and LV ejection fraction (LVEF) were measured at baseline and after 4 weeks of monitoring (control group) or pacing (paced group).

RESULTS

In the control group, LV size decreased with no significant changes in LVEF: 55% at baseline versus 70% at 4 weeks (P = 0.23). In the paced group, LV-EDD decreased with no significant change in LV-ESD. Unlike the control group, LVEF decreased significantly from 69 ± 9% at baseline to 32 ± 22% after 4 weeks of pacing (P = 0.05).

CONCLUSION

We have shown that 4 weeks of coupled pacing simulating atrial bigeminy significantly reduced LV function. Our findings suggest that premature complexes independent of ventricular dyssynchrony might lead to the development of cardiomyopathy.