Background and Purpose:

Atrioventricular (AV) dyssynchrony attenuates oxygen uptake (VO₂) kinetics during the onset to constant work rate exercise. However, the effect of AV dyssynchrony on VO₂ kinetics during recovery from constant work rate exercise remains unknown. Identifying mechanisms responsible for alterations in VO₂ kinetics has the potential to significantly alter clinical management, and improve quality of life in those with cardiac dyssynchrony. Therefore, the purpose of this study was to determine the effect of AV dyssynchrony on VO₂ kinetics during exercise recovery.

Methods:

Seven chronotropically competent male pacemaker dependent patients (mean +/- SEM; age, 76 +/- 3 years; BMI, 28 +/- 1 kg/m²; peak VO₂, 1.24 +/- 0.02 L/min (16.4 +/- 1.6 mL/kg/min); peak work rate, 90 +/- 7 watts) were included in this study. Breath-by-breath VO₂ was collected throughout a 5 min recovery period following exercise termination. VO₂ kinetics were determined with non-linear regression using a monoexponential equation. Stroke volume was determined with impedance cardiography and heart rate with an integrated (lead II) electrocardiogram. Cardiac output was calculated as stroke volume x heart rate.

Results:

The main finding of this study was that VO₂ kinetics during exercise recovery were significantly (P < 0.05) slower during dyssynchronous (82 +/- 6 s; 95% confidence interval, 4.7 s) compared with synchronous (61 +/- 6 s; 95% confidence interval, 4.5 s) AV pacing. Cardiac output and stroke volume responses were also significantly (P < 0.05) reduced at exercise termination and at matched time points throughout recovery during dyssynchronous AV pacing.

Conclusions:

The findings of this study suggest that a reduction in stroke volume associated with AV dyssynchrony contribute to altered VO₂ kinetics, and thus a prolonged exercise recovery time.

Section Description

For more information, contact Marilyn Thomas (204) 488-5854