Effect of left atrial size and function on P-wave dispersion: A study in patients with paroxysmal atrial fibrillation

Background Paroxysmal atrial fibrillation (PAF), a common arrhythmia, is ca used by the fractionated and nonhomogeneous propagation of sinus impulse. Hypothesis: This study was undertaken to examine the effect of left atrial (LA) dimension and function on P-wave dispersion (DeltaP) in unselected pat ients with PAF and healthy controls. Method: In this study, 62 consecutive patients with PAF (32 men, 30 women, mean age 55 +/- 11 years) and 62 age- and gender-matched healthy controls ( 33 men, 29 women, mean age 52 +/- 13 years) were studied to compare the eff ect of LA size, volume, and function on DeltaP (difference between maximum and minimum P-wave duration on 12-lead electrocardiogram). Results: P-wave dispersion in patients with PAF and normal LA diastolic dia meter (LAD) was longer than that in controls with normal LA size (53 +/-8 v s. 34 +/-8 ms, p<0.001). P-wave dispersion increased in patients with PAF ( 62<plus/minus>12 vs. 53 +/-8 ms, p=0.003) and controls (40 +/-7 vs. 34 +/-8 ms, p=0.005) with increased LAD. Presence or absence of PAF did not intera ct with LAD for their effect on DeltaP (2 x 2 analysis of variance test p=0 .20). In the PAF group, DeltaP correlated with LAD (r=0.43, p=0.002), LA di astolic volume (r=0.6, p<0.001), and LA ejection fraction (AEF) (r=-0.33, p =0.05). The AEF was preserved when LAD increased in the patients without PA F (0.52<plus/minus>0.07 vs. 0.57 +/-0.10, p=NS), however was significantly decreased in the PAF group (0.37 +/-0.12 vs. 0.49 +/-0.10, p=0.01). On mult ivariate logistic regression analysis, only DeltaP retained significance on development of PAF. Conclusion: It was concluded that DeltaP increased in patients with PAF and normal LA size. In controls with increased LA size, DeltaP increased but d id not reach the levels attained in patients with PAF. The AEF was decrease d in patients with PAF but was preserved in those without PAF. These findin gs can be explained by the changes in LA microarchitecture which concurrent ly decreased atrial myocardial contraction, increased DeltaP, and predispos ed to PAF.