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

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Abstract
Background: Paroxysmal atrial fibrillation (PAF), a common arrhythmia, is caused by the fractionated and nonhomo-geneous propagation of sinus impulse. Hypothesis: This study was undertaken to examine the effect of left atrial (LA) dimension and function on P-wave dispersion (ΔP) in unselected patients 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 effect of LA size, volume, and function on ΔP (difference between maximum and minimum P-wave duration on 12-lead electrocardiogram). Results: P-wave dispersion in patients with PAF and normal LA diastolic diameter (LAD) was longer than that in controls with normal LA size (53 ± 8 vs. 34 ± 8 ms, p < 0.001). P-wave dispersion increased in patients with PAF (62 ± 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 interact with LAD for their effect on ΔP (2 × 2 analysis of variance test p = 0.20). In the PAF group, ΔP correlated with LAD (r = 0.43, p = 0.002), LA diastolic 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 PAF (0.52 ± 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 multivariate logistic regression analysis, only δP retained significance on development of PAF. Conclusion: It was concluded that δP increased in patients with PAF and normal LA size. In controls with increased LA size, δP increased but did not reach the levels attained in patients with PAF. The AEF was decreased in patients with PAF but was preserved in those without PAF. These findings can be explained by the changes in LA microarchitecture which concurrently decreased atrial myocardial contraction, increased δP, and predisposed to PAF.