EFFECT OF LEFT ATRIA SIZE ON P-WAVE DISPERSION: A STUDY IN PATIENTS WITH PAROXYSMAL ATRIAL FIBRILLATION

INTRODUCTION: Paroxysmal atrial fibrillation (AF) is a common arrhythmia encountered in clinical practice. Experimental and human mapping studies have demonstrated that perpetuation of AF is due to the presence of multiple reentrant wavelets with various sizes in the right and left atria. P-wave dispersion (PWD), defined as the difference between the maximum and minimum P-wave duration, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (AF). This study was undertaken to examine the effect of left atria (LA) dimension on P-wave dispersion in unselected patients with PAF compared to healthy controls. METHODS: In this study, 40 consecutive patients with PAF (25 male, 15 female, mean age 45 ± 9 years) and 40 age and gender matched healthy controls (25 male, 15 female, mean age 46 ± 10 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECG. The difference between the maximum and minimum P wave duration was calculated and defined as P wave dispersion (PWD = Pmax - Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). RESULTS: P-wave dispersion in patients with PAF and normal LA diastolic diameter (LAD) was longer than in controls with normal LA size (51±9 vs. 34±8 ms, P < 0.002). P-wave dispersion increased in patients with PAF (60±14 vs. 50±7 ms, P < 0.001) and controls (39 ± 9 vs. 33 ± 9 ms, P < 0.004) with increased LAD. In the PAF group, P-wave dispersion correlated with LAD (r = 0.40, P = 0.001) and LA diastolic volume (r = 0.62, P < 0.001). On multivariate logistic regression analysis, only P-wave dispersion retained significance on development of PAF. CONCLUSION: P-wave dispersion increased in patients with PAF and normal LA size. In controls with increased LA size, P-wave dispersion increased but did not reach the levels attained in patients with PAF. These findings can be explained by the changes in LA microarchitecture which concurrently decreased atrial myocardial contraction, increased P-wave dispersion and predisposed to PAF.