Purpose: We investigated the relationship between P wave dispersion, as measured on the surface electrocardiogram, and left ventricular diastolic function, in a group of hypertensive patients. Methods: We included 86 patients (52 males, aged between 35–67 years). We excluded patients with previous acute myocardial infarction, thyroid dysfunction, valvular heart disease, cardiomyopathy, electrolyte imbalance, drug use that affects atrial conduction, or alcohol use. P wave dispersions were calculated by measuring minimum and maximum P wave duration values on the surface electrocardiogram. By standard transthoracic echocardiography we investigated the presence and degree of diastolic dysfunction, classified as: stage 1 - prolonged relaxation pattern, stage 2 - pseudonormalization pattern, and stage 3 - restrictive pattern. There were 47 patients with diastolic dysfunction and 39 without. The relationships between P wave dispersion and echocardiographic measurements of diastolic dysfunction were analyzed. Results: P wave dispersion was 62 ± 12 ms in patients with diastolic dysfunction and 49 ± 10 ms in those without (p < 0.01). The maximum P wave duration was 118 ± 9 ms in patients with diastolic dysfunction vs 107 ± 8 ms in the control group (p < 0.05). The minimum P wave duration was 64 ± 11 ms vs 63 ± 10 ms (not significant). When patients were grouped according to the stage of diastolic dysfunction, P wave dispersion was 52 ± 8 ms in stage 1, 58 ± 9 ms in stage 2, and 64 ± 13 ms in stage 3. As the severity of diastolic dysfunction increased, P wave dispersion increased, the difference was statistically significant (p < 0.05). Conclusion: P wave dispersion is increased in hypertensive patients with diastolic dysfunction, and this increase is related to the severity of diastolic dysfunction.

Purpose: A maximum P wave duration (Pmax) of > 110 msec and a P wave dispersion (PWD) > 40 msec are accepted indicators of a disturbance in interatrial conduction and an inhomogeneous propagation of the sinus impulse, respectively. The left atrial (LA) volume is considered to be a marker of atrial remodeling. We aimed to investigate the relationship between LA volume and Pmax or PWD in patients with hypertension. Methods: We included 52 hypertensive patients in sinus rhythm. We recorded for each patient a 12-lead electrocardiogram with a paper speed of 50 mm/s and an amplification of 20 mm/mV. P wave dispersion (PWD) was defined as the difference between the duration of the widest (Pmax) and the narrowest (Pmin) P wave, measured on all leads of the 12-lead electrocardiogram. Measurements were made by a single investigator, in a blinded fashion, using a computerized program; the onset and offset points of the P wave were marked manually. The study population was classified into four groups, according to the Pmax (>/= 110 ms or < 110 ms), and the PWD (>/= 40 ms or < 40 ms). The left atrial volume (LAV) was measured by transthoracic echocardiography. Results: There were significant differences in the ejection fraction, diastolic function, and LAV between patients with a Pmax >/= 110 ms or a PWD >/= 40 ms and those with a Pmax < 110 ms or a PWD < 40 ms. The LAV was independently associated with a disturbance in interatrial conduction and an inhomogeneous propagation of the sinus impulse. The LAV can be used to identify patients with a disturbance in the propagation of the sinus impulse, which are at risk for atrial fibrillation. Conclusion: The maximum duration of the P wave and the P wave dispersion on standard 12-lead electrocardiograms are associated with the LA volume in hypertensive patients.