Abstract
Abstract Introduction Hypertension (HTN) is one of the most important risk factors associated with atrial fibrillation (AF). Prolongation of the PR interval has been associated with an increased risk of incident AF, while PR interval is a component of the Framingham risk score for AF. However, the results regarding PR prolongation as a risk factor for AF are inconsistent. Purpose We aim to evaluate the predictive role of the PR interval for AF development in a large cohort of HTN patients. Methods Consecutive patients with essential hypertension without known AF at baseline were followed up for a mean period of 5.3±3.3 years. A 12-lead ECG and an echocardiography study were performed on each patient at baseline and annually, and 24h Holter rhythm monitoring was used in the event of arrhythmia symptoms. Routine clinical and paraclinical examinations as well as medications were implemented during the follow-up period according to the European Society of Cardiology/ European Society of Hypertension guidelines for HTN management. The PR interval and P wave duration were obtained from the baseline ECG. Results We included 1807 hypertensives (mean age 57±11 years; 49% males) with office systolic blood pressure (SBP)/ diastolic blood pressure (DBP) 144±17/89±11mmHg. During the follow-up period, 65 cases (3%) of new-onset AF were recorded. Patients with new-onset AF (n=67) compared to those without AF (n=1740) had greater baseline P wave duration (115 vs 110 ms) and PR internal (174 vs 157 ms). Multivariable Cox regression analysis showed that higher baseline PR internal is significantly associated with the development of AF (HR 1.01, 95% CI 1.01–1.02; p=0.01), while there was no significant predictive value for baseline P wave duration on the incidence of new-onset AF. Baseline increased DBP was associated with a higher incidence of AF (HR 1.05, 95% 1.003–1.091; p=0.037). Conclusions Baseline PR internal is a significant predictor of new-onset AF in hypertensive patients. The PR prolongation could be considered as a marker for cardiovascular degenerative aging caused by vascular inflammation and myocardial fibrosis. Funding Acknowledgement Type of funding sources: None.
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