Abstract 8488: PR Interval Prolongation is Associated with Endothelial Dysfunction and Activation of Vascular Repair in High Risk Cardiovascular Patients
Background: Recent studies showed that PR prolongation is associated with substantially increased risk of adverse clinical outcomes due to unclear mechanisms.
Objective: To investigate the relations between PR interval and indices of vascular function and endothelial repair in patients at high risk of cardiovascular events.
Methods: A total of 149 patients (mean age 63.6 ± 10.2 years; male 57%) with prior coronary artery disease, ischemic stroke and / or diabetes mellitus (diagnosed >6 months) were recruited from our medical outpatient clinics. Vascular function was non-invasively measured by flow-mediated dilatation (FMD) using high-resolution vascular ultrasound (Agilent Sonos, USA). CD133+/KDR+ circulating endothelial progenitor cells (EPC) were measured by flow cytometry. PR interval was determined from 12-lead electrocardiogram.
Results: Mean PR interval was 170±26 ms, with PR prolongation >200 ms present in 14 subjects (9%). Mean FMD was 3.4±2.5%. PR interval was associated negatively with FMD (Pearson R=−0.27, P=0.001) but positively with CD133+/KDR+ EPC (Pearson R=0.23, P=0.006). Compared with PR interval ≤200ms, patients with PR prolongation >200ms had significantly lower FMD (1.5±1.4% versus 3.6±2.6%, P=0.003,Figure 1) but increased CD133+/KDR+ EPC (log-transformed, unit [x10−3/ ml]) (1.05 ± 0.33 versus 0.70 ± 0.41, P=0.003, Figure 2). Adjusted for potential confounders by the multivariable model (age, gender, smoking history, systolic and diastolic blood pressure, resting heart rate, serum LDL and HDL- cholesterol, triglycerides, fasting glucose, use of aspirin/ statins), PR prolongation was independently associated with reduced FMD by −1.5% (95%CI [−3.0% to −0.1%], P=0.039) and increased CD133+/KDR+ EPC (log, unit [x10−3/ ml]) by 0.26 (95%CI [0.05 to 0.48], P=0.017).
Conclusions: PR prolongation is associated with endothelial dysfunction with evidence of endothelial repair activation in high risk cardiovascular patients.
- © 2011 by American Heart Association, Inc.