Chan YH, et al. – An analysis was performed to examine the role of PR prolongation in pathophysiologically–related adverse cardiovascular events and underlying mechanisms. The researchers concluded that in coronary patients or risk equivalent, PR prolongation strongly predicted new–onset ischemic stroke, myocardial infarction (MI), cardiovascular death, and combined cardiovascular endpoint including congestive heart failure (CHF). The adverse vascular function could implicate an intermediate pathophysiological phenotype or mediating mechanism.

• A total of 597 high-risk cardiovascular outpatients (mean age 66 ± 11 yrs were prospectively examined; male 67%; coronary disease 55%, stroke 22%, diabetes 52%) for new-onset ischemic stroke, myocardial infarction (MI), congestive heart failure (CHF), and cardiovascular death.
• By carotid intima-media thickness (IMT), vascular phenotype was determined.

• At baseline, PR prolongation >200 ms was present in 79 patients (13%).
• PR prolongation >200 ms was correlated with significantly higher mean carotid IMT (1.05 ± 0.37 mm vs 0.94 ± 0.28 mm, P = 0.010).
• Increased PR interval significantly predicted new-onset ischemic stroke (P = 0.006), CHF (P = 0.040), cardiovascular death (P < 0.001), and combined cardiovascular endpoints (P < 0.001) at cut-off >200 ms after mean study period of 63 ± 11 months.
• PR prolongation >200 ms independently predicted new-onset ischemic stroke (HR 8.6, 95% CI: 1.9–37.8, P = 0.005), cardiovascular death (HR 14.1, 95% CI: 3.8–51.4, P < 0.001) and combined cardiovascular endpoints (HR 2.4, 95% CI: 1.30–4.43, P = 0.005) using multivariable Cox regression.
• At the exploratory cut-off >162 ms, PR interval predicted new-onset MI (C-statistic 0.70, P = 0.001; HR: 8.0, 95% CI: 1.65–38.85, P = 0.010).