Abstract
BackgroundWhether PR prolongation independently predicts new-onset ischemic events of myocardial infarction and stroke was unclear. Underlying pathophysiological mechanisms of PR prolongation leading to adverse cardiovascular events were poorly understood. We investigated the role of PR prolongation in pathophysiologically-related adverse cardiovascular events and underlying mechanisms.MethodsWe prospectively investigated 597 high-risk cardiovascular outpatients (mean age 66 ± 11 yrs.; male 67%; coronary disease 55%, stroke 22%, diabetes 52%) for new-onset ischemic stroke, myocardial infarction (MI), congestive heart failure (CHF), and cardiovascular death. Vascular phenotype was determined by carotid intima-media thickness (IMT).ResultsPR prolongation >200 ms was present in 79 patients (13%) at baseline. PR prolongation >200 ms was associated with significantly higher mean carotid IMT (1.05 ± 0.37 mm vs 0.94 ± 0.28 mm, P = 0.010). After mean study period of 63 ± 11 months, 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. Using multivariable Cox regression, 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). PR interval predicts new-onset MI at the exploratory cut-off >162 ms (C-statistic 0.70, P = 0.001; HR: 8.0, 95% CI: 1.65–38.85, P = 0.010).ConclusionsPR prolongation strongly predicts new-onset ischemic stroke, MI, cardiovascular death, and combined cardiovascular endpoint including CHF in coronary patients or risk equivalent. Adverse vascular function may implicate an intermediate pathophysiological phenotype or mediating mechanism.
Highlights
Whether PR prolongation independently predicts new-onset ischemic events of myocardial infarction and stroke was unclear
Clinical utility in the prediction of CV events The clinical utility measures of sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) at specific cut-off points of PR interval in the prediction of each CV event were presented in Additional file 1: Table S6. This is our first recognized study to show that PR prolongation alone is a strong and independent predictor for CV death, new-onset ischemic stroke and myocardial infarction (MI), and combined CV endpoints including congestive heart failure (CHF) among patients with coronary artery disease (CAD) or risk equivalent
Despite the stated observations, adjustment for carotid intima-media thickness (IMT) did not materially alter the prediction of PR prolongation for incident CV events, which suggests that atherosclerosis alone does not fully explain the pathophysiological mechanism along the pathway of PR prolongation leading to clinical events
Summary
Whether PR prolongation independently predicts new-onset ischemic events of myocardial infarction and stroke was unclear. Underlying pathophysiological mechanisms of PR prolongation leading to adverse cardiovascular events were poorly understood. We investigated the role of PR prolongation in pathophysiologically-related adverse cardiovascular events and underlying mechanisms. The roles of PR prolongation in atherosclerotic cardiovascular (CV) disease, as well as outcome prediction in CV patients under clinical care, remained largely unknown. We further showed that PR prolongation when incorporated into the CHADS2 and CHA2DS2-VASc scores, augments their predictive power for new-onset CV events [5]. The individual role of PR prolongation, a precursor to atrial fibrillation, for new-onset ischemic events of stroke and myocardial infarction was not clearly established. Underlying pathophysiological mechanistic basis of how PR prolongation may lead to adverse CV outcomes remained poorly understood
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
