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. 2017 Aug 24;17(1):233.
doi: 10.1186/s12872-017-0667-2.

PR interval prolongation in coronary patients or risk equivalent: excess risk of ischemic stroke and vascular pathophysiological insights

Yap-Hang Chan  1 , Jo Jo Hai  1 , Kui-Kai Lau  2 , Sheung-Wai Li  3 , Chu-Pak Lau  1 , Chung-Wah Siu  1   4 , Kai-Hang Yiu  1 , Hung-Fat Tse  5   6
Affiliations

PR interval prolongation in coronary patients or risk equivalent: excess risk of ischemic stroke and vascular pathophysiological insights

Yap-Hang Chan et al. BMC Cardiovasc Disord. .

Abstract

Background: 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.

Methods: We 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).

Results: PR 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).

Conclusions: PR 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.

Keywords: Cardiovascular death; Carotid intima-media thickness; Ischemic stroke; Myocardial infarction; PR interval prolongation; Pathophysiological mechanism; Vascular function.

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Conflict of interest statement

Ethics approval and consent to participate

We declare that all patients completed written informed consent and the study was adherent to the Declaration of Helsinki and approved by the Ethics Committee, Hospital Authority (Hong Kong West)/ University of Hong Kong.

Consent for publication

We declare that all patients gave informed consent to the research participation and its publication.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
PR Prolongation and Mean Carotid Intima-Media Thickness (IMT). Patients with PR prolongation >200 ms had significantly higher mean carotid IMT (1.05 ± 0.37 versus 0.94 ± 0.28 mm, P = 0.010)
Fig. 2
Fig. 2
Kaplan-Meier Survival Curves for New-Onset Cardiovascular Events by PR Prolongation. Patients with PR prolongation >200 ms had significantly reduced survival from a cardiovascular death (log rank: 14.4, P < 0.001); b Ischemic Stroke (log rank: 8.7, P = 0.003); d CHF (log rank: 5.0, P = 0.026) e Combined Cardiovascular Endpoints (log rank: 14.2, P < 0.001). PR interval > 162 ms was associated with reduced survival from c new-onset MI (log rank: 7.4, P = 0.007)
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