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Article: Abnormal vascular function in PR-interval prolongation

TitleAbnormal vascular function in PR-interval prolongation
Authors
Issue Date2011
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.clinicalcardiology.org
Citation
Clinical Cardiology, 2011, v. 34 n. 10, p. 628-632 How to Cite?
AbstractBackground: Underlying mechanisms of PR-interval prolongation leading to increased risk of adverse cardiovascular outcomes, including atrial fibrillation, are unclear. This study aims to investigate the relation between PR interval and changes in vascular function. Hypothesis: We hypothesize that there exists an intermediate pathological stage between electrocardiographic PR prolongation and adverse cardiovascular outcomes, which could be reflected by changes in surrogate measurements of vascular function. Methods: We recruited 88 healthy subjects (mean age 57.5 ± 9.8 y, 46% male) from a community-based health screening program who had no history of cardiovascular disease or diabetes mellitus. PR interval was determined from a resting 12-lead electrocardiogram. Vascular function was noninvasively assessed by flow-mediated dilation (FMD) using high-resolution ultrasound and brachial-ankle pulse wave velocity (PWV) using a vascular profiling system. Results: Only 3 subjects had a PR-interval length longer than the conventional cutoff of 200 ms. The PR-interval length was associated inversely with FMD (Pearson r = -0.30, P = 0.004) and positively with PWV (r = 0.40, P < 0.001). Adjusting for potential confounders, increased PR-interval length by each 25 ms was independently associated with reduced FMD by -1 unit (absolute %, B = -0.04 [95% confidence interval: -0.080 to -0.002, P = 0.040)] and increased PWV by +103 cm/second (B = +4.1 [95% confidence interval: 0.6-7.6, P = 0.023]). Conclusions: This study shows that PR-interval length, even in the conventionally normal range, is independently associated with endothelial dysfunction and increased arterial stiffness in healthy subjects free of atherosclerotic disease. This suggests the presence of a systemic, intermediate pathologic stage of the vasculature in PR prolongation before clinically manifest cardiovascular events, and could represent a mediating mechanism. © 2011 Wiley Periodicals, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/143767
ISSN
2014 Impact Factor: 2.586
2014 SCImago Journal Rankings: 1.061
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong200907176063
Sun Chieh Yeh Heart Foundation, Hong Kong, China
Funding Information:

This study was supported by the CRCG Small Project Funding of the University of Hong Kong (Project No. 200907176063) and the Sun Chieh Yeh Heart Foundation, Hong Kong, China. Yap-Hang received a Best Paper Award at the Third Asian Preventive Cardiology and Cardiac Rehabilitation Conference, Hong Kong, China, December 11-12, 2010. The authors have no other funding, financial relationships, or conflicts of interest to disclose.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, YHen_HK
dc.contributor.authorSiu, CWen_HK
dc.contributor.authorYiu, KHen_HK
dc.contributor.authorLi, SWen_HK
dc.contributor.authorLau, KKen_HK
dc.contributor.authorLam, THen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorTse, HFen_HK
dc.date.accessioned2011-12-21T08:54:13Z-
dc.date.available2011-12-21T08:54:13Z-
dc.date.issued2011en_HK
dc.identifier.citationClinical Cardiology, 2011, v. 34 n. 10, p. 628-632en_HK
dc.identifier.issn0160-9289en_HK
dc.identifier.urihttp://hdl.handle.net/10722/143767-
dc.description.abstractBackground: Underlying mechanisms of PR-interval prolongation leading to increased risk of adverse cardiovascular outcomes, including atrial fibrillation, are unclear. This study aims to investigate the relation between PR interval and changes in vascular function. Hypothesis: We hypothesize that there exists an intermediate pathological stage between electrocardiographic PR prolongation and adverse cardiovascular outcomes, which could be reflected by changes in surrogate measurements of vascular function. Methods: We recruited 88 healthy subjects (mean age 57.5 ± 9.8 y, 46% male) from a community-based health screening program who had no history of cardiovascular disease or diabetes mellitus. PR interval was determined from a resting 12-lead electrocardiogram. Vascular function was noninvasively assessed by flow-mediated dilation (FMD) using high-resolution ultrasound and brachial-ankle pulse wave velocity (PWV) using a vascular profiling system. Results: Only 3 subjects had a PR-interval length longer than the conventional cutoff of 200 ms. The PR-interval length was associated inversely with FMD (Pearson r = -0.30, P = 0.004) and positively with PWV (r = 0.40, P < 0.001). Adjusting for potential confounders, increased PR-interval length by each 25 ms was independently associated with reduced FMD by -1 unit (absolute %, B = -0.04 [95% confidence interval: -0.080 to -0.002, P = 0.040)] and increased PWV by +103 cm/second (B = +4.1 [95% confidence interval: 0.6-7.6, P = 0.023]). Conclusions: This study shows that PR-interval length, even in the conventionally normal range, is independently associated with endothelial dysfunction and increased arterial stiffness in healthy subjects free of atherosclerotic disease. This suggests the presence of a systemic, intermediate pathologic stage of the vasculature in PR prolongation before clinically manifest cardiovascular events, and could represent a mediating mechanism. © 2011 Wiley Periodicals, Inc.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.clinicalcardiology.orgen_HK
dc.relation.ispartofClinical Cardiologyen_HK
dc.rightsClinical Cardiology (Hoboken). Copyright © John Wiley & Sons, Inc..-
dc.subject.meshAtrioventricular Block - complications - diagnosis - physiopathology-
dc.subject.meshBrachial Artery - physiopathology - ultrasonography-
dc.subject.meshCardiovascular Diseases - etiology - physiopathology-
dc.subject.meshElectrocardiography-
dc.subject.meshVasodilation-
dc.titleAbnormal vascular function in PR-interval prolongationen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, YH:chanwill@hku.hken_HK
dc.identifier.emailSiu, CW:cwdsiu@hkucc.hku.hken_HK
dc.identifier.emailYiu, KH:khkyiu@hku.hken_HK
dc.identifier.emailLau, KK:gkklau@hku.hken_HK
dc.identifier.emailLam, TH:hrmrlth@hkucc.hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityChan, YH=rp01313en_HK
dc.identifier.authoritySiu, CW=rp00534en_HK
dc.identifier.authorityYiu, KH=rp01490en_HK
dc.identifier.authorityLau, KK=rp01499en_HK
dc.identifier.authorityLam, TH=rp00326en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/clc.20958en_HK
dc.identifier.pmid21994083-
dc.identifier.scopuseid_2-s2.0-80054093737en_HK
dc.identifier.hkuros197998en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054093737&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume34en_HK
dc.identifier.issue10en_HK
dc.identifier.spage628en_HK
dc.identifier.epage632en_HK
dc.identifier.eissn1932-8737-
dc.identifier.isiWOS:000296191700008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, YH=22633700600en_HK
dc.identifier.scopusauthoridSiu, CW=7006550690en_HK
dc.identifier.scopusauthoridYiu, KH=35172267800en_HK
dc.identifier.scopusauthoridLi, SW=13807028100en_HK
dc.identifier.scopusauthoridLau, KK=22635159600en_HK
dc.identifier.scopusauthoridLam, TH=7202522876en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK

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