Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/35420
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dc.contributor.authorPuri R.en
dc.contributor.authorWorthley M.I.en
dc.contributor.authorFaull R.J.en
dc.contributor.authorCoates P.T.en
dc.contributor.authorWong D.T.L.en
dc.contributor.authorNelson A.J.en
dc.contributor.authorDundon B.K.en
dc.contributor.authorWorthley S.G.en
dc.contributor.authorRichardson J.D.en
dc.date.accessioned2021-05-14T11:58:02Zen
dc.date.available2021-05-14T11:58:02Zen
dc.date.copyright2019en
dc.date.created20200228en
dc.date.issued2020-02-28en
dc.identifier.citationCoronary Artery Disease. 30 (7) (pp 520-527), 2019. Date of Publication: 01 Nov 2019.en
dc.identifier.issn0954-6928en
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/35420en
dc.description.abstractBackground Cardiovascular disease is the leading cause of death in patients with chronic kidney disease. Studies investigating the disproportionate burden of cardiovascular disease have occurred predominantly in the peripheral vasculature, often used noninvasive imaging modalities, and infrequently recruited patients receiving dialysis. This study sought to evaluate invasive coronary dynamic vascular function in patients with end-stage renal failure (ESRF). Patients and methods Patients referred for invasive coronary angiography prior to renal transplantation were invited to participate. Control patients were recruited in parallel. Baseline characteristics were obtained. Coronary diameter (via quantitative coronary angiography) and coronary blood flow (via Doppler Flowire) were measured; macrovascular endothelial-dependent and independent effects were evaluated in response to intracoronary acetylcholine infusion (10-7 and 10-6 mol/l) and intracoronary glyceryl trinitrate, respectively. Microvascular function was evaluated by response to adenosine and expressed as coronary flow velocity reserve. Mean values were compared. Results Thirty patients were evaluated: 15 patients with ESRF (mean age 52.1 +/- 9, male 73%) and 15 control patients (mean age 53.3 +/- 13, male 60%). Comorbidity profile, aside from ESRF, was well matched. Baseline coronary blood flow was similar between groups (101.6 +/- 10.3 vs. 103.4 +/- 9.1 ml/min, P = 0.71), as was endothelial-dependent response to acetylcholine (159.1 +/- 16.9 vs. 171.1 +/- 16.8 ml/min, P = 0.41). Endothelial-independent response to glyceryl trinitrate was no different between groups (14.3 +/- 3.1 vs. 13.1 +/- 2.3%, P = 0.73. A significantly reduced coronary flow velocity reserve was observed in the ESRF cohort compared to controls (2.34 +/- 0.4 vs. 3.05 +/- 0.3, P = 0.003). Conclusion Patients with ESRF had preserved endothelial-dependent function however compared to controls, demonstrated significantly attenuated microvascular reserve. An impaired response to adenosine may not only represent a component of the pathophysiological milieu in patients with ESRF but may also provide a basis for the suboptimal diagnostic performance of vasodilatory stress in this population.Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.en
dc.languageenen
dc.languageEnglishen
dc.publisherLippincott Williams and Wilkins (E-mail: agents@lww.com)en
dc.relation.ispartofCoronary Artery Diseaseen
dc.subject.meshcardiovascular function-
dc.subject.meshcoronary angiography-
dc.subject.meshcoronary artery blood flow-
dc.subject.meshcoronary blood vessel-
dc.subject.meshcoronary flow reserve-
dc.subject.meshDoppler flowmetry-
dc.subject.meshend stage renal disease-
dc.subject.meshkidney transplantation-
dc.subject.meshacetylcholine-
dc.subject.meshadenosine-
dc.subject.meshglyceryl trinitrate-
dc.subject.meshimaging software-
dc.titleEnd-stage renal failure is associated with impaired coronary microvascular function.en
dc.typeArticleen
dc.identifier.affiliationCardiology (MonashHeart)-
dc.type.studyortrialObservational study (cohort, case-control, cross sectional or survey)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1097/MCA.0000000000000727-
dc.publisher.placeUnited Kingdomen
dc.identifier.pubmedid30883431 [http://www.ncbi.nlm.nih.gov/pubmed/?term=30883431]en
dc.identifier.source630983455en
dc.identifier.institution(Nelson, Worthley) Department of Cardiology, Royal Adelaide Hospital, South Australian Health and Medical Research Institute, Adelaide Medical School, University of Adelaide, Port Road, Adelaide, SA 5000, Australia (Dundon, Wong) Department of Renal Medicine, Royal Adelaide Hospital, Australia (Worthley) GenesisCare Pty Limited, HeartCare Research, Alexandria, Australia (Richardson) Department of Medicine (Monash Medical Center, Monash University and Monash Heart, Monash Health, Monash Cardiovascular Research Center, Melbourne, Australia (Puri) Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom (Coates, Faull) Department of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research, Cleveland Clinic, Cleveland, OH, United Statesen
dc.description.addressA.J. Nelson, Department of Cardiology, Royal Adelaide Hospital, South Australian Health and Medical Research Institute, Adelaide Medical School, University of Adelaide, Port Road, Adelaide, SA 5000, Australia. E-mail: adam.nelson@adelaide.edu.auen
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2020 Elsevier B.V., All rights reserved.en
dc.subect.keywordsendothelial function microvascular renal failureen
dc.identifier.authoremailNelson A.J.; adam.nelson@adelaide.edu.auen
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeArticle-
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