Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/20974
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dc.contributor.authorWarren, Josephine-
dc.contributor.authorNanayakkara, Shane-
dc.contributor.authorAndrianopoulos, Nick-
dc.contributor.authorBrennan, Angela-
dc.contributor.authorDinh, Diem-
dc.contributor.authorYudi, Matias B-
dc.contributor.authorClark, David J-
dc.contributor.authorAjani, Andrew E-
dc.contributor.authorReid, Christopher M-
dc.contributor.authorSelkrig, Laura-
dc.contributor.authorShaw, James-
dc.contributor.authorHiew, Chin-
dc.contributor.authorFreeman, Melanie-
dc.contributor.authorKaye, David-
dc.contributor.authorKingwell, Bronwyn A-
dc.contributor.authorDart, Anthony M-
dc.contributor.authorDuffy, Stephen J-
dc.date.accessioned2019-06-19T06:29:49Z-
dc.date.available2019-06-19T06:29:49Z-
dc.date.issued2019-06-11-
dc.identifier.citationJournal of the American College of Cardiology 2019; 73(22): 2846-2855en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/20974-
dc.description.abstractHigh systolic blood pressure (SBP) increases cardiac afterload, whereas low diastolic blood pressure (DBP) may lead to impaired coronary perfusion. Thus, wide pulse pressure (high systolic, low diastolic [HSLD]) may contribute to myocardial ischemia and also be a predictor of adverse cardiovascular events. The purpose of this study was to determine the relationship between pre-procedural blood pressure and long-term outcome following percutaneous coronary intervention (PCI). The study included 10,876 consecutive patients between August 2009 and December 2016 from the Melbourne Interventional Group registry undergoing PCI with pre-procedural blood pressure recorded. Patients with ST-segment elevation myocardial infarction, cardiogenic shock, and out-of-hospital cardiac arrest were excluded. Patients were divided into 4 groups according to SBP (high ≥120 mm Hg, low <120 mm Hg) and DBP (high >70 mm Hg, low ≤70 mm Hg). Mean pulse pressure was 60 ± 21 mm Hg. Patients with HSLD were older and more frequently women, with higher rates of hypercholesterolemia, renal impairment, diabetes, and multivessel and left main disease (all p ≤ 0.0001). There was no difference in 30-day major adverse cardiac events, but at 12 months the HSLD group had a greater incidence of myocardial infarction (p = 0.018) and stroke (p = 0.013). Long-term mortality was highest for HSLD (7.9%) and lowest for low systolic, high diastolic (narrow pulse pressure) at 2.1% (p = 0.0002). Cox regression analysis demonstrated significantly lower long-term mortality in the low systolic, high diastolic cohort (hazard ratio: 0.50; 99% confidence interval: 0.25 to 0.98; p = 0.04). Pulse pressure at the time of index PCI is associated with long-term outcomes following PCI. A wide pulse pressure may serve as a surrogate marker for risk following PCI and represents a potential target for future therapies.en_US
dc.language.isoeng-
dc.subjectblood pressureen_US
dc.subjectcoronary artery diseaseen_US
dc.subjectoutcomesen_US
dc.subjectpercutaneous coronary interventionen_US
dc.subjectpulse pressureen_US
dc.titleImpact of Pre-Procedural Blood Pressure on Long-Term Outcomes Following Percutaneous Coronary Intervention.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleJournal of the American College of Cardiologyen_US
dc.identifier.affiliationAustin Healthen_US
dc.identifier.affiliationGeelong Hospital, Geelong, Victoria, Australiaen_US
dc.identifier.affiliationRoyal Melbourne Hospital, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationAlfred Hospital, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationBaker Heart and Diabetes Institute, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationCentre of Cardiovascular Research and Education in Therapeutics, Monash University, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Medicine, Nursing and Health Sciences, Monash University, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationBox Hill Hospital, Melbourne, Victoria, Australiaen_US
dc.identifier.doi10.1016/j.jacc.2019.03.493en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0002-3706-4150en_US
dc.identifier.pubmedid31171090-
dc.type.austinJournal Article-
local.name.researcherClark, David J
item.languageiso639-1en-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
crisitem.author.deptCardiology-
crisitem.author.deptCardiology-
crisitem.author.deptUniversity of Melbourne Clinical School-
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