Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11440
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dc.contributor.authorWai, Bryan-
dc.contributor.authorKearney, Leighton G-
dc.contributor.authorHare, David L-
dc.contributor.authorOrd, Michelle-
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorSrivastava, Piyush M-
dc.date.accessioned2015-05-16T01:03:02Z
dc.date.available2015-05-16T01:03:02Z
dc.date.issued2012-02-14en
dc.identifier.citationCardiovascular Diabetology 2012; 11(): 14en
dc.identifier.govdoc22330091en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11440en
dc.description.abstractThe prognostic benefits of beta-blockers (BB) in patients with systolic heart failure (SHF) are known but despite this, in patients with diabetes they are underutilized. The aim of this study was to assess the effect of beta-blockers (BB) on glycaemic control in patients with Type 2 Diabetes (T2DM) and systolic heart failure (SHF) stratified to beta-1 selective (Bisoprolol) vs. nonselective BB (Carvedilol).This observational, cohort study was conducted in patients with T2DM and SHF attending an Australian tertiary teaching hospital's heart failure services. The primary endpoint was glycaemic control measured by glycosylated haemoglobin (HbA1c) at initiation and top dose of BB. Secondary endpoints included microalbuminuria, changes in lipid profile and estimated glomerular filtration rate (eGFR).125 patients were assessed. Both groups were well matched for gender, NYHA class and use of guideline validated heart failure and diabetic medications. The mean treatment duration was 1.9 ± 1.1 years with carvedilol and 1.4 ± 1.0 years with bisoprolol (p = ns). The carvedilol group achieved a reduction in HbA1c (7.8 ± 0.21% to 7.3 ± 0.17%, p = 0.02) whereas the bisoprolol group showed no change in HbA1c (7.0 ± 0.20% to 6.9 ± 0.23%, p = 0.92). There was no significant difference in the change in HbA1c from baseline to peak BB dose in the carvedilol group compared to the bisoprolol group. There was a similar deterioration in eGFR, but no significant changes in lipid profile or microalbuminuria in both groups (p = ns).BB use did not worsen glycaemic control, lipid profile or albuminuria status in subjects with SHF and T2DM. Carvedilol significantly improved glycemic control in subjects with SHF and T2DM and this improvement was non significantly better than that obtained with bisoprolol. BB's should not be withheld from patients with T2DM and SHF.en
dc.language.isoenen
dc.subject.otherAdrenergic beta-Antagonists.therapeutic useen
dc.subject.otherAgeden
dc.subject.otherAged, 80 and overen
dc.subject.otherAlbuminuria.etiologyen
dc.subject.otherBiological Markers.blooden
dc.subject.otherBisoprolol.therapeutic useen
dc.subject.otherCarbazoles.therapeutic useen
dc.subject.otherDiabetes Mellitus, Type 2.blood.complications.drug therapyen
dc.subject.otherDiabetic Nephropathies.etiology.physiopathologyen
dc.subject.otherFemaleen
dc.subject.otherGlomerular Filtration Rate.drug effectsen
dc.subject.otherHeart Failure, Systolic.complications.drug therapyen
dc.subject.otherHemoglobin A, Glycosylated.metabolismen
dc.subject.otherHospitals, Teachingen
dc.subject.otherHumansen
dc.subject.otherHypoglycemic Agents.therapeutic useen
dc.subject.otherLipids.blooden
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherPropanolamines.therapeutic useen
dc.subject.otherProspective Studiesen
dc.subject.otherTime Factorsen
dc.subject.otherTreatment Outcomeen
dc.subject.otherVictoriaen
dc.titleBeta blocker use in subjects with type 2 diabetes mellitus and systolic heart failure does not worsen glycaemic control.en
dc.typeJournal Articleen
dc.identifier.journaltitleCardiovascular diabetologyen
dc.identifier.affiliationDepartment of Cardiology, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1186/1475-2840-11-14en
dc.description.pages14en
dc.identifier.orcid0000-0001-9554-6556-
dc.identifier.pubmedid22330091-
dc.type.austinJournal Articleen
local.name.researcherBurrell, Louise M
item.grantfulltextopen-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextWith Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptCardiology-
crisitem.author.deptCardiology-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
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