Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10614
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dc.contributor.authorMacIsaac, Richard Jen
dc.contributor.authorThomas, Merlin Cen
dc.contributor.authorPanagiotopoulos, Siannaen
dc.contributor.authorSmith, Trudy Jen
dc.contributor.authorHao, Humingen
dc.contributor.authorMatthews, D Geoffreyen
dc.contributor.authorJerums, Georgeen
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorSrivastava, Piyush Men
dc.date.accessioned2015-05-16T00:07:40Z-
dc.date.available2015-05-16T00:07:40Z-
dc.date.issued2008-05-23en
dc.identifier.citationCardiovascular Diabetology 2008; 7: 15en
dc.identifier.govdoc18500986en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10614en
dc.description.abstractIn comparison to the well established changes in compliance that occur at the large vessel level in diabetes, much less is known about the changes in compliance of the cardiovascular system at the end-organ level. The aim of this study was therefore to examine whether there was a correlation between resistance of the intrarenal arteries of the kidney and compliance of the left ventricle, as estimated by measurements of diastolic function, in subjects with type 2 diabetes.We studied 167 unselected clinic patients with type 2 diabetes with a kidney duplex scan to estimate intrarenal vascular resistance, i.e. the resistance index (RI = peak systolic velocity-minimum diastolic velocity/peak systolic velocity) and a transthoracic echocardiogram (TTE) employing tissue doppler studies to document diastolic and systolic ventricular function.Renal RI was significantly higher in subjects with diastolic dysfunction (0.72 +/- 0.05) when compared with those who had a normal TTE examination (0.66 +/- 0.06, p < 0.01). Renal RI values were correlated with markers of diastolic dysfunction including the E/Vp ratio (r = 0.41, p < 0.001), left atrial area (r = 0.36, p < 0.001), the E/A ratio (r = 0.36, p < 0.001) and the E/E' ratio (r = 0.31, p < 0.001). These associations were independent of systolic function, hypertension, the presence and severity of chronic kidney disease, the use of renin-angiotensin inhibitors and other potentially confounding variables.Increasing vascular resistance of the intrarenal arteries was associated with markers of diastolic dysfunction in subjects with type 2 diabetes. These findings are consistent with the hypothesis that vascular and cardiac stiffening in diabetes are manifestations of common pathophysiological mechanisms.en
dc.language.isoenen
dc.subject.otherAdulten
dc.subject.otherAgeden
dc.subject.otherComplianceen
dc.subject.otherDiabetes Mellitus, Type 2.complications.physiopathologyen
dc.subject.otherDiabetic Angiopathies.physiopathologyen
dc.subject.otherDiastole.physiologyen
dc.subject.otherEchocardiographyen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherKidney.blood supplyen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherRenal Artery.physiologyen
dc.subject.otherVascular Resistance.physiologyen
dc.subject.otherVentricular Dysfunction, Left.physiopathology.ultrasonographyen
dc.titleAssociation between intrarenal arterial resistance and diastolic dysfunction in type 2 diabetes.en
dc.typeJournal Articleen
dc.identifier.journaltitleCardiovascular diabetologyen
dc.identifier.affiliationEndocrine Centre, Austin Health & University of Melbourne, Melbourne, Australiaen
dc.identifier.doi10.1186/1475-2840-7-15en
dc.description.pages15en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/18500986en
dc.identifier.orcid0000-0003-1863-7539-
dc.identifier.orcid0000-0002-0845-0001-
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.deptOffice for Research-
crisitem.author.deptRadiology-
crisitem.author.deptEndocrinology-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
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