Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11529
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dc.contributor.authorKearney, Leighton Gen
dc.contributor.authorLu, Ken
dc.contributor.authorOrd, Men
dc.contributor.authorPatel, Sheila Ken
dc.contributor.authorProfitis, Ken
dc.contributor.authorMatalanis, Georgeen
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorSrivastava, Piyush Men
dc.date.accessioned2015-05-16T01:08:34Z
dc.date.available2015-05-16T01:08:34Z
dc.date.issued2012-06-26en
dc.identifier.citationEuropean Heart Journal Cardiovascular Imaging 2012; 13(10): 827-33en
dc.identifier.govdoc22736713en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11529en
dc.description.abstractTo assess the capacity of global longitudinal strain (GLS) in patients with aortic stenosis (AS) to (i) detect the subclinical left ventricular (LV) dysfunction [LV ejection fraction (LVEF) ≥50% patients]; (ii) predict all-cause mortality and major adverse cardiac events (MACE) (all patients), and (iii) provide incremental prognostic information over current risk markers.Patients with AS (n = 146) and age-matched controls (n = 12) underwent baseline echocardiography to assess AS severity, conventional LV parameters and GLS via speckle tracking echocardiography. Baseline demographics, symptom severity class and comorbidities were recorded. Outcomes were identified via hospital record review and subject/physician interview. The mean age was 75 ± 11, 62% were male. The baseline aortic valve (AV) area was 1.0 ± 0.4 cm(2) and LVEF was 59 ± 11%. In patients with a normal LVEF (n = 122), the baseline GLS was controls -21 ± 2%, mild AS -18 ± 3%, moderate AS -17 ± 3% and severe AS -15 ± 3% (P< 0.001). GLS correlated with the LV mass index, LVEF, AS severity, and symptom class (P< 0.05). During a median follow-up of 2.1 (inter-quartile range: 1.8-2.4) years, there were 20 deaths and 101 MACE. Unadjusted hazard ratios (HRs) for GLS (per %) were all-cause mortality (HR: 1.42, P< 0.001) and MACE (HR: 1.09, P< 0.001). After adjustment for clinical and echocardiographic variables, GLS remained a strong independent predictor of all-cause mortality (HR: 1.38, P< 0.001).GLS detects subclinical dysfunction and has incremental prognostic value over traditional risk markers including haemodynamic severity, symptom class, and LVEF in patients with AS. Incorporation of GLS into risk models may improve the identification of the optimal timing for AV replacement.en
dc.language.isoenen
dc.subject.otherAgeden
dc.subject.otherAged, 80 and overen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAortic Valve Stenosis.mortality.pathology.ultrasonographyen
dc.subject.otherBiological Markersen
dc.subject.otherCase-Control Studiesen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherPrognosisen
dc.subject.otherProspective Studiesen
dc.subject.otherRisk Factorsen
dc.subject.otherSeverity of Illness Indexen
dc.subject.otherStroke Volumeen
dc.subject.otherVentricular Function, Leften
dc.subject.otherVictoriaen
dc.titleGlobal longitudinal strain is a strong independent predictor of all-cause mortality in patients with aortic stenosis.en
dc.typeJournal Articleen
dc.identifier.journaltitleEuropean heart journal cardiovascular Imagingen
dc.identifier.affiliationDepartment of Medicine, The University of Melbourne, Austin Health, Victoria, Australiaen
dc.identifier.doi10.1093/ehjci/jes115en
dc.description.pages827-33en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/22736713en
dc.type.austinJournal Articleen
local.name.researcherBurrell, Louise M
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptCardiology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptCardiac Surgery-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
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