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dc.contributor.authorWilliams, Alexandra
dc.contributor.authorAinslie, Philip
dc.contributor.authorAnholm, James
dc.contributor.authorGasho, Christopher
dc.contributor.authorSubedi, Prajan
dc.contributor.authorStembridge, Mike
dc.date.accessioned2019-03-20T11:40:25Z
dc.date.available2019-03-20T11:40:25Z
dc.date.issued2019-05-07
dc.identifierhttps://repository.cardiffmet.ac.uk/bitstream/id/40053/Williams...Stembridge%202019,%20Left%20ventricular%20twist%20is%20augmented%20in%20hypoxia%20by%20%C3%9F1-adrenergic-dependent%20and%20-independent%20factors,%20without%20evidence%20of%20endocardial%20dysfunction%20.pdf
dc.identifier.issn1524-4539
dc.identifier.urihttp://hdl.handle.net/10369/10386
dc.descriptionArticle published in Circulation: Cardiovascular Imaging available at https://doi.org/10.1161/CIRCIMAGING.118.008455en_US
dc.description.abstractBackground. Left ventricular (LV) twist mechanics are augmented with both acute and chronic hypoxemia. Although the underlying mechanisms remain unknown, sympathetic activation and/or a direct effect of hypoxemia on the myocardium have been proposed, the latter of which may produce subendocardial dysfunction that is masked by larger subepicardial torque. This study therefore sought to i) determine the individual and combined influences of ß1-adrenergic receptor (ß1-AR) stimulation and peripheral O2 saturation (SpO2) on LV twist in acute and chronic hypoxia, and ii) elucidate whether endocardial versus epicardial mechanics respond differently to hypoxia. Methods. Twelve males (27±4yr) were tested near sea level (SL) in acute hypoxia (SpO2=83±3%) and following 3-6 days at 5050m (HA; SpO2=83±3%). In both settings, participants received infusions of ß1-AR blocker esmolol and volume-matched saline (double-blind, randomized). LV mechanics were assessed with 2-dimensional speckle-tracking echocardiography, and region-specific analysis to compare subendocardial and subepicardial mechanics. Results. At SL, compared to baseline (14.8±3.0º) LV twist was reduced with esmolol (11.2±3.3º; p=0.007) and augmented during hypoxia (19.6±4.9º; p<0.001), while esmolol+hypoxia augmented twist compared to esmolol alone (16.5±3.3º; p<0.001). At 5050m, LV twist was increased compared to SL (19.5±5.4°; p=0.004), and reduced with esmolol (13.0±3.8°; p<0.001) and SpO2 normalization (12.8±3.4°; p<0.001). Moreover, esmolol+normalized SpO2 lowered twist further than esmolol alone (10.5±3.1°; p=0.036). There was no mechanics-derived evidence of endocardial dysfunction with hypoxia at SL or HA. Conclusions. These findings suggest LV twist is augmented in hypoxia via ß1-AR-dependent and -independent mechanisms (e.g. 1-AR stimulation), but does not appear to reflect endocardial dysfunction.en_US
dc.description.sponsorshipFunding was provided by the Natural Sciences and Engineering Research Council of Canada (P.N.A.), Canadian Research Chairs (P.N.A.) and The Physiological Society UK (A.M.W.).en_US
dc.language.isoenen_US
dc.publisherAmerican Heart Associationen_US
dc.relation.ispartofseriesCirculation: Cardiovascular Imaging;
dc.titleLeft ventricular twist is augmented in hypoxia by ß1-adrenergic-dependent and independent factors, without evidence of endocardial dysfunctionen_US
dc.typeArticleen_US
dc.typeacceptedVersion
dcterms.dateAccepted2019-03-14
rioxxterms.versionAMen_US
rioxxterms.versionofrecordhttps://doi.org/10.1161/CIRCIMAGING.118.008455
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/-all-rights-reserveden_US
rioxxterms.licenseref.startdate2019-03-20
rioxxterms.publicationdate2019-05-07
dc.date.refFCD2019-03-20
rioxxterms.freetoread.startdate2019-11-01


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