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Sökning: onr:"swepub:oai:gup.ub.gu.se/332568" > Blood Pressure Vari...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004962naa a2200421 4500
001oai:gup.ub.gu.se/332568
003SwePub
008240528s2023 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/3325682 URI
0247 a https://doi.org/10.1159/0005337372 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Woods, Andrew G.4 aut
2451 0a Blood Pressure Variability Is Associated with Infarct Growth in Acute Ischaemic Stroke
264 1c 2023
520 a Introduction: Evidence-based blood pressure (BP) targets in acute ischaemic stroke are lacking. Previous observational studies have focused on single baseline BP and clinical outcomes, without consideration for dynamic changes. We aim to determine the association between BP parameters including variability, peak, nadir, median and mean during stroke and infarct growth (primary outcome), risk of haemorrhagic transformation, and functional outcome (secondary outcomes). Methods: Suspected stroke patients were prospectively recruited from a single comprehensive stroke centre. Multimodal computed tomography imaging was used to define infarct core. BP was recorded as per national stroke guidelines during the initial 24 h. Infarct growth and evidence of parenchymal haemorrhage were determined by follow-up magnetic resonance imaging at 24 h. Functional outcome at 3 months was assessed using the modified Rankin Scale. Subgroup analysis was performed according to stroke aetiology and treatment for the association between BP, infarct volume growth, and risk of haemorrhagic transformation. The association between BP parameters and outcomes were determined using regression modelling. Results: A total of 229 patients were included in this study. The median age was 67.4, 64.4% were male, and the baseline National Institutes of Health Stroke Scale was 8. BP variability (BPV) was independently associated with increased infarct growth (multivariate coefficient 1.60, 95% CI: 0.27–2.94, p = 0.19) and an increased odds of parenchymal haemorrhage (adjusted OR 1.21, 95% CI: 1.02–1.44, p = 0.028). The odds of a favourable outcome at 90 days were inversely associated with BPV on simple, but not adjusted logistic regression. On subgroup analysis, only in patients with large vessel occlusions, undergoing endovascular clot retrieval, was BPV associated with infarct growth (multivariate-adjusted coefficient 2.62, 95% CI: 0.53–4.70, p = 0.014) and an increased odds of haemorrhagic transformation (adjusted OR 1.26, 95% CI: 1.01–1.57, p = 0.045). Conclusion: An increase in BPV was associated with infarct expansion, increased risk of haemorrhagic transformation and was negatively associated with favourable functional outcomes at 3 months.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Acute ischaemic stroke
653 a Blood pressure variability
653 a Infarct growth
7001 a Lillicrap, Tom4 aut
7001 a Hood, Rebecca4 aut
7001 a Fletcher, Joseph W.4 aut
7001 a Ranhage, Viktoru Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut
7001 a Larsson, Emilu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut
7001 a Cahlin, Fredriku Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut
7001 a Jood, Katarina,d 1966u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut0 (Swepub:gu)xjooka
7001 a Tatlisumak, Turgutu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut0 (Swepub:gu)xtatlt
7001 a Garcia-Esperon, Carlos4 aut
7001 a Spratt, Neil J.4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap4 org
7730 t Cerebrovascular Diseasesx 1015-9770x 1421-9786
8564 8u https://gup.ub.gu.se/publication/332568
8564 8u https://doi.org/10.1159/000533737

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