ArticleCerebrovascular diseases extra2025
Relative Hypotension is Not Associated with Rapid Progressor Phenotype in Anterior Circulation Large-Vessel Occlusion Acute Ischaemic Stroke: A Retrospective Cohort Study.
Article in Cerebrovascular diseases extra, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionWe aimed to determine whether relative hypotension, defined as a systolic blood pressure (SBP) threshold of <140 mm Hg or 160 mm Hg at the time of neuroimaging, was associated with rapid infarct progressor phenotype, as defined by a high hypoperfusion intensity ratio on MISTAR imaging software (DT6/DT2 >0.318) during anterior circulation large-vessel occlusion (LVO) acute ischaemic stroke (AIS).
methodsIn a retrospective cohort study, consecutive patients admitted to a metropolitan comprehensive stroke centre within South Australia between January 2017 and January 2024 with anterior circulation LVO AIS were included. LVO was defined as either carotid terminus or M1 occlusion. Univariable and multivariable logistic regressions were performed.
resultsA total of 477 patients were included (253 [53.0%] female), of whom 163 (34.2%) had an elevated hypoperfusion intensity ratio (HIR). Hypotension, as defined by either SBP of <160 mm Hg (odds ratio [OR]: 1.2, 95% CI: 0.8-1.8) or SBP of <140 mm Hg (OR 1.7, 95% CI 0.8-1.7), was not associated with elevated HIR. Insular cortex ischaemia (OR: 6.1, 95% CI: 1.7-38.9) and ischaemic heart disease (OR: 2.0, 95% CI: 1.3-3.1) were associated with elevated HIR. Smoking history (OR: 0.5, 95% CI: 0.3-0.9) and obesity (OR: 0.4, 95% CI: 0.2-0.8) were associated with lower HIR.
conclusionRelative hypotension was not significantly associated with rapid infarct progressor phenotype in anterior circulation LVO AIS. Insular cortex ischaemia and ischaemic heart disease were associated with rapid progression phenotype, whilst smoking history and obesity were associated with slower progression phenotype. Further mechanistic studies to elucidate how systemic comorbidities and regional brain vulnerability contribute to infarct evolution are needed.
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