2009
DOI: 10.1161/hypertensionaha.109.134486
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Treating Hypertension in Acute Ischemic Stroke

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Cited by 10 publications
(7 citation statements)
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“…Previous study [41] has also shown that satisfactory control of SBP within 140 to 150 mm Hg was the optimal therapy for improving clinical outcome after acute IS. Therefore, our findings corroborated those of previous studies [42-44]. …”
Section: Discussionsupporting
confidence: 93%
See 1 more Smart Citation
“…Previous study [41] has also shown that satisfactory control of SBP within 140 to 150 mm Hg was the optimal therapy for improving clinical outcome after acute IS. Therefore, our findings corroborated those of previous studies [42-44]. …”
Section: Discussionsupporting
confidence: 93%
“…The impact of blood pressure on clinical outcome after acute IS has been extensively investigated [42-44]. Excessive elevation, reduction, and variability in blood pressure have been reported to be independent prognostic predictors for poor clinical outcome after acute IS [43,44].…”
Section: Discussionmentioning
confidence: 99%
“…Of the patients studied, 80% had hypertension, demonstrating the high prevalence of this risk factor in critical care stroke patients, as observed in other studies 9,10 . Nevertheless, few studies have evaluated the association between BP and the case fatality ratio in acute stroke.…”
Section: Discussionsupporting
confidence: 81%
“…Chronic hypertension causes cerebral vascular remodeling and dysfunction, leading to loss of the cerebral blood flow (CBF) auto-regulation system. 19,20 Under the lost CBF auto-regulation system, further increase of high BP in acute ischemic stroke can promote cerebrovascular over-perfusion and therefore exacerbate ischemic injury by aggravating cerebral edema. 19,20 This reversal of BP elevation by RDN was associated with a significant reduction of CBF in the reperfusion period.…”
Section: Discussionmentioning
confidence: 99%
“…19,20 Under the lost CBF auto-regulation system, further increase of high BP in acute ischemic stroke can promote cerebrovascular over-perfusion and therefore exacerbate ischemic injury by aggravating cerebral edema. 19,20 This reversal of BP elevation by RDN was associated with a significant reduction of CBF in the reperfusion period. 18 As recently demonstrated, cerebral superoxide levels were significantly reduced by RDN post-treatment, and associated with the decrease in cerebral gp91phox, a major subunit of nicotinamide adenine dinucleotide phosphate oxidase.…”
Section: Discussionmentioning
confidence: 99%