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. 2013 Apr;22(3):250-4.
doi: 10.1016/j.jstrokecerebrovasdis.2011.08.006. Epub 2011 Oct 1.

Elevated admission blood pressure and acute ischemic lesions in spontaneous intracerebral hemorrhage

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Elevated admission blood pressure and acute ischemic lesions in spontaneous intracerebral hemorrhage

Ethem Murat Arsava et al. J Stroke Cerebrovasc Dis. 2013 Apr.

Abstract

Concomitant acute ischemic lesions are detected in a subset of patients with intracerebral hemorrhage (ICH). In this study, our aim was to analyze the pattern of acute ischemic lesions detected by diffusion-weighted imaging (DWI) in patients with ICH, and to use this information, in combination with clinical characteristics of patients, to understand the underlying mechanisms of these lesions. We retrospectively analyzed patients with a diagnosis of ICH who underwent DWI within 14 days of symptom onset. We compared demographic, clinical, and imaging characteristics in patients with and without acute ischemic lesions. We also assessed the number, location, and topographic distribution of DWI bright lesions. Acute ischemic lesions were detected in 15 of 86 patients (17.4%); the lesions had a small, dot-like appearance in 13 patients (87%) and were located in an arterial territory separate from the incident ICH in 12 patients (80%). Patients with acute ischemic lesions had higher admission systolic, diastolic, and mean arterial blood pressure levels; greater periventricular leukoaraiosis burden; more microbleeds, and lower admission Glasgow Coma Scale score. In multivariate analyses, admission mean arterial blood pressure (P < .01) and Glasgow Coma Scale score (P =.03) remained as the only significant variables associated with DWI lesion positivity. Our findings highlight the role of elevated admission blood pressure in the development of concomitant acute ischemic lesions in patients with ICH. The pattern of DWI bright lesions, together with a trend toward an increased burden of leukoaraiosis and microbleeds in patients with acute ischemic lesions, suggest an underlying dysfunctional cerebral microvasculature in the etiology of these lesions.

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