Andrea Morotti1, Gregoire Boulouis2, Javier M Romero2, H Bart Brouwers2, Michael J Jessel2, Anastasia Vashkevich2, Kristin Schwab2, Mohammad Rauf Afzal2, Christy Cassarly2, Steven M Greenberg2, Reneé Hebert Martin2, Adnan I Qureshi2, Jonathan Rosand2, Joshua N Goldstein2. 1. From the Department of Neurology, Division of Neurocritical Care and Emergency Neurology (A.M., J.M.R., J.N.G.), Neuroradiology Service, Department of Radiology (J.M.R.), the J.P. Kistler Stroke Research Center (A.M., G.B., J.M.R., M.J.J., A.V., K.S., S.M.G., J.R., J.N.G.), and Department of Emergency Medicine (J.N.G.), Massachusetts General Hospital, Harvard Medical School, Boston; Department of Neuroradiology (G.B.), Université Paris Descartes, INSERM S894, DHU Neurovasc, Centre Hospitalier Sainte-Anne, Paris, France; Department of Neurosurgery (H.B.B.), Brain Center, Rudolf Magnus University Medical Center, Utrecht, the Netherlands; Zeenat Qureshi Stroke Research Center (M.R.A., A.I.Q.), University of Minnesota, Minneapolis; and Department of Public Health Sciences (C.C., R.H.M.), Medical University of South Carolina, Charleston. andrea.morotti85@gmail.com. 2. From the Department of Neurology, Division of Neurocritical Care and Emergency Neurology (A.M., J.M.R., J.N.G.), Neuroradiology Service, Department of Radiology (J.M.R.), the J.P. Kistler Stroke Research Center (A.M., G.B., J.M.R., M.J.J., A.V., K.S., S.M.G., J.R., J.N.G.), and Department of Emergency Medicine (J.N.G.), Massachusetts General Hospital, Harvard Medical School, Boston; Department of Neuroradiology (G.B.), Université Paris Descartes, INSERM S894, DHU Neurovasc, Centre Hospitalier Sainte-Anne, Paris, France; Department of Neurosurgery (H.B.B.), Brain Center, Rudolf Magnus University Medical Center, Utrecht, the Netherlands; Zeenat Qureshi Stroke Research Center (M.R.A., A.I.Q.), University of Minnesota, Minneapolis; and Department of Public Health Sciences (C.C., R.H.M.), Medical University of South Carolina, Charleston.
Abstract
OBJECTIVE: To validate various noncontrast CT (NCCT) predictors of hematoma expansion in a large international cohort of ICH patients and investigate whether intensive blood pressure (BP) treatment reduces ICH growth and improves outcome in patients with these markers. METHODS: We analyzed patients enrolled in the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II) randomized controlled trial. Participants were assigned to intensive (systolic BP <140 mm Hg) vs standard (systolic BP <180 mm Hg) treatment within 4.5 hours from onset. The following NCCT markers were identified: intrahematoma hypodensities, black hole sign, swirl sign, blend sign, heterogeneous hematoma density, and irregular shape. ICH expansion was defined as hematoma growth >33% and unfavorable outcome was defined as modified Rankin Scale score >3 at 90 days. Logistic regression was used to identify predictors of ICH expansion and explore the association between NCCT signs and clinical benefit from intensive BP treatment. RESULTS: A total of 989 patients were included (mean age 62 years, 61.9% male), of whom 186/869 experienced hematoma expansion (21.4%) and 361/952 (37.9%) had unfavorable outcome. NCCT markers independently predicted ICH expansion (all p < 0.01) with overall accuracy ranging from 61% to 78% and good interrater reliability (k > 0.6 for all markers). There was no evidence of an interaction between NCCT markers and benefit from intensive BP reduction (all p for interaction >0.10). CONCLUSIONS: NCCT signs reliably identify ICH patients at high risk of hematoma growth. However, we found no evidence that patients with these markers specifically benefit from intensive BP reduction. CLINICALTRIALSGOV IDENTIFIER: NCT01176565.
OBJECTIVE: To validate various noncontrast CT (NCCT) predictors of hematoma expansion in a large international cohort of ICH patients and investigate whether intensive blood pressure (BP) treatment reduces ICH growth and improves outcome in patients with these markers. METHODS: We analyzed patients enrolled in the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II) randomized controlled trial. Participants were assigned to intensive (systolic BP <140 mm Hg) vs standard (systolic BP <180 mm Hg) treatment within 4.5 hours from onset. The following NCCT markers were identified: intrahematoma hypodensities, black hole sign, swirl sign, blend sign, heterogeneous hematoma density, and irregular shape. ICH expansion was defined as hematoma growth >33% and unfavorable outcome was defined as modified Rankin Scale score >3 at 90 days. Logistic regression was used to identify predictors of ICH expansion and explore the association between NCCT signs and clinical benefit from intensive BP treatment. RESULTS: A total of 989 patients were included (mean age 62 years, 61.9% male), of whom 186/869 experienced hematoma expansion (21.4%) and 361/952 (37.9%) had unfavorable outcome. NCCT markers independently predicted ICH expansion (all p < 0.01) with overall accuracy ranging from 61% to 78% and good interrater reliability (k > 0.6 for all markers). There was no evidence of an interaction between NCCT markers and benefit from intensive BP reduction (all p for interaction >0.10). CONCLUSIONS: NCCT signs reliably identify ICH patients at high risk of hematoma growth. However, we found no evidence that patients with these markers specifically benefit from intensive BP reduction. CLINICALTRIALSGOV IDENTIFIER: NCT01176565.
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