Shoichiro Sato1, Candice Delcourt1, Emma Heeley1, Hisatomi Arima1, Shihong Zhang1, Rustam Al-Shahi Salman1, Christian Stapf1, Daniel Woo1, Matthew L Flaherty1, Achala Vagal1, Christopher Levi1, Leo Davies1, Jiguang Wang1, Thompson Robinson1, Pablo M Lavados1, Richard I Lindley1, John Chalmers1, Craig S Anderson2. 1. From the Neurological and Mental Health Division, George Institute for Global Health, Sydney, New South Wales, Australia (S.S., C.D., E.H., H.A., R.I.L., J.C., C.S.A.); Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan (S.S.); Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia (C.D., E.H., H.A., L.D., R.I.L., J.C., C.S.A.); Neurology Department, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia (C.D., L.D., J.C., C.S.A.); Center for Epidemiologic Research in Asia, Shiga University of Medical Sciences, Shiga, Japan (H.A.); Department of Neurology, West China Hospital, Sichuan University, Chengdu, China (S.Z.); Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom (R.A.-S.S.); Département Hospitalo-Universitaire (DHU) NeuroVasc, Hôpital Lariboisière, Paris, France (C.S.); Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Département de Neurosciences, Université de Montréal, Montréal, Quebec, Canada (C.S.); Department of Neurology (D.W., M.L.F.) and Radiology (A.V.), University of Cincinnati Academic Health Center, OH; Department of Neurology, John Hunter Hospital, University of Newcastle/Hunter Medical Research Institute, Newcastle, New South Wales, Australia (C.L.); The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China (J.W.); Department of Cardiovascular Sciences and NIHR Biomedical Research Unit for Cardiovascular Diseases, University of Leicester, Leicester, United Kingdom (T.R.); Servicio de Neurología, Departamento de Medicina, Clínica Alemana de Santiago, Facultad de Medicina Clinica Alemana Universidad del Desarrollo, Santiago, Chile (P.M.L.); Facultad de Medicina, Universidad de Chile, Santiago, Chile (P.M.L.); and Department of Medicine, Westmead Hospital Clinical School, Westmead, New South Wales, Australia (R.I.L.). 2. From the Neurological and Mental Health Division, George Institute for Global Health, Sydney, New South Wales, Australia (S.S., C.D., E.H., H.A., R.I.L., J.C., C.S.A.); Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan (S.S.); Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia (C.D., E.H., H.A., L.D., R.I.L., J.C., C.S.A.); Neurology Department, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia (C.D., L.D., J.C., C.S.A.); Center for Epidemiologic Research in Asia, Shiga University of Medical Sciences, Shiga, Japan (H.A.); Department of Neurology, West China Hospital, Sichuan University, Chengdu, China (S.Z.); Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom (R.A.-S.S.); Département Hospitalo-Universitaire (DHU) NeuroVasc, Hôpital Lariboisière, Paris, France (C.S.); Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Département de Neurosciences, Université de Montréal, Montréal, Quebec, Canada (C.S.); Department of Neurology (D.W., M.L.F.) and Radiology (A.V.), University of Cincinnati Academic Health Center, OH; Department of Neurology, John Hunter Hospital, University of Newcastle/Hunter Medical Research Institute, Newcastle, New South Wales, Australia (C.L.); The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China (J.W.); Department of Cardiovascular Sciences and NIHR Biomedical Research Unit for Cardiovascular Diseases, University of Leicester, Leicester, United Kingdom (T.R.); Servicio de Neurología, Departamento de Medicina, Clínica Alemana de Santiago, Facultad de Medicina Clinica Alemana Universidad del Desarrollo, Santiago, Chile (P.M.L.); Facultad de Medicina, Universidad de Chile, Santiago, Chile (P.M.L.); and Department of Medicine, Westmead Hospital Clinical School, Westmead, New South Wales, Australia (R.I.L.). canderson@geor
Abstract
BACKGROUND AND PURPOSE: The significance of structural changes associated with cerebral small-vessel disease (SVD), including white matter lesions (WML), lacunes, and brain atrophy, to outcome from acute intracerebral hemorrhage is uncertain. We determined associations of computed tomographic radiological manifestations of cerebral SVD and outcomes, and in terms of any differential effect of early intensive blood pressure-lowering treatment, in the large-scale Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2). METHODS: We graded WML (van Swieten scale), the presence of lacunes, and brain atrophy (2 linear measurements and visual rating) for 2069 of 2839 patients with available baseline brain computed tomography (<6 hours of intracerebral hemorrhage onset) by 3 independent neurologists blind to clinical data. RESULTS: WML grade and 2 linear measurements of brain atrophy were associated with death or major disability at 90 days: multivariable-adjusted odds ratios for WML (grade 3 and 4 versus 0), frontal ratio, and third ventricle Sylvian fissure distance (most versus least severe atrophy quartile) were 1.42 (95% confidence interval, 1.02-1.98), 1.47 (1.08-1.99), and 1.64 (1.21-2.22), respectively (all P for trend <0.05). There was no association between lacunes and outcomes. There were no significant differences in the effects of intensive blood pressure-lowering across subgroups of cerebral SVD. CONCLUSIONS: Preexisting cerebral SVD manifestations of WML and brain atrophy predict poor outcome in acute intracerebral hemorrhage. There is no apparent hazard of early intensive lowering of blood pressure according to the INTERACT2 protocol, in patients with underlying cerebral SVD. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00716079.
BACKGROUND AND PURPOSE: The significance of structural changes associated with cerebral small-vessel disease (SVD), including white matter lesions (WML), lacunes, and brain atrophy, to outcome from acute intracerebral hemorrhage is uncertain. We determined associations of computed tomographic radiological manifestations of cerebral SVD and outcomes, and in terms of any differential effect of early intensive blood pressure-lowering treatment, in the large-scale Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2). METHODS: We graded WML (van Swieten scale), the presence of lacunes, and brain atrophy (2 linear measurements and visual rating) for 2069 of 2839 patients with available baseline brain computed tomography (<6 hours of intracerebral hemorrhage onset) by 3 independent neurologists blind to clinical data. RESULTS: WML grade and 2 linear measurements of brain atrophy were associated with death or major disability at 90 days: multivariable-adjusted odds ratios for WML (grade 3 and 4 versus 0), frontal ratio, and third ventricle Sylvian fissure distance (most versus least severe atrophy quartile) were 1.42 (95% confidence interval, 1.02-1.98), 1.47 (1.08-1.99), and 1.64 (1.21-2.22), respectively (all P for trend <0.05). There was no association between lacunes and outcomes. There were no significant differences in the effects of intensive blood pressure-lowering across subgroups of cerebral SVD. CONCLUSIONS: Preexisting cerebral SVD manifestations of WML and brain atrophy predict poor outcome in acute intracerebral hemorrhage. There is no apparent hazard of early intensive lowering of blood pressure according to the INTERACT2 protocol, in patients with underlying cerebral SVD. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00716079.
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