Cheryl Carcel1, Xia Wang1, Shoichiro Sato1, Christian Stapf1, Else Charlotte Sandset1, Candice Delcourt1, Hisatomi Arima1, Thompson Robinson1, Pablo Lavados1, John Chalmers1, Craig S Anderson2. 1. From the Neurological and Mental Health Division, The George Institute for Global Health, Sydney, New South Wales, Australia (C.C., X.W., S.S., E.C.S., C.D., H.A., J.C., C.S.A.); Sydney Medical School, the University of Sydney, Sydney, New South Wales, Australia (C.C., X.W., C.D., J.C., C.S.A.); Department of Neurology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia (C.C, C.D, J.C., C.S.A.); Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan (S.S.); Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Département de Neurosciences, Université de Montréal, Montréal, Québec, Canada (C.S.); Department of Neurology, Oslo University Hospital, Oslo, Norway (E.C.S.); Department of Preventive Medicine and Public Health, Faculty of Medicine, Fukuoka University, Fukuoka, Japan (H.A.); Department of Cardiovascular Sciences and NIHR Biomedical Research Unit in Cardiovascular Disease, University of Leicester, Leicester, United Kingdom (T.R.); Unidad de Neurología vascular, Servicio de Neurología, Departamento de Medicina, Clínica Alemana, Santiago, Chile (P.L.); and Facultad de Medicina Clínica Alemana Universidad del Desarrollo, Santiago, Chile (P.L.). 2. From the Neurological and Mental Health Division, The George Institute for Global Health, Sydney, New South Wales, Australia (C.C., X.W., S.S., E.C.S., C.D., H.A., J.C., C.S.A.); Sydney Medical School, the University of Sydney, Sydney, New South Wales, Australia (C.C., X.W., C.D., J.C., C.S.A.); Department of Neurology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia (C.C, C.D, J.C., C.S.A.); Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan (S.S.); Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Département de Neurosciences, Université de Montréal, Montréal, Québec, Canada (C.S.); Department of Neurology, Oslo University Hospital, Oslo, Norway (E.C.S.); Department of Preventive Medicine and Public Health, Faculty of Medicine, Fukuoka University, Fukuoka, Japan (H.A.); Department of Cardiovascular Sciences and NIHR Biomedical Research Unit in Cardiovascular Disease, University of Leicester, Leicester, United Kingdom (T.R.); Unidad de Neurología vascular, Servicio de Neurología, Departamento de Medicina, Clínica Alemana, Santiago, Chile (P.L.); and Facultad de Medicina Clínica Alemana Universidad del Desarrollo, Santiago, Chile (P.L.). canderson@georgeinstitute.org.au.
Abstract
BACKGROUND AND PURPOSE:Degree and timing of blood pressure (BP) lowering treatment in relation to hematoma growth were investigated in the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial-2 (INTERACT2). METHODS: INTERACT2 was an international clinical trial of intensive (target systolic BP [SBP], <140 mm Hg) versus guideline-recommended (SBP, <180 mm Hg) BP lowering in 2839 patients within 6 hours of spontaneous intracerebral hemorrhage and elevated SBP (150-220 mm Hg), in which 964 had repeat cranial computed tomography at 24 hours. ANCOVA models assessed categories of SBP reduction and time to target SBP on 24-hour hematoma growth. RESULTS:Greater SBP reduction was associated with reduced hematoma growth (13.3, 5.0, and 3.0 mL for <10, 10-20, and ≥20 mm Hg, respectively; P trend<0.001). In the intensive treatment group (n=491), the least mean hematoma growth was in patients who achieved target SBP <1 hour (2.6 mL) versus to those in target at 1 to 6 (4.7 mL) and >6 hours (5.4 mL). The smallest mean absolute hematoma growth (2.0 mL) was in those achieving target SBP 5 to 8 times versus 3 to 4 (3.1 mL) and 0 to 2 times (5.2 mL). CONCLUSIONS: Intensive BP lowering with greater SBP reduction, which is achieved quickly and maintained consistently, seems to provide protection against hematoma growth for 24 hours. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00716079.
RCT Entities:
BACKGROUND AND PURPOSE: Degree and timing of blood pressure (BP) lowering treatment in relation to hematoma growth were investigated in the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial-2 (INTERACT2). METHODS: INTERACT2 was an international clinical trial of intensive (target systolic BP [SBP], <140 mm Hg) versus guideline-recommended (SBP, <180 mm Hg) BP lowering in 2839 patients within 6 hours of spontaneous intracerebral hemorrhage and elevated SBP (150-220 mm Hg), in which 964 had repeat cranial computed tomography at 24 hours. ANCOVA models assessed categories of SBP reduction and time to target SBP on 24-hour hematoma growth. RESULTS: Greater SBP reduction was associated with reduced hematoma growth (13.3, 5.0, and 3.0 mL for <10, 10-20, and ≥20 mm Hg, respectively; P trend<0.001). In the intensive treatment group (n=491), the least mean hematoma growth was in patients who achieved target SBP <1 hour (2.6 mL) versus to those in target at 1 to 6 (4.7 mL) and >6 hours (5.4 mL). The smallest mean absolute hematoma growth (2.0 mL) was in those achieving target SBP 5 to 8 times versus 3 to 4 (3.1 mL) and 0 to 2 times (5.2 mL). CONCLUSIONS: Intensive BP lowering with greater SBP reduction, which is achieved quickly and maintained consistently, seems to provide protection against hematoma growth for 24 hours. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00716079.
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