{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T08:21:14Z","timestamp":1791534074056,"version":"4.3.4"},"reference-count":25,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2019,8]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Purpose\u2014<\/jats:title>\n                    <jats:p>It is unknown whether blood pressure (BP) reduction influences secondary brain injury in spontaneous intracerebral hemorrhage (ICH). We tested the hypothesis that intensive BP reduction is associated with decreased perihematomal edema expansion rate (PHER) in deep ICH.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods\u2014<\/jats:title>\n                    <jats:p>We performed an exploratory analysis of the ATACH-2 randomized trial (Antihypertensive Treatment of Acute Cerebral Hemorrhage-2). Patients with deep, supratentorial ICH were included. PHER was calculated as the difference in perihematomal edema volume between baseline and 24-hour computed tomography scans divided by hours between scans. We used regression analyses to determine whether intensive BP reduction was associated with PHER and if PHER was associated with poor outcome (3-month modified Rankin Scale score 4\u20136). We then used interaction analyses to test whether specific deep location (basal ganglia versus thalamus) modified these associations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results\u2014<\/jats:title>\n                    <jats:p>\n                      Among 1000 patients enrolled in ATACH-2, 870 (87%) had supratentorial, deep ICH. Of these, 780 (90%) had neuroimaging data (336 thalamic and 444 basal ganglia hemorrhages). Baseline characteristics of the treatment groups remained balanced (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &gt;0.2). Intensive BP reduction was associated with a decrease in PHER in univariable (\u03b2= \u22120.15; 95% CI, \u22120.26 to \u22120.05;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.007) and multivariable (\u03b2=\u22120.12; 95% CI, \u22120.21 to \u22120.02;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.03) analyses. PHER was not independently associated with outcome in all deep ICH (odds ratio, 1.14; 95% CI, 0.93\u20131.41;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.20), but this association was modified by the specific deep location involved (multivariable interaction\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.02); in adjusted analyses, PHER was associated with poor outcome in basal ganglia (odds ratio, 1.42; 1.05\u20131.97;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.03) but not thalamic (odds ratio, 1.02; 95% CI, 0.74\u20131.40;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.89) ICH.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\u2014<\/jats:title>\n                    <jats:p>Intensive BP reduction was associated with decreased 24-hour PHER in deep ICH. PHER was not independently associated with outcome in all deep ICH but was associated with poor outcome in basal ganglia ICH. PHER may be a clinically relevant end point for clinical trials in basal ganglia ICH.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/strokeaha.119.024838","type":"journal-article","created":{"date-parts":[[2019,7,5]],"date-time":"2019-07-05T05:00:48Z","timestamp":1562302848000},"page":"2016-2022","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":46,"title":["Intensive Blood Pressure Reduction and Perihematomal Edema Expansion in Deep Intracerebral Hemorrhage"],"prefix":"10.1161","volume":"50","author":[{"given":"Audrey C.","family":"Leasure","sequence":"first","affiliation":[{"name":"From the Department of Neurology (A.C.L., L.H.S., G.J.F., K.N.S.), Yale School of Medicine, New Haven, CT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adnan I.","family":"Qureshi","sequence":"additional","affiliation":[{"name":"Zeenat Qureshi Stroke Institute, St. Cloud, MN (A.I.Q.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Santosh B.","family":"Murthy","sequence":"additional","affiliation":[{"name":"Department of Neurology, Weill Cornell Medical College, New York, NY (S.B.M. H.K.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hooman","family":"Kamel","sequence":"additional","affiliation":[{"name":"Department of Neurology, Weill Cornell Medical College, New York, NY (S.B.M. H.K.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua N.","family":"Goldstein","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (J.N.G.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyle B.","family":"Walsh","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine (K.B.W.), University of Cincinnati, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Woo","sequence":"additional","affiliation":[{"name":"Department of Neurology and Rehabilitation Medicine (D.W.), University of Cincinnati, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fu-Dong","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Neurology, Barrow Neurological Institute, Phoenix, AZ (F.-D.S.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hagen B.","family":"Huttner","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Erlangen-Nuremberg, Germany (H.B.S.)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wendy C.","family":"Ziai","sequence":"additional","affiliation":[{"name":"Department of Neurology, Johns Hopkins University, Baltimore, MD (W.C.Z., D.F.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel F.","family":"Hanley","sequence":"additional","affiliation":[{"name":"Department of Neurology, Johns Hopkins University, Baltimore, MD (W.C.Z., D.F.H.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles C.","family":"Matouk","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery (C.C.M.), Yale School of Medicine, New Haven, CT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren H.","family":"Sansing","sequence":"additional","affiliation":[{"name":"From the Department of Neurology (A.C.L., L.H.S., G.J.F., K.N.S.), Yale School of Medicine, New Haven, CT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guido J.","family":"Falcone","sequence":"additional","affiliation":[{"name":"From the Department of Neurology (A.C.L., L.H.S., G.J.F., K.N.S.), Yale School of Medicine, New Haven, CT"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin N.","family":"Sheth","sequence":"additional","affiliation":[{"name":"From the Department of Neurology (A.C.L., L.H.S., G.J.F., K.N.S.), Yale School of Medicine, New Haven, CT"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1603460"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1214609"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12975-015-0389-7"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrneurol.2014.264"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/s11940-015-0392-z"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12028-016-0321-3"},{"key":"e_1_3_4_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp-2016-313653"},{"key":"e_1_3_4_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.114.007154"},{"key":"e_1_3_4_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.115.010054"},{"key":"e_1_3_4_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12028-011-9538-3"},{"key":"e_1_3_4_12_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneurol.2010.61"},{"key":"e_1_3_4_13_2","doi-asserted-by":"crossref","first-page":"395","DOI":"10.1093\/neurosurgery\/57.2.395a","article-title":"Effects of recombinant activated factor VII on perilesional edema in patients with acute intracerebral hemorrhage801.","volume":"57","author":"Diringer MN","year":"2005","unstructured":"Diringer, MN, Davalos, A, Mayer, SA, Brun, NC, Begtrup, K, Broderick, J, et al. 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