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Research Article| Volume 6, ISSUE 5, P319-324, July 1997

Regional cerebral hemodynamics among hypertensive patients with lacunar infarctions during blood pressure control in subacute and chronic phases

  • Hiroyuki Hashimoto
    Correspondence
    Address reprint requests to Hiroyuki Hashimoto, MD, The First Department of Medicine, Osaka University School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565, Japan.
    Affiliations
    Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan

    Department of Radiology, National Cardiovascular Center, Osaka, Japan
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  • Yoshihiro Kuriyama
    Affiliations
    Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan

    Department of Radiology, National Cardiovascular Center, Osaka, Japan
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  • Satoshi Imakita
    Affiliations
    Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan

    Department of Radiology, National Cardiovascular Center, Osaka, Japan
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  • Tohru Sawada
    Affiliations
    Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan

    Department of Radiology, National Cardiovascular Center, Osaka, Japan
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  • Hiroaki Naritomi
    Affiliations
    Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Osaka, Japan

    Department of Radiology, National Cardiovascular Center, Osaka, Japan
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      In hypertensive acute stroke patients, the use of antihypertensive treatment is often delayed because autoregulation of cerebral blood flow (CBF) is often impaired during the first 4 weeks after large brain infarctions. However, little is known as to whether such delay is necessary in cases of small to moderate size brain infarction. We compared changes of regional CBF during antihypertensive treatment in subacute and chronic phases of lacunar infarction. Blood pressure was controlled with an angiotensin-converting enzyme inhibitor (n=6) or dihydropyridine calcium antagonist (n=8), administered orally for 2 weeks during the subacute (n=7) and chronic phases after (n=7) lacunar infarction. CBF was measured by the stable xenon-computed tomography (CT) method. Blood pressure decreased significantly from 132±20 mm Hg (mean±standard deviation) to 118±14 mm Hg (P<.05, paired t-test) in subacute patients and from 135±17 mm Hg to 113±12 mm Hg (P<.001, paired t-test) in chronic patients. There was no significant reduction either in mean hemispheric blood flow or in deep white matter blood flow during each phase. We condlude that mild control of blood pressure among hypertensive patients with lacunar infarctions does not produce clinically significant decreases in regional CBF during subacute phases of infarction.

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