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Table of Contents
Vol. 24, No. 2-3, 2007
Issue release date: August 2007
Section title: Original Paper
Cerebrovasc Dis 2007;24:202–209
(DOI:10.1159/000104478)

Effect of the Ca Antagonist Nilvadipine on Stroke Occurrence or Recurrence and Extension of Asymptomatic Cerebral Infarction in Hypertensive Patients with or without History of Stroke (PICA Study)

1. Design and Results at Enrollment

Shinohara Y.a · Tohgi H.c · Hirai S.d · Terashi A.b · Fukuuchi Y.e · Yamaguchi T.f · Okudera T.g
aFederation of National Public Service Personnel Mutual Aid Associations, Tachikawa Hospital, and bNippon Medical School, Tokyo, cDepartment of Neurology, Iwate Medical University, Morioka, dDepartment of Neurology, Gunma University School of Medicine, Maebashi, eAshikaga Red Cross Hospital, Ashikaga, fNational Cardiovascular Center, Suita, gCenter for Higher Brain Dysfunction, Haradoi Hospital, Fukuoka, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 28, 2006
Accepted: February 26, 2007
Published online: June 27, 2007
Issue release date: August 2007

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 2

ISSN: 1015-9770 (Print)
eISSN: 1421-9786 (Online)

For additional information: http://www.karger.com/CED

Abstract

Background: We examined the effect of a Ca antagonist (nilvadipine) on the occurrence or recurrence of symptomatic stroke in hypertensive patients with MRI-defined asymptomatic cerebral infarction (ACI), periventricular hyperintensity (PVH), and deep and subcortical white matter hyperintensity (DSWMH), with or without a history of stroke, and evaluated the effect of long-term treatment on the lesions. Methods: Patients with hypertension and incidental ACI were divided into those with (group B, 235 patients) or without (group A, 181 patients) a history of symptomatic stroke, and were given nilvadipine 4–8 mg/day for 3 years. Primary evaluation points were occurrence of symptomatic ischemic stroke and development or extension of asymptomatic ischemic lesions. Results: Male sex, hyperuricemia, diabetes, maximum diameter of infarction and PVH severity were stronger risk factors for group B. Numbers of cerebral infarctions were 31 ± 28 (group A) and 42 ± 32 (group B) at enrollment (p < 0.001). Infarctions were larger and located more frequently on the internal capsule, putamen, thalamus and brainstem in group B. The severity of PVH and DSWMH paralleled the number of cerebral infarctions in both groups. Conclusion: The study design and status of asymptomatic ischemic brain lesions in hypertensive subjects at enrollment are presented.

© 2007 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: December 28, 2006
Accepted: February 26, 2007
Published online: June 27, 2007
Issue release date: August 2007

Number of Print Pages: 8
Number of Figures: 4
Number of Tables: 2

ISSN: 1015-9770 (Print)
eISSN: 1421-9786 (Online)

For additional information: http://www.karger.com/CED


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