LIPOPROTEIN(A) AND ISCHEMIC CEREBROVASCULAR-DISEASE IN YOUNG-ADULTS

被引:96
作者
NAGAYAMA, M
SHINOHARA, Y
NAGAYAMA, T
机构
[1] Department of Neurology, Tokai University School of Medicine, Isehara
关键词
CEREBRAL INFARCTION; CEREBRAL ISCHEMIA; LIPOPROTEINS; YOUNG ADULTS;
D O I
10.1161/01.STR.25.1.74
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose Serum lipoprotein(a) level is genetically determined and remains almost constant throughout life. Based on this property, we investigated the serum lipoprotein(a) levels of ischemic stroke patients in the chronic stage (mean period after stroke, 27 months) and its relation to the types of ischemic stroke. Methods We measured serum lipoprotein(a) levels in 101 patients with chronic ischemic stroke and 37 normal control subjects, taking the clinical profiles into consideration. Results Lipoprotein(a) levels in patients with atherothrombotic stroke were 28.0+/-19.6 mg/dL (mean+/-SD), which were significantly (P<.01) higher than those in patients with lacunar stroke and in normal control subjects (16.4+/-13.5 and 11.7+/-10.5 mg/dL, respectively). The lipoprotein(a) levels in patients with atherothrombotic stroke were significantly higher in the subgroup who were a younger age at onset: onset before age 50 years, 35.3+/-20.5; onset at age 50 to 59, 35.4+/-21.7; onset at age 60 to 69, 17.0+/-12.8; and onset at age 70 or older, 16.3+/-6.8 mg/dL (P<.01 for onset before age 50 versus 60 to 69 years or 70 years or older; P<.01 for onset at 50 to 59 years versus 60 to 69 years or 70 years or older). Serum lipoprotein( a) was significantly increased (40.2+/-20.1 mg/dL) in young adults with atherothrombotic stroke (onset at younger than age 45 years) compared with that in patients older than 45 years (P<.01). Conclusions We conclude that lipoprotein(a) is a genetic, independent, and critical risk factor for ischemic stroke, especially in young adults.
引用
收藏
页码:74 / 78
页数:5
相关论文
共 29 条
[1]   ENZYME-LINKED IMMUNOSORBENT-ASSAY OF LIPOPROTEIN(A) IN SERUM AND CORD BLOOD [J].
ABE, A ;
MAEDA, S ;
MAKINO, K ;
SEISHIMA, M ;
SHIMOKAWA, K ;
NOMA, A ;
KAWADE, M .
CLINICA CHIMICA ACTA, 1988, 177 (01) :31-40
[2]  
ABE A, 1990, JPN J CLIN PATHOL, V38, P722
[3]   REDUCTION OF LECITHIN-CHOLESTEROL ACYLTRANSFERASE, APOLIPOPROTEIN D AND THE LP(A) LIPOPROTEIN WITH THE ANABOLIC-STEROID STANOZOLOL [J].
ALBERS, JJ ;
TAGGART, HM ;
APPLEBAUMBOWDEN, D ;
HAFFNER, S ;
CHESNUT, CH ;
HAZZARD, WR .
BIOCHIMICA ET BIOPHYSICA ACTA, 1984, 795 (02) :293-296
[4]   IMMUNOCHEMICAL QUANTIFICATION OF HUMAN PLASMA LP(A) LIPOPROTEIN [J].
ALBERS, JJ ;
HAZZARD, WR .
LIPIDS, 1974, 9 (01) :15-26
[5]   LP(A) LIPOPROTEIN IN PATIENTS WITH ACUTE STROKE [J].
ASPLUND, K ;
OLSSON, T ;
VIITANEN, M ;
DAHLEN, G .
CEREBROVASCULAR DISEASES, 1991, 1 (02) :90-96
[6]  
BERG K, 1963, ACTA PATHOL MIC SC, V59, P369
[7]  
BERG K, 1974, CLIN GENET, V6, P230
[8]   LIPOPROTEIN(A) REDUCTION BY N-ACETYLCYSTEINE [J].
GAVISH, D ;
BRESLOW, JL .
LANCET, 1991, 337 (8735) :203-204
[9]   LIPOPROTEIN(A) MODULATION OF ENDOTHELIAL-CELL SURFACE FIBRINOLYSIS AND ITS POTENTIAL ROLE IN ATHEROSCLEROSIS [J].
HAJJAR, KA ;
GAVISH, D ;
BRESLOW, JL ;
NACHMAN, RL .
NATURE, 1989, 339 (6222) :303-305
[10]   REDUCTION OF SERUM LIPOPROTEIN(A) USING ESTROGEN IN A MAN WITH FAMILIAL HYPERCHOLESTEROLEMIA [J].
HIRAGA, T ;
HARADA, K ;
KOBAYASHI, T ;
MURASE, T .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1992, 267 (17) :2328-2328