Parental history of myocardial infarction: lipid traits, gene polymorphisms and lifestyle

被引:13
作者
Boer, JMA
Feskens, EJM
Kuivenhoven, JA
Schouten, EG
Havekes, LM
Kastelein, JJP
Seidell, JC
Kromhout, D
机构
[1] Natl Inst Publ Hlth & Environm, Dept Chron Dis Epidemiol, NL-3720 BA Bilthoven, Netherlands
[2] Natl Inst Publ Hlth & Environm, Div Publ Hlth Res, NL-3720 BA Bilthoven, Netherlands
[3] Univ Wageningen & Res Ctr, Div Human Nutr & Epidemiol, Wageningen, Netherlands
[4] Natl Inst Hlth Sci, NIHES, Rotterdam, Netherlands
[5] Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1105 AZ Amsterdam, Netherlands
[6] TNO Prevent & Hlth, IVVO, Gaubius Lab, NL-2300 AK Leiden, Netherlands
[7] Leiden Univ, Med Ctr, Dept Cardiol, Leiden, Netherlands
[8] Leiden Univ, Med Ctr, Dept Internal Med, Leiden, Netherlands
关键词
D O I
10.1016/S0021-9150(00)00521-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To investigate the relationship between parental history of myocardial infarction (MI), lipid traits and gene polymorphisms involved in lipid metabolism, we examined Dutch men and women, who were selected from a large population-based study. Subjects whose father (n = 112), mother (n = 115) or both parents (n = 115) suffered from a premature MI presented with significantly higher apolipoprotein B (apo B) levels than subjects without a parental history (n = 114). Genetic analyses revealed that the apo E4 isoform and the D9N mutation of lipoprotein lipase (LPL) were more frequent among subjects with a parental history (P less than or equal to0.05). A similar trend was found for the LPL N291S mutation. In contrast, the LPL S447X mutation and polymorphisms at the cholesteryl ester transfer protein (TaqIB) and apo CIII (SstI) loci proved to be noninformative. Body mass index and lifestyle could not explain differences in apo B levels between parental history groups. In contrast, the apo E polymorphism and the LPL D9N mutation accounted for some, but not all, of the higher apo B levels in subjects with a parental history. Therefore, other genetic or lifestyle-related factors must be responsible for the increased levels of apo B in individuals with a family history of myocardial infarction. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:149 / 156
页数:8
相关论文
共 34 条
[1]   Physical activity modulates the effect of a lipoprotein lipase mutation (D9N) on plasma lipids and lipoproteins [J].
Boer, JMA ;
Kuivenhoven, JA ;
Feskens, EJM ;
Schouten, EG ;
Havekes, LM ;
Seidell, JC ;
Kastelein, JJP ;
Kromhout, D .
CLINICAL GENETICS, 1999, 56 (02) :158-163
[2]  
BOER JMA, 1997, CIRCULATION S, V96, P413
[3]   Apolipoprotein E and atherosclerosis: insight from animal and human studies [J].
Davignon, J ;
Cohn, JS ;
Mabile, L ;
Bernier, L .
CLINICA CHIMICA ACTA, 1999, 286 (1-2) :115-143
[4]  
De Backer G, 1999, J CARDIOVASC RISK, V6, P183
[5]  
Gerdes C, 1997, CIRCULATION, V96, P733
[6]  
Goldberg IJ, 1996, J LIPID RES, V37, P693
[7]   HIGH-DENSITY LIPOPROTEIN CHOLESTEROL AND CARDIOVASCULAR-DISEASE - 4 PROSPECTIVE AMERICAN-STUDIES [J].
GORDON, DJ ;
PROBSTFIELD, JL ;
GARRISON, RJ ;
NEATON, JD ;
CASTELLI, WP ;
KNOKE, JD ;
JACOBS, DR ;
BANGDIWALA, S ;
TYROLER, HA .
CIRCULATION, 1989, 79 (01) :8-15
[8]   Verification of parental history of coronary artery disease and associations with adult offspring risk factors in a community sample: The Bogalusa Heart Study [J].
Greenlund, KJ ;
Valdez, R ;
Bao, WH ;
Wattigney, WA ;
Srinivasan, SR ;
Berenson, GS .
AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 1997, 313 (04) :220-227
[9]  
HANSEN PS, 1993, HUM GENET, V91, P45
[10]  
HAVEKES LM, 1987, J LIPID RES, V28, P455