Serotonin transporter gene polymorphism and myocardial infarction - Etude Cas-te'moins de' l'Infarctus du Myocarde (ECTIM)

被引:63
作者
Fumeron, F
Betoulle, D
Nicaud, V
Evans, A
Kee, F
Ruidavets, JB
Arveiler, D
Luc, G
Cambien, F
机构
[1] Univ Paris 07, EA 3516, F-75870 Paris 18, France
[2] INSERM, U525, Paris, France
[3] MONICA Project, Belfast, Antrim, North Ireland
[4] MONICA Project, Toulouse, France
[5] MONICA Project, Strasbourg, France
[6] MONICA Project, Lille, France
关键词
serotonin transporter; genes; myocardial infarction; risk factors;
D O I
10.1161/01.CIR.0000022603.92986.99
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Depression is a risk factor for myocardial infarction (MI). Selective serotonin reuptake inhibitors reduce this risk. The site of action is the serotonin transporter (SLC6A4), which is expressed in brain and blood cells. A functional polymorphism in the promoter region of the SLC6A4 gene has been described. This polymorphism may be associated with the risk of MI. Methods and Results-The SLC6A4 polymorphism has been investigated by polymerase chain reaction in 671 male patients with MI and in 688 controls from the Etude Cas-Temoins de l'Infarctus du Myocarde (ECTIM) multicentric study. Percentages for LL, LS, and SS genotypes were 35.5%, 45.4%, and 19.1%, respectively, for cases versus 28.1%, 49.1%, and 22.8%, respectively, for controls. S allele frequency was 41.8% and 47.4% for cases and controls, respectively. After adjustment for age,and center by using multivariable logistic regression, the odds ratio for MI associated with the LL genotype was 1.40 (95% Cl 1.11 to 1.76, P=0.0047). Conclusions-The LL genotype of the SLC6A4 polymorphism is associated with a higher risk of MI. This could be attributable to the effect of the polymorphism on serotonin-mediated platelet activation or smooth muscle cell proliferation or on other risk factors, such as depression or response to stress.
引用
收藏
页码:2943 / 2945
页数:3
相关论文
共 22 条
[1]  
[Anonymous], 1988, J CLIN EPIDEMIOL, V41, P105, DOI DOI 10.1016/0895-4356(88)90084-4
[2]  
Arinami T, 1999, THROMB HAEMOSTASIS, V81, P853
[3]   PLATELET-INDUCED VASCULAR SMOOTH-MUSCLE CELL-PROLIFERATION IS MODULATED BY THE GROWTH AMPLIFICATION FACTORS SEROTONIN AND ADENOSINE-DIPHOSPHATE [J].
CROWLEY, ST ;
DEMPSEY, EC ;
HORWITZ, KB ;
HORWITZ, LD .
CIRCULATION, 1994, 90 (04) :1908-1918
[4]   Serotonin transporter overexpression is responsible for pulmonary artery smooth muscle hyperplasia in primary pulmonary hypertension [J].
Eddahibi, S ;
Humbert, M ;
Fadel, E ;
Raffestin, B ;
Darmon, M ;
Capron, F ;
Simonneau, G ;
Dartevelle, P ;
Hamon, M ;
Adnot, S .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (08) :1141-1150
[5]   Association of a functional 5-HT transporter gene polymorphism with anorexia nervosa and food intake [J].
Fumeron, F ;
Betoulle, D ;
Aubert, R ;
Herbeth, B ;
Siest, G ;
Rigaud, D .
MOLECULAR PSYCHIATRY, 2001, 6 (01) :9-10
[6]  
Gelernter J, 1999, AM J MED GENET, V88, P61, DOI 10.1002/(SICI)1096-8628(19990205)88:1<61::AID-AJMG11>3.0.CO
[7]  
2-K
[8]   DIVERGENT EFFECTS OF SEROTONIN ON CORONARY-ARTERY DIMENSIONS AND BLOOD-FLOW IN PATIENTS WITH CORONARY ATHEROSCLEROSIS AND CONTROL PATIENTS [J].
GOLINO, P ;
PISCIONE, F ;
WILLERSON, JT ;
CAPPELLIBIGAZZI, M ;
FOCACCIO, A ;
VILLARI, B ;
INDOLFI, C ;
RUSSOLILLO, E ;
CONDORELLI, M ;
CHIARIELLO, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 324 (10) :641-648
[9]  
Greenberg BD, 1999, AM J MED GENET, V88, P83, DOI 10.1002/(SICI)1096-8628(19990205)88:1<83::AID-AJMG15>3.0.CO
[10]  
2-0