Antibodies to human heat shock protein 60, hypertension and dyslipidemia.: A study of joint effects on coronary risk

被引:29
作者
Kervinen, H
Huittinen, T
Vaarala, O
Leinonen, M
Saikku, P
Manninen, V
Mänttäri, M
机构
[1] Univ Helsinki, Cent Hosp, Maria Hosp, Dept Med, Helsinki 00180, Finland
[2] Kyvinkaa Hosp, Dept Med, Hyvinkaa, Finland
[3] Natl Publ Hlth Inst, Oulu, Finland
[4] Oulu Univ, Dept Microbiol, Oulu, Finland
关键词
autoimmunity; heat shock protein; interaction; coronary heart disease;
D O I
10.1016/S0021-9150(03)00229-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: High IgA-class (but not IgG-class) Anti-Heat-shock-protein 60 antibody level is a predictor of coronary risk in dyslipidemic middle-aged men. In this paper we studied the joint effects of high Anti-Hsp60-antibody level and the classical coronary risk factors. Methods: We used nested case-control design and logistic regression analyses. The cases consisted of 233 middle-aged men with myocardial infarction or coronary death during 8.5-year follow-up in Helsinki Heart Study, a coronary primary prevention study with gemfibrozil. The controls were subjects without coronary events, matched for drug treatment and the geographical area. Results: The relative coronary risks (Odds Ratios (ORs); 95% confidence interval) were 1.41 (0.96-2.05) for high IgA-class Anti-Hsp60 antibody level and 1.98 (1.35-2.90) for hypertension, defined as mean arterial pressure > 114 mmHg. With simultaneous occurrence of high Anti-Hsp60 antibody level and hypertension, the ORs were 2.32 (1.26-4.27) for systolic and 2.99 (1.63-5.48) for diastolic hypertension. Similar patterns of joint effects were found between high Anti-Hsp60 antibody and lipoprotein cholesterol levels as well as antibodies against oxidized low-density lipoprotein. Conclusions: Our results suggest that, while high IgA-class Anti-Hsp60 antibody level predicts coronary risk, the effect is modest without simultaneous occurrence of other classical risk factors. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:339 / 344
页数:6
相关论文
共 32 条
[1]   Immunization of low-density lipoprotein receptor deficient (LDL-RD) mice with heat shock protein 65 (HSP-65) promotes early atherosclerosis [J].
Afek, A ;
George, J ;
Gilburd, B ;
Rauova, L ;
Goldberg, I ;
Kopolovic, J ;
Harats, D ;
Shoenfeld, Y .
JOURNAL OF AUTOIMMUNITY, 2000, 14 (02) :115-121
[2]  
BERBERIAN PA, 1990, AM J PATHOL, V136, P71
[3]   Association between antibodies to heat shock protein 65 and coronary atherosclerosis - Possible mechanism of action of Helicobacter pylori and other bacterial infections in increasing cardiovascular risk [J].
Birnie, DH ;
Holme, ER ;
McKay, IC ;
Hood, S ;
McColl, KEL ;
Hillis, WS .
EUROPEAN HEART JOURNAL, 1998, 19 (03) :387-394
[4]   BLOOD-PRESSURE AND HEAT-SHOCK PROTEIN EXPRESSION IN RESPONSE TO ACUTE AND CHRONIC STRESS [J].
BLAKE, MJ ;
KLEVAY, LM ;
HALAS, ES ;
BODE, AM .
HYPERTENSION, 1995, 25 (04) :539-544
[5]   HELSINKI HEART-STUDY - PRIMARY-PREVENTION TRIAL WITH GEMFIBROZIL IN MIDDLE-AGED MEN WITH DYSLIPIDEMIA - SAFETY OF TREATMENT, CHANGES IN RISK-FACTORS, AND INCIDENCE OF CORONARY HEART-DISEASE [J].
FRICK, MH ;
ELO, O ;
HAAPA, K ;
HEINONEN, OP ;
HEINSALMI, P ;
HELO, P ;
HUTTUNEN, JK ;
KAITANIEMI, P ;
KOSKINEN, P ;
MANNINEN, V ;
MAENPAA, H ;
MALKONEN, M ;
MANTTARI, M ;
NOROLA, S ;
PASTERNACK, A ;
PIKKARAINEN, J ;
ROMO, M ;
SJOBLOM, T ;
NIKKILA, EA .
NEW ENGLAND JOURNAL OF MEDICINE, 1987, 317 (20) :1237-1245
[6]   Induction of heat shock protein in monocytic cells by oxidized low density lipoprotein [J].
Frostegard, J ;
Kjellman, B ;
Gidlund, M ;
Andersson, B ;
Jindal, S ;
Kiessling, R .
ATHEROSCLEROSIS, 1996, 121 (01) :93-103
[7]  
FROSTEGARD J, 1997, HYPERTENSION, V29, P940
[8]   Enhanced fatty streak formation in C57BL/6J mice by immunization with heat shock protein-65 [J].
George, J ;
Shoenfeld, Y ;
Afek, A ;
Gilburd, B ;
Keren, P ;
Shaish, A ;
Kopolovic, J ;
Wick, G ;
Harats, D .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1999, 19 (03) :505-510
[9]   Fluid shear stress induces heat shock protein 60 expression in endothelial cells in vitro and in vivo [J].
Hochleitner, BW ;
Hochleitner, EO ;
Obrist, P ;
Eberl, T ;
Amberger, A ;
Xu, QB ;
Margreiter, R ;
Wick, G .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (03) :617-623
[10]   Changes of serum antibodies to heat-shock protein 65 in coronary heart disease and acute myocardial infarction [J].
Hoppichler, F ;
Lechleitner, M ;
Traweger, C ;
Schett, G ;
Dzien, A ;
Sturm, W ;
Xu, QB .
ATHEROSCLEROSIS, 1996, 126 (02) :333-338