The metabolic syndrome as a link between smoking and cardiovascular disease

被引:41
作者
Dzien, A
Dzien-Bischinger, C
Hoppichler, F
Lechleitner, M
机构
[1] Univ Innsbruck Hosp, Dept Internal Med, A-6020 Innsbruck, Austria
[2] Med Ctr Hentschelhof, Innsbruck, Austria
[3] Hosp Barmherzige Brueder, Salzburg, Austria
关键词
insulin resistance; smoking;
D O I
10.1111/j.1462-8902.2004.00324.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: Smoking is associated with a significant increase in the cardiovascular risk. The possible relationship of smoking with insulin resistance might further enhance the cardiovascular risk of the patients and is therefore of great clinical interest. Design, Setting and Subjects: We have retrospectively evaluated data of 3804 non-diabetic men attending a medical outdoor clinic. Clinical [body mass index (BMI), percentage of body fat, waist-to-hip ratio] and laboratory results were compared between smokers (n = 124) and non-smokers (n = 1915) without cardiovascular disease, as well as between smokers (n = 759) and non-smokers (n = 1006) with cardiovascular disease. Results: Smokers without clinically manifest cardiovascular disease revealed significantly higher fasting glucose (5.8 +/- 0.6 mmol/l) and triglyceride levels (1.8 +/- 0.9 mmol/l) than non-smokers (fasting glucose: 5.1 +/- 0.7 mmol/l, p < 0.010; triglycerides: 1.5 +/- 0.8 mmol/l, p < 0.030). The adverse metabolic profile of smokers was even more pronounced in patients with cardiovascular disease. An age-matched analysis of smokers could demonstrate that cardiovascular patients revealed higher BMI values (27.3 +/- 2.4 kg/m(2)) and a higher percentage of body fat (25.5 +/- 5.5%) than those without cardiovascular disease (BMI: 25.7 +/- 2.2 kg/m(2), p < 0.010; percentage of body fat: 23.0 +/- 5.5%, p < 0.030). Conclusion: In men with and without clinically manifest cardiovasular disease, smoking was associated with a metabolic profile indicating a higher degree of insulin resistance.
引用
收藏
页码:127 / 132
页数:6
相关论文
共 32 条
[1]   Smoking is associated with altered endothelial-derived fibrinolytic and antithrombotic factors - An in vitro demonstration [J].
Barua, RS ;
Ambrose, JA ;
Saha, DC ;
Eales-Reynolds, LJ .
CIRCULATION, 2002, 106 (08) :905-908
[2]   BODY-WEIGHT CHANGE, ALL-CAUSE MORTALITY, AND CAUSE-SPECIFIC MORTALITY IN THE MULTIPLE RISK FACTOR INTERVENTION TRIAL [J].
BLAIR, SN ;
SHATEN, J ;
BROWNELL, K ;
COLLINS, G ;
LISSNER, L .
ANNALS OF INTERNAL MEDICINE, 1993, 119 (07) :749-757
[3]   Effects of atorvastatin on glucose homeostasis, postprandial triglyceride response and C-reactive protein in subjects with impaired fasting glucose [J].
Costa, A ;
Casamitjana, R ;
Casals, E ;
Alvarez, L ;
Morales, J ;
Masramón, X ;
Hernández, G ;
Gomis, R ;
Conget, I .
DIABETIC MEDICINE, 2003, 20 (09) :743-745
[4]   The association between inflammation markers, coronary artery disease and smoking [J].
de Maat, MPM ;
Kluft, C .
VASCULAR PHARMACOLOGY, 2002, 39 (03) :137-139
[5]   Smoking cessation improves insulin sensitivity in healthy middle-aged men [J].
Eliasson, B ;
Attvall, S ;
Taskinen, MR ;
Smith, U .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1997, 27 (05) :450-456
[6]   Insulin resistance as a predictor of age-related diseases [J].
Facchini, FS ;
Hua, N ;
Abbasi, F ;
Raven, GM .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2001, 86 (08) :3574-3578
[7]   INSULIN RESISTANCE AND CIGARETTE-SMOKING [J].
FACCHINI, FS ;
HOLLENBECK, CB ;
JEPPESEN, J ;
CHEN, YDI ;
REAVEN, GM .
LANCET, 1992, 339 (8802) :1128-1130
[8]  
Freund K M, 1993, Ann Epidemiol, V3, P417, DOI 10.1016/1047-2797(93)90070-K
[9]   Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes [J].
Gaede, P ;
Vedel, P ;
Larsen, N ;
Jensen, GVH ;
Parving, H ;
Pedersen, O .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (05) :383-393
[10]   Xanthine oxidase inhibition reverses endothelial dysfunction in heavy smokers [J].
Guthikonda, S ;
Sinkey, C ;
Barenz, T ;
Haynes, WG .
CIRCULATION, 2003, 107 (03) :416-421