Progression of coronary artery disease in young male post-infarction patients is linked to disturbances of carbohydrate and lipoprotein metabolism and to impaired fibrinolytic function

被引:57
作者
Bavenholm, P [1 ]
de Faire, U
Landou, C
Efendic, S
Nilsson, J
Wiman, B
Hamsten, A
机构
[1] Karolinska Hosp, Dept Emergency & Cardiovasc Med, Div Internal Med, S-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Thorac Radiol, S-17176 Stockholm, Sweden
[3] Karolinska Hosp, Dept Endocrinol, S-17176 Stockholm, Sweden
[4] Karolinska Hosp, Dept Clin Chem & Blood Coagulat, S-17176 Stockholm, Sweden
[5] Karolinska Inst, King Gustaf V Res Inst, Atherosclerosis Res Unit, Stockholm, Sweden
关键词
lipoproteins; plasminogen activator inhibitor-1; glucose; insulin; myocardial infarction; coronary angiography;
D O I
10.1053/euhj.1997.0752
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aims To assess determinants of coronary artery disease progression in men with previous myocardial infarction. Methods and Results A total of 102 unselected nondiabetic Swedish men (age 40.4+/-3.6, range 23-44 years) entered the study 3-6 months after a first myocardial infarction. The programme included metabolic and haemostatic investigations and routine coronary angiography at baseline, followed by re-angiography 5 years later. Of the original cohort, 76 patients underwent a second angiogram. Separate semiquantitative scoring systems were used for diffuse coronary atherosclerosis and distinct stenoses in 15 proximal coronary segments. Smoking, global severity of coronary atherosclerosis and presence of multi-vessel disease at baseline (P<0.001) characterized patients with severe progression of both diffuse and focal lesions. Higher plasma levels of low density lipoprotein cholesterol (P<0.01) and low density lipoprotein triglycerides (P<0.05), a lower plasma high density lipoprotein, cholesterol level (P<0.05) and higher plasma plasminogen activator inhibitor-1 activity (P<0.05), together with a high baseline stenosis score (P<0.001) characterized patients with severe progression of coronary atherosclerosis. On the other hand, more pronounced fasting and post-prandial glycaemia (P<0.05), together with higher plasma plasminogen activator inhibitor-1 activity (P<0.01) characterized severe progressors with respect to coronary stenosis. Multivariate analysis identified the presence of multi-vessel disease as an independent predictor of progression of both coronary atherosclerosis (P=0.008) and stenoses (P=0.007), whereas a high low density lipoprotein triglyceride level (P<0.01) was independently related to progression of coronary atherosclerosis and a high fasting glucose level (P=0.02) to progression of coronary stenoses. Conclusion Disturbances in carbohydrate and lipoprotein metabolism and impaired fibrinolytic function are associated with progression of coronary artery disease in young male post-infarction patients.
引用
收藏
页码:402 / 410
页数:9
相关论文
共 47 条
[1]  
Austen W. G., 1975, CIRCULATION, V51, P7
[2]  
AUSTIN MA, 1988, JAMA-J AM MED ASSOC, V260, P1917
[3]   ATHEROGENIC LIPOPROTEIN PHENOTYPE - A PROPOSED GENETIC-MARKER FOR CORONARY HEART-DISEASE RISK [J].
AUSTIN, MA ;
KING, MC ;
VRANIZAN, KM ;
KRAUSS, RM .
CIRCULATION, 1990, 82 (02) :495-506
[4]   PLASMA TRIGLYCERIDE AND CORONARY HEART-DISEASE [J].
AUSTIN, MA .
ARTERIOSCLEROSIS AND THROMBOSIS, 1991, 11 (01) :2-14
[5]   INSULIN, INTACT AND SPLIT PROINSULIN, AND CORONARY-ARTERY DISEASE IN YOUNG MEN [J].
BAVENHOLM, P ;
PROUDLER, A ;
TORNVALL, P ;
GODSLAND, I ;
LANDOU, C ;
DEFAIRE, U ;
HAMSTEN, A .
CIRCULATION, 1995, 92 (06) :1422-1429
[6]   ASSOCIATION OF INSULIN AND INSULIN PROPEPTIDES WITH AN ATHEROGENIC LIPOPROTEIN PHENOTYPE [J].
BAVENHOLM, P ;
KARPE, F ;
PROUDLER, A ;
TORNVALL, P ;
CROOK, D ;
HAMSTEN, A .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1995, 44 (11) :1481-1488
[7]  
BAVENHOLM P, 1995, THROMB HAEMOSTASIS, V73, P568
[8]  
BEUMONT JL, 1970, B WORLD HEALTH ORGAN, V43, P891
[9]   PREDICTION OF ANGIOGRAPHIC CHANGE IN NATIVE HUMAN CORONARY-ARTERIES AND AORTOCORONARY BYPASS GRAFTS - LIPID AND NONLIPID FACTORS [J].
BLANKENHORN, DH ;
ALAUPOVIC, P ;
WICKHAM, E ;
CHIN, HP ;
AZEN, SP .
CIRCULATION, 1990, 81 (02) :470-476
[10]  
Carlson K, 1973, J Clin Pathol Suppl (Assoc Clin Pathol), V5, P32