Involvement of the hemostatic system in the insulin resistance syndrome. A study of 1500 patients with angina pectoris. The ECAT Angina Pectoris Study Group.
- 1 December 1993
- journal article
- abstracts
- Published by Wolters Kluwer Health in Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
- Vol. 13 (12), 1865-1873
- https://doi.org/10.1161/01.atv.13.12.1865
Abstract
Hyperinsulinemia, a major indicator of insulin resistance, may exert its influence on the risk of coronary artery disease partially through disturbances of the hemostatic system. The relations of fasting insulin concentrations with the degree of coronary atherosclerosis, other coronary risk factors (including some markers of the insulin resistance syndrome such as body mass index and triglyceride), markers of inflammation, and hemostatic factors were investigated in 1484 patients with angina pectoris. Mean insulin levels were higher in patients with one or more coronary vessel stenoses than in those without (9.9 microU/mL compared with 9.0 microU/mL, P < .0001). However, the association the presence of vessel stenoses was stronger in patients with a previous myocardial infarction than in those without. Insulin increased markedly (P < .0001) and independently of other risk factors with age body mass index, triglyceride concentration, and markers of inflammation, such as white blood cell count and C-reactive protein. The strongest relations between insulin and hemostatic factors were observed with fibrinolytic variables, particularly plasminogen activator inhibitor-1 (PAI-1) levels (r = .44, P < .0001). This relation decreased somewhat (r = .29) after simultaneous adjustment for markers of the insulin resistance syndrome, mainly body mass index and triglycerides, but not after adjustment for markers of inflammation. Therefore, we propose that increased PAI-1 levels, which are essentially related to the classic metabolic aspect of the insulin resistance syndrome, have to be included in this syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)Keywords
This publication has 36 references indexed in Scilit:
- Plasminogen activator inhibitor-1 synthesis in the human hepatoma cell line Hep G2. Metformin inhibits the stimulating effect of insulin.Journal of Clinical Investigation, 1993
- Insulin and Atheroma: 20-Yr PerspectiveDiabetes Care, 1990
- Plasma plasminogen activator inhibitor-1 in angina pectoris. Influence of plasma insulin and acute-phase response.Arteriosclerosis: An Official Journal of the American Heart Association, Inc., 1989
- PLASMINOGEN ACTIVATOR INHIBITOR IN PLASMA: RISK FACTOR FOR RECURRENT MYOCARDIAL INFARCTIONThe Lancet, 1987
- Fibrinogen as a Risk Factor for Stroke and Myocardial InfarctionNew England Journal of Medicine, 1984
- Fatty acids, fibrinogen and blood flow: A general mechanism for hyperfibrinogenemia and its pathologic consequencesMedical Hypotheses, 1980
- Coronary Heart Disease Incidence and Cardiovascular Mortality in Busselton with Reference to Glucose and Insulin ConcentrationsDiabetes Care, 1979
- Effect of insulin in the induction and regression of experimental cholesterol atherosclerosis in the rabbitPublished by Oxford University Press (OUP) ,1978
- Development of Vascular Lesions in Insulin-treated Animals Fed a Normal DietBMJ, 1970
- INSULIN-STIMULATED LIPOGENESIS IN ARTERIAL TISSUE IN RELATION TO DIABETES AND ATHEROMAThe Lancet, 1968