METABOLIC FEATURES OF PATIENTS WITH AND WITHOUT CORONARY HEART-DISEASE BUT WITH A SUPERIMPOSABLE CLUSTER OF CARDIOVASCULAR RISK-FACTORS

Background: Many studies have shown a significant association between the magnitude of insulin resistance and the plasma insulin levels in n on-diabetic patients. It has also been shown that all major cardiovasc ular risk factors are associated with the presence of hyperinsulinemia or insulin resistance. However, studies have not addressed the possib le metabolic differences in insulin action that can occur in patients with and without coronary heart disease (CHD) but with a superimposabl e cluster of risk factors. Methods: Three groups of patients matched f or age, sex, and lean body mass, but different in their absence of ris k factors (group A; n = 8), presence of risk factors but no clinical a nd electrocardiographic signs of CHD (group B; n = 12), and the presen ce of risk factors, family history of CHD, and clinical and electrocar diographic signs of CHD (group C; n = 14) volunteered for the study. P atients in groups B and C were also matched for main risk factors. All patients were submitted to a euglycemic hyperinsulinemic glucose clam p during which a an infusion of 3H-glucose and indirect calorimetry fa cilitated the determination of glucose turnover parameters and substra te oxidation. Results: Patients with CHD (group C) had the highest fas ting plasma insulin levels (98+/-13 pmol/l) compared with patients in group B (86+/-4 pmol/l; P<0.05) and in group A (63+/-4 pmol/l; P<0.05) and the lowest insulin-mediated stimulation in non-oxidative glucose metabolism. Fasting lipid oxidation was similar in the three groups, b ut a stronger insulin-mediated inhibition in the control patients (gro up A) was found. Multiple regression analysis of the pooled data from the patients in groups B and C (n=26) demonstrated that all risk facto rs considered correlated (t=1.58, P<0.04) with total body glucose disp osal (TBGD) and accounted for 77% of the variability in TBGD. Furtherm ore, a separate analysis for groups B and C demonstrated a different c ontribution of all risk factors (89% and 65% for groups B and C, respe ctively) to the variability in TBGD. In group C patients, a multiple l ogistic regression analysis encompassing all risk factors studied, but also the family history of CHD, explained 92% of the variability in T BGD. Conclusion: In patients with and without CHD but with similar ris k factors, a significant reduction in non-oxidative glucose metabolism occurs; nevertheless, such impaired glucose handling seems to be wors ened in the presence of CHD. Further studies will be needed to determi ne the cause of such differences.