Search

White blood cell (WBC) count has been shown as a risk factor for cardiovascular disease. Decreased insulin sensitivity has been suggested as the link between these two entities. Our aim was to study the potential relation between insulin sensitivity and WBC count in patients with coronary artery disease. In order to assess insulin sensitivity, we performed 83 insulin suppression tests before and after therapy in 50 patients with coronary artery disease. Patients with glucose intolerance, arterial hypertension or obesity were excluded. Steady-state plasma glucose (SSPG) and insulin sensitivity index (ISI=1 000 x glucose infusion rate/SSPG) were considered as a measure of insulin sensitivity. WBC count, blood platelets, fibrinogen, microalbuminuria, creatinine, urea and HbA1c were also assessed. Simple and multiple correlation analysis were carried out between insulin sensitivity parameters and the other variables measured. There were significant correlation between SSPG and WBC count (r=0,32: p=0,003) and microalbuminuria (r=0,28: p=0,012). We also found statistically significant correlation between ISI and WBC count (r=0,27: p=0,015) and microalbuminuria (r=0,24: p=0,029). No correlation could be detected between either SSPG or ISI and the other variables measured. In multiple regression analysis, WBC count was found to be an independent predictor of both SSPG (p<0.01) and ISI (p<0.05). Our data show the existence of a significant relationship between decreased insulin sensitivity and WBC count in patients with coronary artery disease. The results of this study suggest that an elevated WBC count could be postulated as part of the insulin resistant syndrome.

The objective of the study was to examine the evolution of insulin sensitivity in a group of patients with stable coronary artery disease receiving one of four different pharmacological therapies. Insulin sensitivity was evaluated using an insulin suppression test in 40 newly diagnosed patients with coronary artery disease and no previous history of metabolic disorders, who were not taking any medication which might affect insulin sensitivity. The insulin suppression test consisted of a constant infusion of glucose, insulin and somatostatin for 150 min; insulin resistance was estimated by determining the steady-state plasma glucose concentrations during the last 60 minutes of the test. The insulin sensitivity index was calculated by the formula: insulin sensitivity index = (glucose infusion rate/steady state plasma glucose concentrations) x 10(3). A second insulin suppression test was performed after 6 months' therapy with either isosorbide mononitrate, atenolol, diltiazem or captopril in 30 of the 40 patients. There were no differences between any of the groups before therapy was initiated. After 6 months, patients treated with captopril and, to a lesser extent, those treated with diltiazem showed statistically significantly decreased steady state plasma glucose concentrations and increased insulin sensitivity index compared to basal values. No statistically significant differences were found in the other two groups. We conclude that captopril and, to a lesser extent, diltiazem improve insulin sensitivity in patients with stable coronary artery disease.

Obesity is a metabolic disorder in which multiple clinical and biochemical alterations coexist. However, the progression of these alterations in relation to weight gain has not been investigated in detail. Therefore, we studied the evolution of insulin resistance and associated risk factors in a model of experimental obesity in dogs. We also studied whether chronic exposure to these pathogenic factors could induce cardiac and vascular alterations. Twenty male age- and body weight-matched beagle dogs were divided into four groups (n = 5), according to diet and pharmacologic therapy received, and followed for 2 years. Control animals were maintained with a regular diet, while the 15 remaining animals were fed a high-fat diet. The Obese group of dogs received no therapy, whereas the Capto group received 25 mg/12 h captopril, and the Prava+Capto was treated with 10 mg/24 h pravastatin plus the same dose of captopril throughout the study. Periodical determinations of clinical and biochemical parameters were made, and the degree of insulin resistance was also estimated. After the 2-year follow-up, the dogs were killed and vascular thickening in the aorta and the coronary arteries was evaluated. In addition, cardiac hypertrophy was estimated by heart weight and free-wall left ventricular width. Chronic pravastatin plus captopril treatment, together with decreasing weight gain rate, ameliorated the progression of insulin resistance and associated risk factors (hyperinsulinemia, hypercholesterolemia) related to this severe model. In addition, this combined therapy showed cardioprotective action, as cardiac and vascular hypertrophy observed in the Obese group was prevented. These positive results seems to emerge from the synergistic effects of both drugs, as captopril as monotherapy induced only a slight benefit on these parameters.

Objective: To evaluate insulin sensitivity, and serum levels of sex hormone-binding globulin (SHBG) and dehydroepiandrosterone sulfate (DHEA-sulfate), in patients with essential hypertension., Design and Methods: In 15 non-treated hypertensive patients, insulin resistance was measured by an insulin suppression test (IST). Serum levels of DHEA-sulfate and SHBG were measured at the beginning and at the end of the IST. The results were compared to those of a control group of 10 healthy normotensive subjects matched for age, sex and body mass index (BMI).

Insulin resistance has been related to the pathogenesis and development of ischemic heart disease (IHD). Dehydroepiandrosterone sulfate (DHEA-S) has been suggested as the possible link between these two entities. The aim of this study was to clarify the relationship between insulin resistance and DHEA-S in patients with IHD. Thirty-two male patients with newly-diagnosed IHD and without known metabolic disorders and 11 healthy matched controls were included in this study. Insulin sensitivity was assessed by an insulin suppression test, and DHEA-S levels were measured before the test (basal) and at the end of the test (during hyperinsulinemia). Insulin resistance, defined as an insulin sensitivity index (ISI) below the normal range derived from the control group, was present in 78% of IHD patients; they also displayed, as a group, lower ISI (P < 0.0001) than controls. DHEA-S levels were lower in IHD than in controls, both basal and during hyperinsulinemia (P < 0.05). DHEA-S levels decreased when hyperinsulinemia was achieved, both in IHD patients and controls (P < 0.0005). The magnitude of the decrease was the same in both groups. No correlation between ISI and DHEA-S levels was found. In conclusion, insulin sensitivity is lower in patients with IHD, even when major metabolic abnormalities associated with insulin resistance are excluded. These patients also show decreased DHEA-S levels, which are further reduced when acute induced hyperinsulinemia is achieved, although, as the decline was similar to that of controls, there does not seem to be resistance to this particular action of insulin.

Objective: To elucidate whether insulin resistance is present in coronary artery disease (CAD) at diagnosis and to study its relationship with other known cardiovascular risk factors., Methods: We evaluated the incidence of insulin resistance in 40 newly diagnosed CAD patients. Fifteen healthy subjects were used as a control group. The patients and controls had no previous history of metabolic disorders, and were not being administered any medication that might have affected their insulin sensitivity. Immediately after diagnosis of CAD, a standard 75 g oral glucose-tolerance test (OGTT) and an insulin suppression test (IST) were performed on separate days. The IST consisted of a constant infusion of glucose, insulin and somatostatin for 150 min; insulin resistance was estimated by determining the steady-state plasma glucose (SSPG) concentrations during the last 60 min of the test. The insulin sensitivity index (ISI) was calculated by the formula ISI = (glucose infusion rate/SSPG]x10(3)., Results: Insulin resistance, defined by an ISI below the normal range derived from the control group, was present in 82.5% of the CAD patients. As a group, the patients with CAD displayed lower ISI (means +/- SD:29.23 +/- 11.23 versus 50.33 +/- 9.37 dl/kg per min, P < 0.001) than did controls. Serum triglycerides and uric acid were higher and high-density lipoprotein cholesterol levels were lower in patients than they were in controls. No differences were observed in fasting plasma insulin, glucose, total and low-density lipoprotein cholesterol concentration. An abnormal OGTT result was observed in 27 patients. The ISI was low in 88.8% of the patients with an abnormal OGTT result and in 69% of the 13 patients with a normal OGTT result., Conclusions: Insulin resistance and even impaired glucose tolerance are common findings in CAD at diagnosis. The changes in the lipid profile and in uric acid levels paralleled the changes in insulin sensitivity. These results suggest that insulin resistance might play a role in the development of coronary atherosclerosis and that its early diagnosis might be important in the prophylaxis of CAD.

Soon after the discovery of insulin, the importance of insulin sensitivity assessment was recognised. Recently, the role of insulin resistance in cardiovascular morbidity and mortality has been widely accepted and many methods for in vivo assessment of insulin resistance have been developed. They may be classified as 'closed-loop' techniques (in which insulin and glucose concentrations are allowed to interact freely), 'open-loop' techniques (in which insulin and/or glucose levels are fixed) and 'model methods' (which use a mathematical model to analyse the interactions between insulin secretion patterns and glucose disposal). Although there is no ideal method available to date, open-loop techniques avoid many of the difficulties involved in the interpretation of closed-loop or model methods, and are preferred by most investigators. The glucose clamp technique is recognised as the 'gold standard' for assessment of insulin sensitivity; however, the insulin suppression test is adequate in most circumstances and is much simpler to perform.