Blood Glucose Levels In Range Research Articles

Is Nondiabetic Hyperglycemia a Risk Factor for Cardiovascular Disease?

Although hyperglycemia increases the risk of cardiovascular disease (CVD) in diabetic patients, the risk associated with blood glucose levels in the nondiabetic range remains unsettled. We identified 38 reports in which CVD incidence or mortality was an end point, blood glucose levels were measured prospectively, and the relative risk (RR) and information necessary to calculate the variance were reported comparing groups of nondiabetic people. These reports were prospective studies, published in English-language journals. First author, publication year, participant age and sex, study duration, CVD end points, glucose assessment methods, control for confounding, range of blood glucose levels, RR, and confidence intervals (CIs) or P values were extracted. Using a random effects model, we calculated pooled RRs and 95% CIs. The group with the highest postchallenge blood glucose level (midpoint range, 150-194 mg/dL [8.3-10.8 mmol/L]) had a 27% greater risk for CVD compared with the group with the lowest level (midpoint range, 69-107 mg/dL [3.8-5.9 mmol/L]) (RR, 1.27 [95% CI, 1.09-1.48]). The results were similar when combining studies regardless of type of blood glucose assessment (RR, 1.36 [95% CI, 1.23-1.52]) and when using strict criteria for exclusion of diabetic subjects (RR, 1.26 [95% CI, 1.11-1.43]). Adjustment for CVD risk factors attenuated but did not abolish this relationship (RR, 1.19 [95% CI, 1.07-1.32]). The RR was greater in cohorts including women than in cohorts of men (RR, 1.56 vs 1.24 [P = .03]). Blood glucose level is a risk marker for CVD among apparently healthy individuals without diabetes.

Blood glucose and platelet-dependent thrombosis in patients with coronary artery disease

OBJECTIVESTo investigate the influence of blood glucose on platelet-dependent thrombosis (PDT).BACKGROUNDElevated blood glucose is a predictor of adverse cardiovascular risk independent of a diagnosis of diabetes, possibly due to adverse effects promoting thrombosis. The effects of blood glucose on PDT have not been characterized.METHODSAn ex vivo extracorporeal perfusion protocol was used to measure PDT in 42 patients with stable coronary artery disease (CAD). The Badimon chamber was perfused with unanticoagulated venous blood and PDT evaluated using computerized morphometry. Whole blood impedance aggregometry and flow cytometry evaluated platelet aggregation and P-selectin expression, respectively.RESULTSUsing a multivariate stepwise regression model, blood glucose was the best independent predictor of PDT (R2= 0.19, p < 0.008), followed by apolipoprotein B (R2= 0.18, p = 0.002) and intracellular magnesium levels (R2= 0.12, p = 0.02). Platelet-dependent thrombosis was significantly greater in patients with blood glucose >, compared with ≤, the median value of 4.9 mmol/l (159 ± 141 vs. 67 ± 69 μm2/mm, p < 0.01). Neither platelet aggregation nor P-selectin expression was significantly different between the two groups. Insulin levels correlated with blood glucose (r = 0.56, p = 0.0003), but were not independently associated with either PDT, platelet aggregation or P-selectin expression. A two-way analysis of variance demonstrated an interaction between insulin (>126 pmol/l) and blood glucose (>4.9 mmol/l) in modulating PDT (F [1,38] = 8.5, p < 0.006).CONCLUSIONSBlood glucose is an independent predictor of PDT in stable CAD patients. The relationship is evident even in the range of blood glucose levels considered normal, indicating that the risk associated with blood glucose may be continuous and graded. These findings suggest that the increased CAD risk associated with elevated blood glucose may be, in part, related to enhanced platelet-mediated thrombogenesis.

Cardiorespiratory fitness, glycemic status, and mortality risk in men.

To determine the association of baseline cardiorespiratory fitness to all-cause mortality across the range of blood glucose levels. Data from a prospective study of 8715 men (average age 42 yr), followed for an average of 8.2 yr (range 1-15 yr), were analyzed. Cardiorespiratory fitness was assessed by maximal-exercise treadmill testing. Men with evidence of clinical vascular disease or who did not achieve 85% of their age-predicted maximum heart rate during exercise testing were excluded from analyses. Age-adjusted death rates increased with higher levels, of fasting blood glucose. Regardless of glycemic status, fit men had lower age-adjusted all-cause death rates than their less fit counterparts. For men with fasting blood glucose greater than or equal to 7.8 mM or physician-diagnosed non-insulin-dependent diabetes mellitus (NIDDM), the age-adjusted death rates per 10,000 person-yr of follow-up in unfit and fit subjects were 82.5 and 45.9, respectively. The age-adjusted relative risk of death due to all causes was significantly elevated in the lower-fitness group within each of three glycemic status levels: fasting blood glucose less than 6.4 mM; relative risk (RR) = 1.93 (95% confidence interval [95% CI] 1.15-3.26); fasting blood glucose 6.4-7.8 mM; RR = 3.42 (95% CI 2.27-5.15); and fasting blood glucose greater than or equal to 7.8 mM or with NIDDM, RR = 1.80 (95% CI = 1.25-2.58). Multivariate analyses, controlling for risk factors of mortality (age, resting systolic blood pressure, serum cholesterol, body mass index, family history of heart disease, follow-up interval, and smoking habit) showed a higher risk of death due to all causes for unfit compared with fit men. Multivariate risks of death associated with low fitness, compared with higher fitness (RR), in the three glycemic status groups were: fasting blood glucose less than 6.4 mM, RR = 1.38 (95% CI 1.09-1.74); fasting blood glucose 6.4-7.8 mM, RR = 1.61 (95% CI 0.91-2.86); and fasting blood glucose greater than or equal to 7.8 mM or with NIDDM, RR = 1.92 (95% CI 0.75-4.90).