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Background: Microalbuminuria in Type 2 diabetes is associated with arterial endothelial dysfunction, but the venous bed was never evaluated., Aim: To study the endothelial function in the venous and arterial bed in patients with Type 2 diabetes with normoalbuminuria or microalbuminuria., Material and Methods: We evaluated 28 patients with Type 2 diabetes, glycated hemoglobin (HbA(₁c)) <7.5%, who were classified as normo- (albuminuria <30 mg/24 h; no.=16) or microalbuminuric (albuminuria 30-300 mg/24 h; no.=12). Venous and arterial endothelial function were assessed by the dorsal hand vein technique (venodilation by acetylcholine) and brachial artery flow-mediated vasodilation, respectively., Results: Patients were normotensive (systolic arterial pressure: 131.1±10.6 mmHg) and on good metabolic control (HbA(₁c): 6.6±0.6%). Microalbuminuric patients presented impaired venous (32.9±17.4 vs 59.3±26.5%; p=0.004) and arterial vasodilation (1.8±0.9 vs 5.1±2.4; p<0.001), as compared to normoalbuminuric patients. There was a negative correlation between acetylcholine-induced venodilation and albuminuria (r=-0.62; p<0.001) and HbA(₁c) (r=-0.41; p=0.032). The same was observed between flow mediated arterial vasodilation and albuminuria (r=-0.49; p=0.007) and HbA(₁c) (r=-0.44; p=0.019). Venous and arterial vasodilation was positively correlated (r=0.50; p=0.007)., Conclusions: Both venous and arterial endothelial function are impaired in Type 2 microalbuminuric diabetics, in spite of good metabolic control, suggesting that other factors are involved in its pathogenesis.

Background: The association between TGF-beta1 levels and long-term major adverse cardiovascular events (MACE) in patients with coronary artery disease (CAD) is controversial. No study specifically addressed patients with CAD and diabetes mellitus (DM). The association between TGF-beta1 levels and long-term major adverse cardiovascular events (MACE) in patients with coronary artery disease (CAD) is controversial. No study specifically addressed patients with CAD and diabetes mellitus (DM)., Methods: Patients (n = 135, 30-80 years) referred for coronary angiography were submitted to clinical and laboratory evaluation, and the coronary angiograms were evaluated by two operators blinded to clinical characteristics. CAD was defined as the presence of a 70% stenosis in one major coronary artery, and DM was characterized as a fasting glycemia > 126 mg/dl or known diabetics (personal history of diabetes or previous use of anti-hyperglycemic drugs or insulin). Based on these criteria, study patients were classified into four groups: no DM and no CAD (controls, C n = 61), DM without CAD (D n = 23), CAD without DM (C-CAD n = 28), and CAD with DM (D-CAD n = 23). Baseline differences between the 4 groups were evaluated by the chi2 test for trend (categorical variables) and by ANOVA (continuous variables, post-hoc Tukey). Patients were then followed-up during two years for the occurrence of MACE (cardiac death, stroke, myocardial infarction or myocardial revascularization). The association of candidate variables with the occurrence of 2-year MACE was assessed by univariate analysis., Results: The mean age was 58.2 +/- 0.9 years, and 51% were men. Patients with CAD had a higher mean age (p = 0.011) and a higher percentage were male (p = 0.040). There were no significant baseline differences between the 4 groups regarding hypertension, smoking status, blood pressure levels, lipid levels or inflammatory markers. TGF-beta1 was similar between patients with or without CAD or DM (35.1 x/: 1.3, 33.6 x/: 1.6, 33.9 x/: 1.4 and 31.8 x/: 1.4 ng/ml in C, D, C-CAD and D-CAD, respectively, p = 0.547). In the 2-year follow-up, independent predictors of 2-year MACE were age (p = 0.007), C-reactive protein (p = 0.048) and systolic blood pressure (p = 0.008), but not TGF-beta1., Conclusion: Serum TGF-beta1 was not associated with CAD or MACE occurrence in patients with or without DM.

This study evaluated the association between progressively higher levels of fasting glycemia (G) and insulin resistance parameters with coronary artery disease (CAD) in patients referred for coronary angiography. All 145 patients (age 58.4+/-0.9 years, 51.7% men) underwent clinical and laboratory evaluation before coronary angiography and subjects were divided into four groups: normal (N, <88 mg/dl), high-normal (H-N, 89-99 mg/dl), impaired fasting glucose (IFG, 100-125 mg/dl) and diabetes (DM, >126 mg/dl or known diabetics). Arteriographic evidence of CAD was determined by two criteria: (1) a 30% or greater diameter stenosis in at least one major coronary artery; (2) a 70% or greater diameter stenosis in at least one major coronary artery. HOMA-IR increased progressively according to each group: N=1.74+/-0.2, H-N=3.14+/-0.3, IFG=4.67+/-0.6 and DM=8.00+/-2.9; p=0.001. The proportion of patients with CAD according to both criteria increased with each G level: CAD criteria 1: N=39.4%, H-N=50%, IFG=60% and DM=69.6%, p=0.006; CAD criteria 2: N=27.3%, H-N=30%, IFG=36% and DM=50%, p=0.03. We demonstrated a significant association between subtle disturbances of the glucose metabolism, assessed by subnormal levels of fasting glucose and insulin resistance parameters, and angiographically documented coronary artery disease.