The Effects of Carvedilol vs. Metoprolol on Endothelial Function and Oxidative Stress in Patients with Type 2 Diabetes Mellitus.

Carvedilol does not worsen glycemic control in patients with type 2 diabetes mellitus (T2DM) and possesses anti-oxidant properties that might provide vascular protection. We sought to compare the effects of carvedilol and metoprolol tartrate on endothelial function and oxidative stress in a head to head trial. Thirty-four patients with T2DM and hypertension were randomized to receive either carvedilol (n = 16) or metoprolol (n = 18) in addition to their current anti-hypertensive medications for five months. The following variables were "measured pre- and post-treatment: blood pressure, fasting glucose and insulin, homeostasis model assessment, hemoglobin A1c, lipids, C-reactive protein (CRP), 8-isoprostane, asymmetric dimethylarginine, oxidized LDL cholesterol, ultrasound assessment of brachial artery flow-mediated dilation (FMD), nitroglycerin-induced endothelium-independent dilation (EID), brachial and carotid artery distension, distensibility, and compliance. Changes in variables between groups over time were compared with 2X2 (group by time) ANOVA. Background medications were similar between groups. Both carvedilol and metoprolol treatment resulted in significant and equivalent decreases in systolic (p<0.05) and diastolic (p<0.0001) blood pressure. There were no differences between groups for any of the glycemic or lipid variables except HDL cholesterol, which significantly decreased (p<0.05) in the metoprolol compared to carvedilol group. No differences were observed between groups for CRP or the markers of oxidative stress. However, compared to metoprolol, carvedilol significantly improved FMD (carvedilol: 3.5 ± 0.8% to 6.2 ± 0.1% vs. metoprolol: 5.5 ± 0.9% to 4.1 ± 0.9%, p<0.001). There were no differences between groups for EID or arterial stiffness. Compared to metoprolol, carvedilol significantly improves endothelial function in patients with T2DM. Differences in glycemic control and oxidative stress do not seem to explain the observed improvements in FMD, suggesting other mechanisms may be involved. [ABSTRACT FROM AUTHOR]