Metformin, but not glimepiride, improves carotid artery diameter and blood flow in patients with type 2 diabetes mellitus

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

Depressive symptoms are related with hemostatic factors in middle-aged women: A report from the Study of Women Health Across the Nation (SWAN)

OBJECTIVE: Depression may be a risk factor for coronary heart disease (CHD) morbidity and mortality, but the mechanism(s) for the association are not established. The present study examined the relationship between one possible mechanism, hemostatic factors, and depressive symptoms in middle-aged women. METHOD: We measured levels of fibrinogen, Factor VIIc, plasminogen activator inhibitor antigen-1 (PAI-1), and tissue plasminogen activator antigen (TPA-ag) in 3,016 women aged 42-52 years enrolled in the Study of Women's Health Across the Nation (SWAN). Depressive symptoms were measured by the Center for Epidemiological Studies Depression Scale (CES-D), with scores > 16 suggestive of depression. RESULTS: Depressed women had high levels of all four hemostatic factors ( all p <0 .01). After controlling for age, smoking, ethnicity, prevalent cardiovascular disease, osteoarthritis, and dia-betes, and use of medications (including psychotropics), depressed women still had elevated levels of fibrinogen (mean, 95% confidence intervals 299, 304 ­ 295 mg/dl vs. 291, 294 ­ 288mg/dl, p= 0.003) and Factor VIIc (124, 127 ­ 121 ng/dl vs. 119, 121 ­ 117 ng/dl, p= 0.01) levels, compared to nondepressed women. CONCLUSIONS: These findings suggest that hemostatic factors may be a key me-chanism accounting for the relationship between depression and CHD. [Castilla RC, Bromberger JT, Zhang Y, Perel JM, Matthews KA. Depressive symptoms are related with hemostatic factors in middle-aged women: A report from the Study of Women Health Across the Nation (SWAN). MedUNAB 2004; 7:57-64