ATLANTA — Adolescents with type 1 diabetes may have early evidence of atherosclerosis, Dr. Maria V. Karantza reported at the annual scientific sessions of the American Diabetes Association.
The increased risk appears to be related to conventional cardiovascular disease risk factors such as dyslipidemia, hemoglobin A1c, and tobacco exposure rather than nontraditional risk factors related to endothelial function, suggesting that strategies targeting modifiable risk factors could benefit these patients, said Dr. Karantza of the University of California, Los Angeles.
Carotid artery intima-medial thickening (IMT), considered an indirect measure of cardiovascular disease (CVD), was evaluated by B-mode ultrasound in 90 adolescents with type 1 diabetes (mean age 16.6 years) with 16 of their healthy siblings (mean age 16.7 years). Overall, IMT was significantly greater among the diabetic group than the controls (0.564 mm vs. 0.54 mm), she reported.
There were no differences between the two groups in body mass index, blood pressure, gender, or family history of diabetes/CVD. None of the controls smoked, while six of the diabetics (all male) were smokers; the difference was not statistically significant.
The two groups also did not differ by conventional risk factors such as cholesterol, triglycerides, or microalbumin/creatinine ratio, or by nontraditional risk factors such as fibrinogen, von Willebrand factor antigen, plasminogen activator inhibitor-1, or IL-6.
When broken down by gender, significant differences in IMT between diabetic and control subjects were only seen among the males (0.582 mm vs. 0.524 mm), and not the females (0.548 mm vs. 0.556 mm).
Among the males with diabetes, IMT was significantly correlated with HbA1c and tobacco exposure, as well as with total cholesterol and apolipoprotein B. Among the female diabetics, IMT was correlated positively with a family history of CVD and negatively correlated with HDL cholesterol.
The findings suggest that conventional CVD risk factors result in increased IMT, and probably cause the initial endothelial dysfunction in these young people. The subsequent loss of normal endothelial homeostatic properties would eventually lead to a “proinflammatory, proadhesive, and procoagulant endothelial surface that is not yet present in our cohort. Early treatment of modifiable risk factors could avert the chronic inflammatory process which, if unabated, will result in the advanced chronic plaque formation,” she said.