Family histories of Type II diabetes and hypertension predict intima–media thickness in patients with Type I diabetes
Aims/hypothesis. Hyperglycaemia predicts microvascular complications but data on macrovascular disease are limited. We searched for predictors of carotid artery intima–media thickness in young adults with Type I (insulin-dependent) diabetes mellitus.
Methods. A total of 71 children (F/M = 34/37) were followed after their diagnosis until they reached 32 ± 1 years of age, when duration of diabetes averaged 22 ± 1 years. Cardiovascular risk markers [lipids, blood pressure, smoking, urinary albumin excretion rate, lifetime glycaemic exposure (A1c months), exercise habits, alcohol consumption, family history] were evaluated at age 21 ± 1 for the baseline examination and at age 32 ± 1 years for the follow-up examination years. During follow-up, intima–media thickness of common and internal carotid arteries and the carotid bulb were quantitated using a high-resolution B-mode ultrasound.
Results. In univariate analysis, age, BMI, blood pressure, lifetime glycaemic exposure, a positive family history of Type II (non-insulin-dependent) diabetes mellitus, hypertension and cardiovascular disease were predictors of carotid intima–media thickness. In multivariate analysis, a positive family history of Type II diabetes predicted maximal (p < 0.05) and common (p < 0.005) carotid artery intima–media thickness, family history of hypertension predicted increases in maximal (p < 0.04), and far wall (p < 0.006) carotid artery intima–media thickness, and lifetime glycaemic exposure was an independent predictor of increased carotid bulb thickness (p < 0.03).
Conclusion/interpretation. Positive family histories of Type II diabetes and hypertension are independent predictors of carotid intima–media thickness in patients with Type I diabetes, and could therefore predispose these patients to atherosclerosis
- Family histories of Type II diabetes and hypertension predict intima–media thickness in patients with Type I diabetes
Volume 45, Issue 5 , pp 711-718
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- A1. University of Helsinki, Department of Medicine, Division of Diabetes, P.O. Box 340, 00029 HUCH, Helsinki, Finland
- A2. Department of Medicine, Division of Cardiology, Helsinki University Central Hospital, Helsinki, Finland
- A3. Department of Medicine, Division of Ophthalmology, Helsinki University Central Hospital, Helsinki, Finland