Oana Maftei1, Alexia S Pena2, Thomas Sullivan3, Timothy W Jones4, Kim C Donaghue5, Fergus J Cameron6, Elizabeth Davis4, Andrew Cotterill7, Maria E Craig5, Roger Gent1, Neil Dalton8, Denis Daneman9, David Dunger10, John Deanfield11, Jenny J Couper12. 1. Departments of Endocrinology and Diabetes and Medical Imaging, Women's and Children's Hospital, Adelaide, Australia. 2. Departments of Endocrinology and Diabetes and Medical Imaging, Women's and Children's Hospital, Adelaide, Australia Robinson Institute and Discipline of Paediatrics, University of Adelaide, Adelaide, Australia. 3. School of Population Health, University of Adelaide, Adelaide, Australia. 4. Department of Endocrinology and Diabetes, Princess Margaret Hospital for Children, Subiaco, Australia Telethon Institute for Child Health Research, University of Western Australia, Subiaco, Australia School of Paediatrics and Child Health, University of Western Australia, Subiaco, Australia. 5. Institute of Endocrinology and Diabetes, The Children's Hospital at Westmead, Sydney, Australia. 6. Department of Endocrinology and Diabetes, Royal Children's Hospital, Melbourne, Australia Department of Paediatrics, University of Melbourne, Melbourne, Australia Murdoch Childrens Research Institute, Melbourne, Melbourne, Australia. 7. Department of Paediatric Endocrinology, Mater Children's Hospital, Brisbane, Australia. 8. WellChild Laboratory, St. Thomas' Hospital, London, U.K. 9. Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Canada. 10. University Department of Paediatrics, Addenbrooke's Hospital, Cambridge, U.K. 11. National Centre for Cardiovascular Disease Prevention and Outcomes, University College London, London, U.K. 12. Departments of Endocrinology and Diabetes and Medical Imaging, Women's and Children's Hospital, Adelaide, Australia Robinson Institute and Discipline of Paediatrics, University of Adelaide, Adelaide, Australia jennifer.couper@adelaide.edu.au.
Abstract
OBJECTIVE: The origins of cardiovascular and renal disease in type 1 diabetes begin during childhood. We aimed to evaluate carotid (cIMT) and aortic intima-media thickness (aIMT) and their relationship with cardiovascular risk factors and urinary albumin excretion in adolescents with type 1 diabetes in the Adolescent Type 1 Diabetes cardio-renal Intervention Trial (AdDIT). RESEARCH DESIGN AND METHODS: A total of 406 adolescents with type 1 diabetes, who were 14.1 ± 1.9 years old with type 1 diabetes duration of 6.7 ± 3.7 years, and 57 age-matched control subjects provided clinical and biochemical data and ultrasound measurements of vascular structure (cIMT and aIMT). Vascular endothelial and smooth muscle function was also measured in 123 of 406 with type 1 diabetes and all control subjects. RESULTS: In type 1 diabetic subjects, mean/maximal aIMT (P < 0.006; <0.008), but not mean/maximal cIMT, was greater than in control subjects. Mean/maximal aIMT related to urinary albumin-to-creatinine ratio (multiple regression coefficient [SE], 0.013 [0.006], P = 0.03; 0.023 [0.007], P = 0.002), LDL cholesterol (0.019 [0.008], P = 0.02; 0.025 [0.011], P = 0.02), and age (0.010 [0.004], P = 0.004; 0.012 [0.005], P = 0.01), independent of other variables. Mean/maximal cIMT was greater in males (0.023 [0.006], P = 0.02; 0.029 [0.007], P < 0.0001), and mean cIMT related independently to systolic blood pressure (0.001 [0.001], P = 0.04). Vascular smooth muscle function related to aIMT and cIMT but not to urinary albumin excretion. CONCLUSIONS: aIMT may be a more sensitive marker of atherosclerosis than cIMT in type 1 diabetes during mid-adolescence. Higher urinary albumin excretion, even within the normal range, is associated with early atherosclerosis and should direct clinical attention to modifiable cardiovascular risk factors.
OBJECTIVE: The origins of cardiovascular and renal disease in type 1 diabetes begin during childhood. We aimed to evaluate carotid (cIMT) and aortic intima-media thickness (aIMT) and their relationship with cardiovascular risk factors and urinary albumin excretion in adolescents with type 1 diabetes in the Adolescent Type 1 Diabetes cardio-renal Intervention Trial (AdDIT). RESEARCH DESIGN AND METHODS: A total of 406 adolescents with type 1 diabetes, who were 14.1 ± 1.9 years old with type 1 diabetes duration of 6.7 ± 3.7 years, and 57 age-matched control subjects provided clinical and biochemical data and ultrasound measurements of vascular structure (cIMT and aIMT). Vascular endothelial and smooth muscle function was also measured in 123 of 406 with type 1 diabetes and all control subjects. RESULTS: In type 1 diabetic subjects, mean/maximal aIMT (P < 0.006; <0.008), but not mean/maximal cIMT, was greater than in control subjects. Mean/maximal aIMT related to urinary albumin-to-creatinine ratio (multiple regression coefficient [SE], 0.013 [0.006], P = 0.03; 0.023 [0.007], P = 0.002), LDL cholesterol (0.019 [0.008], P = 0.02; 0.025 [0.011], P = 0.02), and age (0.010 [0.004], P = 0.004; 0.012 [0.005], P = 0.01), independent of other variables. Mean/maximal cIMT was greater in males (0.023 [0.006], P = 0.02; 0.029 [0.007], P < 0.0001), and mean cIMT related independently to systolic blood pressure (0.001 [0.001], P = 0.04). Vascular smooth muscle function related to aIMT and cIMT but not to urinary albumin excretion. CONCLUSIONS: aIMT may be a more sensitive marker of atherosclerosis than cIMT in type 1 diabetes during mid-adolescence. Higher urinary albumin excretion, even within the normal range, is associated with early atherosclerosis and should direct clinical attention to modifiable cardiovascular risk factors.
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