Aortic Intima Media Thickness is an Early Marker of Atherosclerosis in Children with Type 1 Diabetes Mellitus - 07/03/14
, Alexia S. Peña, MD, PhD a, d, Roger Gent, DMU b, Craig Hirte, BSC (hons) c, Jennifer Couper, MD, FRACP a, d
Reprint requests: Jennifer Harrington, Endocrinology and Diabetes Department, Women’s and Children’s Hospital, 72 King William Rd N, Adelaide, SA 5006, Australia.Abstract |
Objective |
To compare aortic intima media thickness (aIMT) to carotid intima media thickness (cIMT) as a marker of early atherosclerosis in children with type 1 diabetes mellitus and to examine the associations of aIMT to known cardiovascular risk factors.
Study design |
66 children with type 1 diabetes mellitus (age, 14.1 ± 2.5 years; 37 male) and 32 healthy control subjects (age, 14.2 ± 3 years; 15 male) underwent assessment of vascular structure (cIMT and aIMT) and vascular function (flow mediated dilatation [FMD] and glyceryl trinitrate induced dilatation [GTN]). Fasting blood tests were taken to measure levels of hemoglobin A1c, high sensitive C reactive protein, total homocyst(e)ine, serum folate, red cell folate, and lipids.
Results |
aIMT, but not cIMT, was significantly greater in the children with type 1 diabetes mellitus than in control subjects (P < .001). In children with type 1 diabetes mellitus, aIMT correlated with glycosylated hemoglobin (r = 0.31, P = .01) and was independently associated with age (β = 0.38, P = .001) and low-density lipoprotein cholesterol level (β = 0.38, P = .001). Vascular function (GTN) was worse in children with type 1 diabetes mellitus who had an aIMT >95th percentile, as defined with the control subjects.
Conclusions |
aIMT is an earlier marker than cIMT of preclinical atherosclerosis in children with type 1 diabetes mellitus and relates to known cardiovascular risk factors and metabolic control.
Le texte complet de cet article est disponible en PDF.Mots-clés : aIMT, cIMT, CV, FMD, GTN, HbA1c, IMT, LDL, RCF, tHcy
Plan
| Supported by a National Health and Medical Research Council grant (#519245) and the Diabetes Australia Research trust. J.H. was supported by the MS McLeod Medical Postgraduate Scholarship. A.P. was supported by Juvenile Diabetes Research Foundation Fellowship provided by The Royal Australasian College of Physicians. The authors declare no conflicts of interest. |
Vol 156 - N° 2
P. 237-241 - février 2010 Retour au numéro
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