کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5944342 | 1172343 | 2015 | 5 صفحه PDF | دانلود رایگان |

- Contrast-enhanced ultrasonography was used to assess the vasa vasorum signal in type 1 diabetes.
- Increased carotid wall vasa vasorum signal was found in type 1 diabetic patients.
- The results confirm that vasa vasorum are a site for diabetic microangiopathy.
- Microangiopathy of large vessel wall may contribute to diabetic atherosclerosis.
ObjectiveWe hypothesize that in type 1 diabetes vasa vasorum (VV) are affected by microangiopathic changes. For this purpose, we assessed the status of the VV signal in patients with type 1 diabetes.MethodsThe VV signal at the arterial adventitia of the common carotid artery was evaluated by contrast-enhanced ultrasound imaging. The VV contrast agent signal was quantified in an plaque-free arterial segment as the ratio of the adventitial signal and that of the lumen of the artery. We studied 113 type 1 diabetic patients, 60 with and 53 without retinopathy and without known cardiovascular disease, and a group of 78 non-diabetic subjects free of cardiovascular risk factors. All study subjects underwent a clinical evaluation.ResultsThe mean ± standard deviation VV signal of healthy subjects was 0.562 ± 0.135. Type 1 diabetic patients showed a higher adventitial VV signal (0.723 ± 0.128) than non-diabetic subjects (P < 0.0001). After adjustment for cardiovascular risk confounders, this difference remained significant. No differences in VV signal, or common carotid intima-media thickness, between subjects with and without retinopathy were found.ConclusionsType 1 diabetic patients, independently of their retinopathy status, show an increased angiogenesis of the VV of the common carotid artery compared with non-diabetic subjects. Diabetic microangiopathy, that according to our results would also affect the wall of the large arteries, could be a factor contributing to atherosclerosis in type 1 diabetes mellitus.
Journal: Atherosclerosis - Volume 241, Issue 2, August 2015, Pages 334-338