Esther Rubinat1, Emilio Ortega2, Alicia Traveset3, Maria V Arcidiacono4, Nuria Alonso5, Angels Betriu4, Minerva Granado-Casas6, Marta Hernández7, Jordi Soldevila3, Manel Puig-Domingo5, Carmen Jurjo3, Elvira Fernández4, Didac Mauricio8. 1. Institut de Recerca Biomedica de Lleida, University of Lleida, Rovira Roure, 80, 25198 Lleida, Spain; Unitat de Detecció i Tractament de Malalties Aterotrombòtiques, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain. 2. Department of Endocrinology and Nutrition, Institut d'Investigacions Biomediques August Pi Suñer, Hospital Clinic, Villarroel, 170, 08036 Barcelona, Spain. 3. Department of Ophthalmology, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain. 4. Unitat de Detecció i Tractament de Malalties Aterotrombòtiques, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain; Department of Nephrology, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain. 5. Department of Endocrinology & Nutrition, University Hospital and Health Sciences Research Institute Germans Trias Pujol, Carretera Canyet S/N, 08916 Badalona, Spain. 6. Unitat de Detecció i Tractament de Malalties Aterotrombòtiques, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain. 7. Unitat de Detecció i Tractament de Malalties Aterotrombòtiques, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain; Department of Endocrinology and Nutrition, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain. 8. Unitat de Detecció i Tractament de Malalties Aterotrombòtiques, Hospital Universitari Arnau de Vilanova, Rovira Roure, 80, 25198 Lleida, Spain; Department of Endocrinology & Nutrition, University Hospital and Health Sciences Research Institute Germans Trias Pujol, Carretera Canyet S/N, 08916 Badalona, Spain. Electronic address: didacmauricio@gmail.com.
Abstract
OBJECTIVE: We 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. METHODS: The 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. RESULTS: The 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. CONCLUSIONS: Type 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.
OBJECTIVE: We 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. METHODS: The 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 diabeticpatients, 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. RESULTS: The mean ± standard deviation VV signal of healthy subjects was 0.562 ± 0.135. Type 1 diabeticpatients 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. CONCLUSIONS: Type 1 diabeticpatients, 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.