Abstract

Diabetic cardiomyopathy alterations include the presence of interstitial fibrosis. Diabetes also increases the occurrence of arrhythmias, but the pathophysiology remains unclear. To describe a non-invasive method using high-resolution myocardial T2 time measurement to assess myocardial fibrosis in diabetic mice in vivo and to correlate this fibrosis with ventricular arrhythmias. Cine-FLASH sequences for morphology and function were followed by two multi-slice spin-echo sequences for T2 time assessment, respectively at 20 and 9 ms echo time (resolution 85×85 μm2, slice thickness 1.0 mm, imaging time 15 minutes), in ten 16-week old C57Bl/6J after 8 weeks of streptozotocin-induced diabetes, and ten control mice, under isoflurane anesthesia, on a 11.75T magnet. Programmed stimulation was then realized to assess atrial and ventricular inducibility in both groups. MRI measurements were compared with histological quantification of collagen deposits using picrosirius red staining. T2 time was lower in diabetic mice (13.8 ± 2.8 ms versus 18.9 ± 2.3 ms in the control group ; p < 0.05). This was associated with a significant increase in collagen deposits, as evaluated by picrosirius red staining, in diabetic mice. Morphologic and functional analysis showed no difference in terms of ejection fraction (60.70 ± 5% versus 60.35 ± 4%) between the two groups, but end-systolic(1.28 ± 0.26 μL/g versus 1.04 ± 0.24 μL/g) and end-diastolic volumes (3.22 ± 0.60 μL/g versus 2.67 ± 0.65μL/g) were significantly increased in the diabetic group. During the electrophysiological study, 3 non sustained ventricular tachycardias were induced in diabetic mice (none in the control group) and 4 supra-ventricular arrhythmias (none in the control group). In diabetic cardiomyopathy, T2 assessment can detect the presence of fibrosis at an early stage. Myocardial fibrosis is a potential substrate for the genesis of (supra)-ventricular arrhythmias in diabetes mellitus.

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