BackgroundCoronary microvascular dysfunction (CMD) is an early character of type 2 diabetes mellitus (T2DM), and is indicative of adverse events. The present study aimed to validate the performance of the stress T1 mapping technique on cardiac magnetic resonance (CMR) for identifying CMD from a histopathologic perspective and to establish the time course of CMD-related parameters in a rabbit model of T2DM.MethodsNew Zealand white rabbits (n = 30) were randomly divided into a control (n = 8), T2DM 5-week (n = 6), T2DM 10-week (n = 9), and T2DM 15-week (n = 7) groups. The CMR protocol included rest and adenosine triphosphate (ATP) stress T1-mapping imaging using the 5b(20b)3b-modified look-locker inversion-recovery (MOLLI) schema to quantify stress T1 response (stress ΔT1), and first-pass perfusion CMR to quantify myocardial perfusion reserve index (MPRI). After the CMR imaging, myocardial tissue was subjected to hematoxylin-eosin staining to evaluate pathological changes, Masson trichrome staining to measure collagen volume fraction (CVF), and CD31 staining to measure microvascular density (MVD). The associations between CMR parameters and pathological findings were determined using Pearson correlation analysis.ResultsThe stress ΔT1 values were 6.21 ± 0.59%, 4.88 ± 0.49%, 3.80 ± 0.40%, and 3.06 ± 0.54% in the control, T2DM 5-week, 10-week, and 15-week groups, respectively (p < 0.001) and were progressively weakened with longer duration of T2DM. Furthermore, a significant correlation was demonstrated between the stress ΔT1 vs. CVF and MVD (r = −0.562 and 0.886, respectively; p < 0.001).ConclusionThe stress T1 response correlated well with the histopathologic measures in T2DM rabbits, indicating that it may serve as a sensitive CMD-related indicator in early T2DM.
Purpose: The purpose of this paper was to verify that the linear high-intensity signal on late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) may represent the contrast enhancement of vessels rather than scars or fibrosis, and to assess whether this linear high-intensity signal will affect the quantification of myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM).Methods: A total of 58 patients who underwent both coronary computed tomography angiography (CCTA) and LGE-CMR in our hospital were ultimately enrolled. The definitions of positive linear LGE (LLGE+) were as follows: (1) LLGE in the basal anterior septum or lateral wall, and (2) LLGE observable at 10 mm or more. All other patients were regarded as negative LLGE (LLGE-). In LLGE+ patients, the length of the LLGE located in the anterior septum and lateral wall was compared with the length of the septal perforator artery and the circumflex artery on CCTA, respectively. For nine patients with HCM, the LGE% was measured before and after removal of LLGE.Results: Among the 58 patients, 40 of whom showed LLGE+ and 18 of whom showed LLGE-. For patients with LLGE in the anterior septum, there was a strong correlation between LLGE and anterior septal perforator arteries in length (r=0.887, p<0.001). For patients with LLGE in the lateral wall, LLGE also correlated well with the circumflex arteries in length (r=0.962, p<0.001). In nine patients with HCM, the LGE% decreased significantly after the removal of LLGE (18.6 [14.15 - 27.5] vs. 12.4 [9.8 - 17.5], p<0.05).Conclusions: The LLGE in the anterior septum and lateral wall may represent contrast enhancement of the anterior septal perforator artery and the circumflex artery, respectively. This LLGE may overestimate the extent of myocardial fibrosis in patients with hypertrophic cardiomyopathy.
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