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Noninvasive Assessment of Cardiac Abnormalities in Experimental Autoimmune Myocarditis by Magnetic Resonance Microscopy Imaging in the Mouse
Published on: June 20, 2014
Hypertrophic cardiomyopathy: Cardiac structural and microvascular abnormalities as evaluated with multi-parametric
Yu-Dong Zhang1, Meijiao Li2, Liang Qi1
1Department of Radiology, the First Affiliated Hospital with Nanjing Medical University, China.
Purpose:
To determine the relationship between myocardial structural and microvascular abnormality in hypertrophic cardiomyopathy (HCM) by multi-parametric cardiac MRI.
Materials And Methods:
Twenty-four HCM and eighteen controls were retrospectively included. Left ventricle mass (LVM), LV end-systolic and end-diastolic volume (LVESV, LVEDV), LV ejection fraction (LVEF), and 16-segment wall thickness at ES and ED (SESWT, SEDWT) were assessed with a 2D cine-MRI. Myocardial perfusion (reflected by K(trans)), interstitial volume (Ve) and mean transmit time (MTT) were evaluated with a model-dependent dynamic contrast-enhanced MRI. Myocardial fibrosis was assessed with late gadolinium enhancement (LGE) imaging.
Results:
K(trans) was significantly decreased in LGE-present (0.74±0.15mL/g/min) against LGE-absent (0.55±0.14mL/g/min, p=0.030) and normal group (0.81±0.32mL/g/min, p<0.001), but was unchanged in LGE-absent against normal group (p>0.05). Ve and MTT were significantly increased in LGE-present (Ve: 26.7±15.7%; MTT: 28.6±21.3s) against LGE-absent (37.6±18.3%; 49.8±30.5s) and normal group (19.7±6.9%; 15.1±3.9s; all p<0.001), and were significantly increased in LGE-absent against normal group (p<0.001). LGE significantly correlated to K(trans), Ve, MTT, and SESWT (ρ=0.232, -0.247, -0.443, and -0.207, respectively). K(trans) negatively correlated to SEDWT and SESWT (ρ=-0.224 and -0.231). Ve and MTT positively correlated to SEDWT (Ve: ρ=0.223; MTT: ρ=0.239) and SESWT (Ve: ρ=0.248; MTT: ρ=0.254).
Conclusions:
Consistent relationship was determined between myocardial structural abnormality and microvascular dysfunction in HCM.
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