Hypertrophic cardiomyopathy: Cardiac structural and microvascular abnormalities as evaluated with multi-parametric MRI

Highlights: • LGE-present HCM had lower K^trans, higher V_e and MTT against LGE-absent HCM and normal group. • LGE-absent had significantly higher V_e and MTT against normal group. • K^trans was not changed between LGE-absent and normal group Microcirculatory dysfunction in HCM closely correlated to structural abnormality. - Abstract: 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 (V_e) 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 ± 0.15 mL/g/min) against LGE-absent (0.55 ± 0.14 mL/g/min, p = 0.030) and normal group (0.81 ± 0.32 mL/g/min, p < 0.001), but was unchanged in LGE-absent against normal group (p > 0.05). V_e and MTT were significantly increased in LGE-present (V_e: 26.7 ± 15.7%; MTT: 28.6 ± 21.3 s) against LGE-absent (37.6 ± 18.3%; 49.8 ± 30.5 s) and normal group (19.7 ± 6.9%; 15.1 ± 3.9 s; all p < 0.001), and were significantly increased in LGE-absent against normal group (p < 0.001). LGE significantly correlated to K^trans, V_e, 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). V_e and MTT positively correlated to SEDWT (V_e: ρ = 0.223; MTT: ρ = 0.239) and SESWT (V_e: ρ = 0.248; MTT: ρ = 0.254). Conclusions: Consistent relationship was determined between myocardial structural abnormality and microvascular dysfunction in HCM