Altered regional myocardial velocities by tissue phase mapping and feature tracking in pediatric patients with hypertrophic cardiomyopathy

Background Hypertrophic cardiomyopathy (HCM) is associated with heart failure, atrial fibrillation and sudden death. Reduced myocardial function has been reported in HCM despite normal left ventricular (LV) ejection fraction. Additionally, LV fibrosis is associated with elevated T1 and might be an outcome predictor. Objective To systematically compare tissue phase mapping and feature tracking for assessing regional LV function in children and young adults with HCM and pediatric controls, and to evaluate structure–function relationships among myocardial velocities, LV wall thickness and myocardial T1. Materials and methods Seventeen pediatric patients with HCM and 21 age-matched controls underwent cardiac MRI including standard cine imaging, tissue phase mapping (two-dimensional cine phase contrast with three-directional velocity encoding), and modified Look-Locker inversion recovery to calculate native global LV T1. Maximum LV wall thickness was measured on cine images. LV radial, circumferential and long-axis myocardial velocity time courses, as well as global and segmental systolic and diastolic peak velocities, were quantified from tissue phase mapping and feature tracking. Results Both tissue phase mapping and feature tracking detected significantly decreased global and segmental diastolic radial and long-axis peak velocities (by 12–51%, P <0.001–0.05) in pediatric patients with HCM vs. controls. Feature tracking peak velocities were lower than directly measured tissue phase mapping velocities (mean bias = 0.3–2.9 cm/s). Diastolic global peak velocities correlated moderately with global T1 ( r = −0.57 to −0.72, P <0.01) and maximum wall thickness ( r = −0.37 to −0.61, P <0.05). Conclusion Both tissue phase mapping and feature tracking detected myocardial velocity changes in children and young adults with HCM vs. controls. Associations between impaired diastolic LV velocities and elevated T1 indicate structure–function relationships in HCM.