Hypertrophic cardiomyopathy (HCM) is a complex genetic disease, characterized by thickening of the myocardial wall and associated with progressive heart failure. Determinants of heart failure include left-ventricular (LV) outflow obstruction due to systolic anterior motion (SAM) of the mitral valve and diastolic dysfunction¹. As a consequence, HCM induced LV hemodynamics in patients with HCM during the ejection and filling phase may be altered compared to healthy controls. Current hemodynamic assessment in HCM is limited to the assessment of peak left ventricular outflow tract (LVOT). Recently, Allen et al. showed that deranged 3D flow patterns in the ascending aorta, measured with 4D flow MRI, correlated with SAM and LVOT gradient². Altered LV hemodynamics may thus contribute to the occurrence of heart failure, but a systematic assessment of 3D hemodynamic changes in the LV in HCM patients has not been performed to date. Therefore, the aim of this was study was to employ 4D flow MRI to derive LV hemodynamics of the ejection and filling phase. Our goal was to to identify regions with altered velocity in HCM patients based on the concept of an 'LV flow atlas' derived from healthy controls.Eight patients (mean age: 43±19 years, range: 18-68 years, 5 men) with asymmetric basal-septal hypertrophy were referred for cardiac MRI as part of HCM assessment. Additionally, 11 healthy controls (mean age: 54±15 years, range: 20-74 years, 8 men) were included. All subjects underwent an MRI examination on 1.5T systems (Magnetom Avanto and Aera, Siemens, Erlangen, Germany) that included three-chamber CINEs for the evaluation of the presence of SAM, and respiratory and ECG gated 4D flow MRI to measure time-resolved 3D blood flow velocities with full volumetric coverage of the LV. Pulse sequence parameters were as follows: spatial resolution: 2.9-4.0 x 2.1-2.8 x 2.8-3.2 mm3; temporal resolution: 37-40 ms, TE/TR/FA: 2.2-2.5ms/4.6-4.9ms/7-15°; VENC= 120-250 cm/s. Data preprocessing included correction for background phase correction and velocity aliasing. Three-dimensional phase contrast MR angiograms were created by multiplication of phase contrast magnitude images with absolute velocity images, which were subsequently averaged over time (figure 1a). From these images, the left ventricle was semi-automatically segmented using commercial software (Mimics, Materialise, Leuven, Belgium), see figure 1b. The ejection and filling phase were defined as the cardiac time frame in the first and second half of the cardiac cycle with the highest averaged velocity in the left ventricle, respectively (figure 1c). To investigate whether HCM is characterized by abnormal LV velocity, two atlas-based methods were used: ‘LV Flow Atlas’ and ‘LV Heat maps’. Both maps were created as previously described for aortas³. For this purpose, a ‘shared geometry’ was created for both cohorts. The difference in voxel-wise overlap between the individual LV geometries and the ‘shared’ geometry was quantified.LV volumes in the control cohort were significantly smaller compared to HCM patients (63±18 mL vs. 89±25 mL, Wilcoxon rank sum test: P<0.05). SAM was present in 50% of the patients. In figure 2, overlap maps of the LV geometries for both cohorts are displayed. The mean difference between the individual LV geometries and the ‘shared geometry’ was 15±3% for the HCM patients and 13±3% for the controls. Figure 3 displays the LV flow atlases for the ejection and filling phases for both cohorts. For both cohorts the velocity vectors point towards the LV outflow tract in the ejection phase. During LV filling, a clear pattern with blood flowing in from the left atrium is evident. Figure 4 shows four representative LV heat maps illustrating abnormally elevated (red volume) and decreased (blue volume) blood flow in HCM patients. In the ejection phase, abnormally elevated velocity is found in the LV outflow tract, whereas the filling phase showed elevated velocity in the LV apex. Table 1 summarizes the LV volumes of abnormal velocity in HCM patients compared to controls. In this study, the feasibility of creating LV flow atlases and LV heat maps was shown and applied in patients with HCM. SAM may play an important role in the elevated velocity fields as seen in the HCM atlas and the velocity heat maps for the ejection phase. However, there was no difference in abnormally elevated velocity volumes for patients with SAM compared to without SAM, caused by a high velocity volume in one patient without SAM. The inclusion of more patients is warranted to further investigate the relationship between LV hemodynamics and SAM. LV atlases and heat maps show that left ventricular velocity fields are elevated in the ejection and filling phase in HCM patients.