Introduction: Left ventricular non-compaction (LVNC) is associated with an increase risk of heart fa-ilure (HF). If LVNC or hypertrabeculation in HF with preserved ejection fraction (HFpEF) is an adaptive or stand-alone condition that contribute to generation of HF is not clearly understood yet.

Objective: To describe LV functional and structural parameters in HFpEF with LVNC by comparison with HFpEF without LVNC.

Methods: We assessed 42 patients with HFpEF, 21 with LVNC (61 ± 9 years) and 21 without LVNC (LVC), aged and risk factor matched, by NTproBNP, 2D echo-cardiography (2DE), speckle-tracking (STE) and cardiac magnetic resonance (CMR). LVNC diagnosis was based on Petersen and Jacquier criteria, by the NC/C ratio and the percentage of NC myocardium. We measured global longitudinal strain (GLS) and we defined furthermore a global deformation for basal strain (LSb), apical strain (LSa) and also for endocardial and epicardial layers. Two gradients were calculated: a base to apex gradient (LV base-apex) and an endo-epicardial gradient (LV endo-epi). T1 mapping with extra-cellular volume (ECV) quantification was performed and mean value of native T1 for apical segments (apical T1), mean value of ECV for apical (apical ECV) and basal segments (basal ECV) and gradient between them (ECV base-apex gradient) were calculated.

Results: In the LVNC, mean NC/C ratio was 2.9 ± 0.5 and the percentage of NC myocardium was 24.41 ± 8.8%. NTproBNP was significant higher in LVNC group (294 ± 282pg/ml vs. 163 ± 71pg/ml, p= 0.047). Functional echocardiographic findings were consis-tent with the structural changes from CMR. We found lower values for LSa in LVNC group compared with LVC group (-21.1 ± 4.4% vs. -24.7 ± 3.1%, p= 0.004) with significant lower LV base-apex (3.27 ± 4.1% vs. 6.81 ± 3.8%, p= 0.006) and LV endo-epi gradients (3.98 ± 0.9% vs. 4.95 ± 1.1%, p= 0.003). Accordingly, LVNC patients have higher native apical T1 (1059 ± 73ms vs. 1007 ± 40ms, p= 0.007). ECV was globally expanded in LVNC compared to LVC (p= 0.002) suggesting diffuse fibrosis, but the difference between groups was more relevant for apical ECV (29.6 ± 3.9% vs. 25.1 ± 2.8%, p< 0.001), with a higher ECV base-apex gradient (3.27 ± 3.1% vs. 0.94 ± 1.8%, p= 0.007) in LVNC group. ECV base-apex was negatively correlated with the percenta-ge of NC myocardium (p= 0.003, R= 0.64).

Conclusions: Patients with HFpEF with LVNC have more fibrosis, with more severe changes in the apical segments on CMR than patients with HFpEF without NC. They have also significantly decreased apical deformation, lower base to apex deformation gradient and lower transmural deformation gradient, due to non-compaction itself, which involves the endocardial layers. This findings suggests that NC in HFpEF is an independent condition rather than an adaptive one.