Abstract Background Adult heart failure in industrialized nations is primarily due to dilated (DCM) and ischemic cardiomyopathy (ICM). Both diseases are characterized by different pathological pathways. While ICM is predominantly caused by local, subendocardial myocyte necrosis, DCM is characterized by a general myocyte apoptosis involving all myocardial layers. Using feature tracking, longitudinal, circumferential, and radial motion of the left ventricle (LV) can be measured, which allows the function of subendocardial, mostly longitudinal orientated, and subepicardial, mostly circumferential orientated fibers to be assessed independently. Purpose It was the aim of our study to detect differences of LV motion between DCM and ICM patients in a propensity score-matched cohort. Methods Between April 2017 and December 2018 we included 845 patients with a clinical indication for CMR in our tertiary care center registry. Out of this cohort we identified 273 patients with ICM and 126 with DCM. Propensity score matching was used to pair patients in each group based on their indexed enddiastolic volume (EDVi), ejection fraction (EF), septal T1. Feature tracking technique was used for strain analyses quantified on steady state free precession cine CMR images yielding six strain parameters. Results Propensity score matching yielded 59 patients in each group (ICM mean age 59.4±13.0 years, 11 females; DCM mean age 66.5±10.6 years, 15 females; LV-EF 32.6±11.4% vs. 33.0±14.2%, p=0.8178; EDVi 124.2±36 ml/m2 vs. 132.9±42 ml/m2, p=0.0909; native T1 values 1161±66 ms vs. 1164±59 ms, p=0.7049). There was no difference in global longitudinal strain between ICM and DCM patients (−10.9±4.4% vs. −10.6±5.8%, p=0.686), whereas global circumferential strain and radial strain were reduced in DCM patients (−12.0±4.3% vs. −10.31±4.8%, p=0.0190 and 21.1±8.9% vs. 18.0±15.5%, p=0.0386). Conclusion Our data confirm the inherently different mechanics of ICM and DCM patients. While myocardial fibres are globally affected in DCM, myocardial damage is predominantly confined to subendocardial layers in ICM despite equally reduced EF.