Introduction: Diastolic dysfunction represents a significant pathophysiology in cardiomyopathies and heart failure (HF), yet limited therapies exist for treatment. Direct Mechanical Ventricular Actuation (DMVA) is a non-blood contacting device highly unique in its ability to provide both diastolic and systolic support. The purpose of this study was to further evaluate DMVA’s effect on diastolic function in the failing heart. Methods: Adult canine (63.7 ± 13.4 lb, n=9) underwent repeated cycles of ventricular fibrillation to generate progressive levels of acute HF. DMVA was applied to support HF after defibrillation. Intracardiac echocardiography was used to quantify LV longitudinal strain/strain rates using speckle-tracking algorithms. Strain/strain rate peak magnitudes and composite waveforms were analyzed during baseline (n = 35), DMVA (n = 127), and non-support HF (n = 127). One-way ANOVA with post-hoc Tukey’s HSD was used to assess statistical differences (p<0.05) for all comparisons. Results: LV strain metrics were augmented during DMVA support (strain: 20.0 ± 0.5 %, strain rate: systolic, -1.64 ± 0.03 1/s, diastolic, 1.68 ± 0.04 1/s) versus non-supported HF (strain: 9.9 ± 0.2 %, p<0.001, strain rate: systolic, -0.83 ± 0.02 1/s, p<0.001, diastolic, 0.86 ± 0.02 1/s, p<0.001). All strain metrics were increased during DMVA compared to baseline (strain: 14.2 ± 0.4 %, p<0.001, strain rate: systolic, -1.11 ± 0.03 1/s, p<0.001, diastolic, 1.14 ± 0.04 1/s, p<0.001). Composite strain waveforms aligned by systolic peak revealed an early diastolic boost during DMVA relative to baseline (see figure). Conclusions: Diastolic strain dynamics were significantly improved during DMVA in this model of progressive HF. Direct cardiac compression devices can impair diastolic function, which limits feasibility for circulatory support. This study further validates that DMVA restores near physiologic LV strain patterns during HF and uniquely augments diastolic function.