Abstract

Introduction: Available forms of mechanical circulatory support are associated with significant complications related to blood contact. Direct cardiac compression (DCC) devices avoid blood contact but may impair diastolic function. This derogatory effect of DCC devices may be related to a negative impact on RV function. Direct mechanical ventricular actuation (DMVA) uniquely augments LV diastolic function. The purpose of this study was to evaluate DMVA’s effect on RV function. Methods: Ischemic heart failure (HF) was induced using 5 mins of ventricular fibrillation (VF) circulatory arrest in large mature canines (n=9). Hearts were defibrillated and DMVA applied for 15 mins. VF circulatory arrest was subsequently re-induced for 5 mins to generate progressive HF. The experimental protocol was continued for 3 hrs. Intracardiac echocardiography was used to quantify longitudinal strain and peak strain rates in the RV and LV using speckle-tracking algorithms. Two-way ANOVA with Tukey HSD tests were used to evaluate statistical differences in strain metrics (baseline vs. HF vs. DMVA support and LV vs. RV). Results: DMVA increased RV fractional area change (DMVA: 0.282 ± 0.011, Mean ± SEM) relative to either baseline (0.221 ± 0.15, p=0.004) or HF (0.170 ± 0.006, p<0.001). DMVA statistically significantly augmented all RV strain metrics relative to either baseline or HF (Table). Additionally, all DMVA strain metrics were statistically significantly greater in the RV than the LV (LV strain: 18.8 ± 0.5 %, p<0.001, LV strain rate: systolic, -1.46 ± 0.04 1/s, p<0.001, diastolic, 1.51 ± 0.04 1/s, p<0.001). Conclusions: DMVA substantially improved RV strain dynamics compared to baseline or HF in this model. During DMVA support, strain dynamics in the RV were amplified more than the LV. This RV augmentation is important to achieving balanced biventricular DMVA support. Enhanced diastolic RV and LV augmentation during DMVA remains highly unique when compared to any other devices.

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