Mark P. Anstadt, M.D. (Advisor); David R. Cool, Ph.D. (Committee Member); David L. Goldstein, Ph.D. (Committee Member); Lucile E. Wrenshall, M.D., Ph.D. (Committee Member); Christopher N. Wyatt, Ph.D. (Committee Member)
Doctor of Philosophy (PhD)
Objectives: Heart failure (HF) refractory to medical management can be effectively treated with mechanical support. However, available devices are frequently associated with complications due to blood contact. Direct cardiac compression (DCC) devices augment LV systolic pump function by externally compressing the heart surface. Direct Mechanical Ventricular Actuation (DMVA) is a unique DCC method providing not only systolic but, importantly, diastolic support. However, DCC in general remains a relatively poorly understood modality. The purpose of this study was to examine DMVA’s effect on restoration of physiologic function in the failing heart. Methods: Global ischemic HF was induced with 5 mins of ventricular fibrillation (VF) and circulatory arrest in large mature canines (n=14). Hearts were defibrillated and DMVA was applied to support HF for 15 mins. VF circulatory arrest was re-induced in subsequent cycles to generate progressively worsening HF. Cycling was continued for up to 3 hrs or until defibrillation was no longer successful. Animals were instrumented to record aortic and LV hemodynamics. Intracardiac echocardiography was used to quantify longitudinal strain and strain rates using speckle-tracking algorithms. Four areas relevant to function during cardiac assist were analyzed: (1) pump function, (2) contractile function, (3) intraventricular dyssynchrony, and (4) device/heart coordination. Results were compared between baseline, HF, and DMVA. ANOVA with Tukey HSD tests were used to assess statistical differences (p<0.05). Results: Aortic indicators of pump function during DVMA were attenuated compared to baseline, but indicators of pulsatility were substantially increased. Strain and strain rate waveforms were dramatically augmented by DMVA when applied to the failing heart. Early diastolic strain rates were substantially augmented during DMVA compared to baseline. DMVA increased dyssynchrony in a transient manner that was immediately reversed upon device removal. Increased coordination between the device and heart motions was strongly associated with higher pressure and pressure slopes. Poor coordination was characterized by premature intrinsic contraction. Conclusions: DMVA augmented heart function significantly during severe HF. Significant boosts to pulsatility and strain-based metrics even during mild HF were found to be an important feature of DMVA. Some of these findings may be a characteristic of DCC in general, but diastolic support is a unique feature of DMVA.
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