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Left ventricular assist device (LVAD) inflow cannula malposition is a significant risk for pump thrombosis. Thrombus development is influenced by altered flow dynamics, such as stasis or high shear that promote coagulation. The goal of this study was to measure the intraventricular flow field surrounding the apical inflow cannula of the Evaheart centrifugal LVAD, and assess flow stasis, vortex structures, and pulsatility for a range of cannula insertion depths and support conditions. Experimental studies were performed using a mock loop with a customized silicone left ventricle (LV) and the Evaheart LVAD. A transparent inflow cannula was positioned at 1, 2, or 3 cm insertion depth into the LV and the velocity field in the LV midplane was measured for 2 levels of LVAD support: 1800 and 2300 rpm. The LV velocity field exhibits a diastolic vortex ring whose size, path, and strength are affected by the flow conditions and cannula position. During diastole, the large clockwise midplane vortex grows, but its circulation and kinetic energy are reduced with cannula insertion depth. The counterclockwise vortex is smaller and exhibits more complex behavior, reflecting a flow split at 3 cm. Overall, the 1 cm cannula insertion depth produces the flow pattern that exhibits the least apical flow stasis and greatest pulsatility and should correlate to a lower risk of thrombus formation.

Abstracts S319position had the greatest pulsatility and the least flow stasis of all three positions, especially in the apical region. The results of this study indicate that the C_3 position, in which the cannula is inserted the furthest into the LV, produces a flow pattern with a lower apical thrombus risk than the C_2 pattern. Conclusion: Overall, the C_1 cannula position exhibits the least apical flow stasis and greatest pulsatility and is predicted to have the lowest thromboembolic risk of the three cannula positions studied. ( 880) WITHDRAWN ( 881)Purpose: Advanced heart failure (HF) is a characterized by poor functional capacity, fluid retention, elevated filling pressures and increased arrhythmia burden. Autonomic imbalance leading to sympathetic activation and reduced vagal activity plays a key role in mediating these symptoms. Heart rate variability (HRV) is a physiologic marker that provides an assessment of autonomic function. The EACP device is a chronic counterpulsation therapy consisting of an external cuff wrapped around the ascending aorta. We report the chronic effects of EACP therapy on autonomic function in advanced HF patients using HRV derived from implantable CRT/ICD devices. Methods: We retrospectively obtained HRV reports from patients in the US Feasibility study which evaluated preliminary safety and efficacy of EACP from 2010-2012. Patients (N= 4) were identified, 3M, NYHA Class III, 42.3±4.3 years, CRT (N= 2), ICD (N= 4). All patients received maximally tolerated, guideline directed medical therapy. HRV was measured using CRM device algorithm. Briefly, 5 minute median intervals were derived from atrial sensed cycle lengths. HRV was defined as the standard deviation of these intervals (SDAAM) for each 24 hour period. Results: SDAAM was measured without EACP 130±17.3 days and 185±36.9 days with EACP (p= NS). SDAAM demonstrated significant improvement with chronic EACP therapy increasing from 55±4.6ms to 85±5.4 (p< 0.01). No significant change in heart rate was observed between no EACP 78.5±3.8 min-1 and chronic EACP 79.3±6 min-1. All data mean±se. Conclusion: In this small cohort, treatment with EACP was associated with clinically relevant improvement in autonomic balance assessed by chronic HRV measurements derived from an independent, validated algorithm. Studies have shown SDAMM ≤ 50ms predicts significant mortality risk. Thus, EACP may be expected to significantly impact the risk of cardiovascular death and hospitalization. Further studies are warranted to assess the mechanisms whereby counterpulsation may influence sympathetic/parasympathetic balance, which may include increased baroreceptor signaling arising from enhanced pulsatility.

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