Pump Speed Modulation Research Articles

Impact of the HeartMate 3 Pump Speed Modulation Algorithm on Derived Pump Parameters and Measured Haemodynamic Variables

Impact of the HeartMate 3 Pump Speed Modulation Algorithm on Derived Pump Parameters and Measured Haemodynamic Variables

Numerical simulation analysis of multi-scale computational fluid dynamics on hemodynamic parameters modulated by pulsatile working modes for the centrifugal and axial left ventricular assist devices

Continuous flow (CF) left ventricular assist devices (LVAD) operate at a constant speed mode, which could result in increased risk of adverse events due to reduced vascular pulsatility. Consequently, pump speed modulation algorithms have been proposed to augment vascular pulsatility. However, the quantitative local hemodynamic effects on the aorta when the pump is operating with speed modulation using different types of CF-LVADs are still under investigation. The computational fluid dynamics (CFD) study was conducted to quantitatively elucidate the hemodynamic effects on a clinical patient-specific aortic model under different speed patterns of CF-LVADs. Pressure distribution, wall shear stress (WSS), time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), relative residence time (RRT), and velocity were calculated to compare their differences at constant and pulsatile speeds under centrifugal and axial LVAD support. Results showed that pulse pressure on the aorta was significantly larger under pulsatile speed mode than that under constant speed mode for both CF-LVADs, indicating enhanced aorta pulsatility, as well as the higher peak blood flow velocity on some representative slices of aorta. Pulsatile speed modulation enhanced peak WSS compared to constant speed; high TAWSS region appeared near the branch of left common carotid artery and distal aorta regardless of speed modes and CF-LVADs but these regions also had low OSI; RRT was almost the same for all the cases. This study may provide a basis for the scientific and reasonable selection of the pulsatile speed patterns of CF-LVADs for treating heart failure patients.

Encouraging Regular Aortic Valve Opening for EVAHEART 2 LVAD Support Using Virtual Patient Hemodynamic Speed Modulation Analysis.

This study focuses on investigating the EVAHEART 2 left ventricular assist device (LVAD) toward designing optimal pump speed modulation (PSM) algorithms for encouraging aortic valve (AV) flow. A custom-designed virtual patient hemodynamic model incorporating the EVAHEART 2 pressure-flow curves, cardiac chambers, and the systemic and pulmonary circulations was developed and used in this study. Several PSM waveforms were tested to evaluate their influence on the mean arterial pressure (MAP), cardiac output (CO), and AV flow for representative heart failure patients. Baseline speeds were varied from 1,600 to 2,000 rpm. For each baseline speed, the following parameters were analyzed: 1) PSM ratio (reduced speed/baseline speed), 2) PSM duration (3-7 seconds), 3) native ventricle contractility, and 4) patient MAP of 70 and 80 mm Hg. More than 2,000 rpm virtual patient scenarios were explored. A lower baseline speed (1,600 and 1,700 rpm) produced more opportunities for AV opening and more AV flow. Higher baseline speeds (1,800 and 2,000 rpm) had lower or nonexistent AV flow. When analyzing PSM ratios, a larger reduction in speed (25%) over a longer PSM (5+ seconds) duration produced the most AV flow. Lower patient MAP and increased native ventricle contractility also contributed to improving AV opening frequency and flow. This study of the EVAHEART 2 LVAD is the first to focus on leveraging PSM to enhance pulsatility and encourage AV flow. Increased AV opening frequency can benefit aortic root hemodynamics, thereby improving patient outcomes.

P19: Modeling the Effects of Heartbeat Synchronized Speed Modulation for a Pediatric LVAD

Study: Increasing the pulsatility of combined LVAD and heart output can be done by modulating the speed of the pump driver in synchrony with the heart rhythm. Increased pulsatility is closer to the physiological norm, lessens blood stagnation, and improves baroreceptor feedback for pressure regulation. This study is a first step to model the systemic response to pump speed modulation to develop the precise synchronization timing and controls for an optimized outcome and to analyze the results. Methods: A previously validated computational model of a mock circulatory loop is used as a platform to observe the hemodynamic effects of synchronized pump speed modulation on the heart. A model of a brushless DC motor used to drive the pediatric LVAD is established using the speed, torque, and inertia constants of the manufacturer specification sheet to represent the motor’s ability to change speed. The pressure and flow HQ curve of the LVAD impeller is used to calculate the pump output flow at different pressures and impeller speeds. The flow of the set speed LVAD is 3L/min, and the flow of the speed modulated LVAD varies between 1 L/min and 5 L/min at diastole and systole respectively. A PID controller is used to control the pump speed to reach the desired flow output. Results: The modulated LVAD flow results in larger changes in aortic pressure. The speed modulated LVAD had an aortic pressure difference of 20 mmHg between the minimum diastole and maximum systole values while the set speed LVAD had a difference of 7 mmHg. The set speed LVAD and the speed modulated LVAD had similar average aortic pressure values of 93mmHg and 91mmHg respectively. The changes in aortic pressure at systole and diastole resulting from the speed modulated flow show that synchronized motor speed modulation results in physiologic conditions closer to the norm.Figure 1. Overview of the Mock Circulatory Loop model and LVAD motor speed controller.Figure 2. Left Ventricular and Aortic Pressure with a set speed LVAD and a speed modulated LVAD.

P84: The impact of temporal synchronization on platelet activation in LVAD patients: CFD and PIV study for the HeartMate3 pulsatility mode.

Study: LVAD patients continue to experience high rates of stroke. Stasis and high shear stresses contribute to platelet activation in the left ventricle, that can lead to thrombus formation. A pulsatility mode was incorporated into the HeartMate3 to improve in-pump washout. The pump speed modulation occurs every two seconds, independently of the cardiac cycle even in patients with preserved native contractility. This study examines intraventricular washout under different LVAD pulsatility/native cardiac cycle synchronization. Methods: A patient-specific 3D time-resolved computational fluid dynamics (CFD) simulation captures the hemodynamics in the left ventricle implanted with an LVAD. Lagrangian particle tracking models platelet motion from the mitral valve, across the left ventricle and out through the outflow cannula. The residence time and shear stress history for each platelet is tracked to determine its risk of activation. Four different temporal synchronizations between the LVAD pulsatility and the native contractility are studied: contraction, peak contraction, relaxation, and peak relaxation. The flow rate through the cannula is prescribed from flow meter data in the experimental campaign. Particle image velocimetry (PIV) experiments measured the in-plane and through plane velocity fields at two orthogonal planes in the ventricle. This PIV data is compared to the CFD to benchmark the simulations. Results: The different pulsatility mode synchronizations result in significantly different time-dependent flow rates through the cannula. The difference between these flow rates results in different hemodynamics patterns in the ventricle. The velocity fields from the CFD models agree closely with the results from the PIV experiments, and take these in a new direction with the use of Lagrangian platelet tracking. Recirculation zones develop underneath the aortic valve and around the cannula/apex pocket, resulting in areas of stasis for the platelets. By identifying platelets that experience both high shear stress history and long residence time, the thrombogenicity of the different synchronizations is evaluated.

Pulsatility hemodynamics during speed modulation of continuous-flow total artificial heart in a chronic in vivo model.

BackgroundThe evaluation of pulsatile flow created by the new Cleveland Clinic continuous‐flow total artificial heart (CFTAH100), which has a re‐designed right impeller and motor, had not been tested in vivo. The purpose of this study was to evaluate the feasibility of pulsatility with the CFTAH100 during the application of pump speed modulation protocols in a chronic animal model.MethodsA 30‐day chronic animal experiment was conducted with a calf. Five pulsatile studies were performed on the alert animal. The mean pump speed was set at 2800 rpm, and modulated sinusoidally within a range of 0 to ± 35% of mean speed, in increments of 5% at 80 beats per minute (bpm). The pressures and pump flow were collected and a pulsatility index (PI) was calculated.ResultsThe calf was supported with the CFTAH100 without any major complications. The maximum and minimum pump flows changed significantly from baseline in all conditions, while the mean pump flow did not change. All flow pulsatility (FP) readings in all conditions significantly increased from baseline, and the percent modulation (%S) and FP had a strong positive correlation (r = 0.99, p < 0.01). The PI also increased significantly in all conditions (maximum at %S of 35%, 2.2 ± 0.05, p < 0.01), and a positive correlation between %S and PI (r = 0.99, p < 0.01) was observed.ConclusionThe CFTAH100 showed the feasibility of creating pulsatile circulation with sinusoidal pump speed modulation.

Effects of Pulsatility on Arterial Endothelial and Smooth Muscle Cells

Continuous flow ventricular assist device (CFVAD) support in advanced heart failure patients causes diminished pulsatility, which has been associated with adverse events including gastrointestinal bleeding, end organ failure, and arteriovenous malformation. Recently, pulsatility augmentation by pump speed modulation has been proposed as a means to minimize adverse events. Pulsatility primarily affects endothelial and smooth muscle cells in the vasculature. To study the effects of pulsatility and pulse modulation using CFVADs, we have developed a microfluidic co-culture model with human aortic endothelial (ECs) and smooth muscle cells (SMCs) that can replicate physiologic pressures, flows, shear stresses, and cyclical stretch. The effects of pulsatility and pulse frequency on ECs and SMCs were evaluated during (1) normal pulsatile flow (120/80 mmHg, 60 bpm), (2) diminished pulsatility (98/92 mmHg, 60 bpm), and (3) low cyclical frequency (115/80 mmHg, 30 bpm). Shear stresses were estimated using computational fluid dynamics (CFD) simulations. While average shear stresses (4.2 dynes/cm²) and flows (10.1 mL/min) were similar, the peak shear stresses for normal pulsatile flow (16.9 dynes/cm²) and low cyclic frequency (19.5 dynes/cm²) were higher compared to diminished pulsatility (6.45 dynes/cm²). ECs and SMCs demonstrated significantly lower cell size with diminished pulsatility compared to normal pulsatile flow. Low cyclical frequency resulted in normalization of EC cell size but not SMCs. SMCs size was higher with low frequency condition compared to diminished pulsatility but did not normalize to normal pulsatility condition. These results may suggest that pressure amplitude augmentation may have a greater effect in normalizing ECs, while both pressure amplitude and frequency may be required to normalize SMCs morphology. The co-culture model may be an ideal platform to study flow modulation strategies.

Control strategy to enhance pulmonary vascular pulsatility for implantable cavopulmonary assist devices: A simulation study

ObjectiveFontan failure can be potentially addressed with an implantable pump in the cavopulmonary junction (cavopulmonary assist device, CPAD) to replace the missing subpulmonary power source. Fontan pulmonary circulation lacks pulsatility due to the absence of the right ventricle, which has adverse physiological consequences. CPAD can augment pulmonary flow and improve Fontan hemodynamics. However, CPAD operating at a constant pump speed does not provide pulmonary arterial pulsatility, provide physiologic flow to match cardiac demand, or avoid suction. To overcome these limitations, a sensorless control strategy for CPAD is proposed. MethodsCPAD pump speed measurement, an intrinsic pump parameter, was used to estimate cavopulmonary pressure head (CPPH). A gain scheduled proportional-integral controller alternates CPPH between high/low setpoints (CPPHHr/CPPHLr) that generates pulsatility, while simultaneously adapting to cardiac demand and avoiding suction. Computer simulations were performed to quantify the overall performance of the proposed algorithm at rest and exercise, rapid transition from exercise to rest, and doubling of the vena caval resistance. The performance was compared against CPPH measured using pressure sensors, and a constant pump speed control strategy. ResultsThe sensorless algorithm generated a pulmonary vascular pulsatility of approximately 10 mmHg, and matched the cardiac demand at rest and exercise. The frequency of pump speed modulation was 10–15 cycles per minute and no suction was observed. Conclusion and significanceThe sensorless strategy outperformed constant CPAD speed control algorithm for improvement of pulmonary vascular pulsatility and physiologic perfusion. Further validation is needed using mock loop and animal tests.

Low Peak VO2 and Pulse Pressure Augmentation on Exercise in LVAD Patients with Recovery and Pump Explant

<h3>Purpose</h3> Recovered LVAD patients have normal EF and hemodynamics, but knowledge of their exercise response is scarce. We compared exercise responses in LVAD vs. HF and normal subjects. <h3>Methods</h3> In 2016-20, 25 LVAD patients had upright ergometer CPET with first-pass radionuclide imaging (n=20), with (n=13) or without (n=12) invasive hemodynamic monitoring. Five had pump explant for recovery after exercising at low pump speeds. LVAD patients were compared to HFrEF (EF < 40%, n=31) vs. normal subjects (EF ≥ 50%, rest mean PAP ≤ 20, PAWP < 15 mmHg, n=41). Values are expressed as median (25^th-75^th interquartile range). P < 0.05 was considered significant comparison across all groups. <h3>Results</h3> Median EF was 55% (explant), 19% (no-explant), 23% (HFrEF), and 63% (normal) (p<0.01). On exercise, LVAD patients did not augment EF as other groups. Peak VO₂ was 14 (explant), 10.1 (no-explant), 11.9 (HFrEF), and 22.7 mL/kg/min (normal) (p<0.01). Max-predicted heart rate (HR) was 90% (explant), 69% (no-explant), 68% (HFrEF), and 89% (normal) (p<0.01). Explant patients did not widen radial artery pulse pressure as normal subjects (Δ pulse pressure 18 vs. 32 mmHg, p<0.01) (Fig 1A). At rest, from supine to upright position, filling pressures dropped in HF and normal subjects but were unchanged in LVAD patients. Peak CO was similar between explant and normal (13.9 L/min [9.9-14.6] vs. 13.9 [11.9-17.1]), but low in no-explant and HF groups (6.9 [6.3-10.5] vs. 7.1 [5.8-9.1]). PAWP/CO slope was lowest in explant and normal (1.4 mmHg/L/min [0.8-2.2] vs. 1.1 [0.9-1.6]), but high in no-explant and HFrEF groups (3.2 [2.2-4.5] vs. 4.2 [2.3-5.4]) (Fig 1B). <h3>Conclusion</h3> Explant patients had higher peak CO, peak HR and lower PAWP/CO slope than no-explant group. Despite normal EF and hemodynamics, explant patients did not completely normalize peak VO₂ or pulse pressure augmentation on exercise. Efforts aimed at improving CO (e.g. pump speed modulation) and reducing chronotropic incompetence may help improve exercise tolerance for LVAD patients.

Effect of Mechanical Circulatory Support on Exercise Hemodynamics among Individuals with Advanced Heart Failure

<h3>Purpose</h3> The primary objective of this study was to determine why exercise capacity is limited among HF patients following left ventricular assist device (LVAD) implantation. <h3>Methods</h3> Thirteen HF patients (N=11 males; 59±10 yrs) completed invasive cardiopulmonary exercise testing (CPET) on upright cycle ergometry pre- and post-LVAD implantation on three visits: Visit 1: Pre-LVAD baseline testing; Visit 2: Post-LVAD testing with pump speed held at baseline; Visit 3: Post-LVAD testing with stepwise increases in pump speed (Heartware=40RPM/min; Heartmate 3=100RPM/min). On all visits, cardiac hemodynamics and gas-exchange parameters were monitored by Swan-Ganz catheter and indirect calorimetry, respectively. <h3>Results</h3> Cohort characteristics are displayed in <b>Table 1</b>. Compared to Visit 1, maximal oxygen uptake (VO₂Max) did not improve and was severely reduced on Visits 2 and 3 (<b>Figure 2</b>). Cardiac hemodynamics increased significantly with exercise on Visits 2-3 and were similar to values obtained from Visit 1. Cardiac output reserve was severely blunted on all visits and did not improve despite pump speed increases on Visit 3. Ventilatory efficiency improved modestly but remained impaired on Visits 2 and 3, compared to Visit 1 (Visits 1, 2, and 3: 47±13 v. 43±11 v. 39±7, respectively, ANOVA P=0.0047). <h3>Conclusion</h3> VO₂Max among LVAD patients is limited by severe increases in pulmonary arterial and left-sided filling pressures, and blunted cardiac output reserve. Pump speed modulations during exercise do not improve exercise performance. LVAD patients exhibit signs of residual and severe heart failure with exercise.

Ex vivo assessment of erythrocyte tolerance to the HeartWare ventricular assist device operated in three discrete configurations.

Despite technological advances in ventricular assist devices (VADs) to treat end-stage heart failure, hemocompatibility remains a constant concern, with supraphysiological shear stresses an unavoidable reality with clinical use. Given that impeller rotational speed is related to the instantaneous shear within the pump housing, it is plausible that the modulation of pump speed may regulate peak mechanical shear stresses and thus ameliorate blood damage. The present study investigated the hemocompatibility of the HeartWare HVAD in three configurations typical of clinical applications: standard systemic support left VAD (LVAD), pediatric support LVAD, and pulmonary support right VAD (RVAD) conditions. Two ex vivo mock circulation blood loops were constructed using explanted HVADs, in which pump speed and external loop resistance were manipulated to reflect the flow rates and differential pressures reported in configurations for standard adult LVAD (at 3150rev⸱min-1 ), pediatric LVAD (at 2400 rev⸱min-1 ), and adult RVAD (at 1900 rev⸱min-1 ). Using bovine blood, the mock circulation blood loops were tested at 37°C over a period of 6hours (consistent with ASTM F1841-97) and compared with static control. Hemocompatibility assessments were conducted for each test condition, examining hematology, hemolysis (absolute and normalized index), osmotic fragility, and blood viscosity. Regardless of configuration, continuous exposure of blood to the VAD over the 6-hour period significantly altered hematological and rheological blood parameters, and induced increased hemolysis when compared with a static control sample. Comparison of the three operational VAD configurations identified that the adult LVAD condition-associated with the highest pump speed, flow rate, and differential pressure across the pump-resulted in increased normalized hemolysis index (NIH; 0.07) when compared with the lower pump speed "off-label" counterparts (NIH of 0.04 in pediatric LVAD and 0.01 in adult RVAD configurations). After normalizing blood residence times between configurations, pump speed was identified as the primary determinant of accumulated blood damage; plausibly, blood damage could be limited by restricting pump speed to the minimum required to support matched cardiac output, but not beyond.

Right ventricular function and cardiopulmonary performance among patients with heart failure supported by durable mechanical circulatory support devices

Patients with continuous-flow left ventricular assist devices (CF-LVADs) experience limitations in functional capacity and frequently, right ventricular (RV) dysfunction. We sought to characterize RV function in the context of global cardiopulmonary performance during exercise in this population. A total of 26 patients with CF-LVAD (aged 58 ± 11 years, 23 males) completed a hemodynamic assessment with either conductance catheters (Group 1, n = 13) inserted into the right ventricle to generate RV pressure‒volume loops or traditional Swan‒Ganz catheters (Group 2, n = 13) during invasive cardiopulmonary exercise testing. Hemodynamics were collected at rest, 2 sub-maximal levels of exercise, and peak effort. Breath-by-breath gas exchange parameters were collected by indirect calorimetry. Group 1 participants also completed an invasive ramp test during supine rest to determine the impact of varying levels of CF-LVAD support on RV function. In Group 1, pump speed modulations minimally influenced RV function. During upright exercise, there were modest increases in RV contractility during sub-maximal exercise, but there were no appreciable increases at peak effort. Ventricular‒arterial coupling was preserved throughout the exercise. In Group 2, there were large increases in pulmonary arterial, left-sided filling, and right-sided filling pressures during sub-maximal and peak exercises. Among all participants, the cardiac output‒oxygen uptake relationship was preserved at 5.8:1. Ventilatory efficiency was severely abnormal at 42.3 ± 11.6. Patients with CF-LVAD suffer from limited RV contractile reserve; marked elevations in pulmonary, left-sided filling, and right-sided filling pressures during exercise; and severe ventilatory inefficiency. These findings explain mechanisms for persistent reductions in functional capacity in this patient population.

Shear stress and blood trauma under constant and pulse-modulated speed CF-VAD operations: CFD analysis of the HVAD.

Modulation of pump speed has been proposed and implemented clinically to improve vascular pulsatility in continuous flow ventricular assist device patient. The flow dynamics of the HVAD with a promising asynchronous pump speed modulation and its potential risk for device-induced blood trauma was investigated numerically. The boundary conditions at the pump inlet and outlet were defined using the pressure waveforms adapted from the experimentally recorded ventricular and arterial pressure waveforms in a large animal ischemic heart failure (IHF) model supported by the HVAD operated at constant and modulated pump speeds. Shear stress fields and hemolysis indices were derived from the simulated flow fields. The overall features of the computationally generated flow waveforms at simulated constant and pulse-modulated speed operations matched with those of the experimentally recorded flow waveforms. The simulations showed that the shear stress field and hemolysis index vary throughout the cardiac cycle under the constant speed operation, and also as a function of modulation profile under modulated speed operation. The computational model did not demonstrate any differences in the time average hemolysis index between constant and modulated pump speed operations, thereby predicting pulse-modulated speed operation may help to restore vascular pulsatility without any further increased risk of blood trauma. Graphical abstract The streamline inside the HVAD pump and the wall shear stress distribution on the impeller surface at six discrete time instants over one cardiac cycle under constant speed operation (3000rpm) (a) and under pulse-modulated speed operation (b). c Computationally predicted flow rate waveform under pulse-modulated speed operation. d Computationally predicted time-varying HI generated by the HVAD pump under the two operation modes constant speed (dash line) and pulse-modulated speed (solid line). These figures indicate that the pulse-modulated speed operation may help to restore vascular pulsatility without any further increased risk of blood trauma.

The Influence of Rotary Blood Pump Speed Modulation on the Risk of Intraventricular Thrombosis.

Rotary left ventricular assist devices (LVADs) are commonly operated at a constant speed, attenuating blood flow pulsatility. Speed modulation of rotary LVADs has been demonstrated to improve vascular pulsatility and pump washout. The effect of LVAD speed modulation on intraventricular flow dynamics is not well understood, which may have an influence on thromboembolic events. This study aimed to numerically evaluate intraventricular flow characteristics with a speed modulated LVAD. A severely dilated anatomical left ventricle was supported by a HeartWare HVAD in a three-dimensional multiscale computational fluid dynamics model. Three LVAD operating scenarios were evaluated: constant speed and sinusoidal co- and counter-pulsation. In all operating scenarios, the mean pump speed was set to restore the cardiac output to 5.0L/min. Co- and counter-pulsation was speed modulated with an amplitude of 750rpm. The risk of thrombosis was evaluated based on blood residence time, ventricular washout, kinetic energy densities, and a pulsatility index map. Blood residence time for co-pulsation was on average 1.8 and 3.7% lower than constant speed and counter-pulsation mode, respectively. After introducing fresh blood to displace preexisting blood for 10 cardiac cycles, co-pulsation had 1.5% less old blood in comparison to counter-pulsation. Apical energy densities were 84 and 27% higher for co-pulsation in comparison to counter-pulsation and constant speed mode, respectively. Co-pulsation had an increased pulsatility index around the left ventricular outflow tract and mid-ventricle. Improved flow dynamics with co-pulsation was caused by increased E-wave velocities which minimized blood stasis. In the studied scenario and from the perspective of intraventricular flow dynamics, co-pulsation of rotary LVADs could minimize the risk of intraventricular thrombosis.

Early in vivo experience with the pediatric continuous-flow total artificial heart.

Heart transplantation in infants and children is an accepted therapy for end-stage heart failure, but donor organ availability is low and always uncertain. Mechanical circulatory support is another standard option, but there is a lack of intracorporeal devices due to size and functional range. The purpose of this study was to evaluate the in vivo performance of our initial prototype of a pediatric continuous-flow total artificial heart (P-CFTAH), comprising a dual pump with one motor and one rotating assembly, supported by a hydrodynamic bearing. In acute studies, the P-CFTAH was implanted in 4 lambs (average weight: 28.7 ± 2.3 kg) via a median sternotomy under cardiopulmonary bypass. Pulmonary and systemic pump performance parameters were recorded. The experiments showed good anatomical fit and easy implantation, with an average aortic cross-clamp time of 98 ± 18 minutes. Baseline hemodynamics were stable in all 4 animals (pump speed: 3.4 ± 0.2 krpm; pump flow: 2.1 ± 0.9 liters/min; power: 3.0 ± 0.8 W; arterial pressure: 68 ± 10 mm Hg; left and right atrial pressures: 6 ± 1 mm Hg, for both). Any differences between left and right atrial pressures were maintained within the intended limit of ±5 mm Hg over a wide range of ratios of systemic-to-pulmonary vascular resistance (0.7 to 12), with and without pump-speed modulation. Pump-speed modulation was successfully performed to create arterial pulsation. This initial P-CFTAH prototype met the proposed requirements for self-regulation, performance, and pulse modulation.

Initial in vitro testing of a paediatric continuous-flow total artificial heart.

Mechanical circulatory support has become standard therapy for adult patients with end-stage heart failure; however, in paediatric patients with congenital heart disease, the options for chronic mechanical circulatory support are limited to paracorporeal devices or off-label use of devices intended for implantation in adults. Congenital heart disease and cardiomyopathy often involve both the left and right ventricles; in such cases, heart transplantation, a biventricular assist device or a total artificial heart is needed to adequately sustain both pulmonary and systemic circulations. We aimed to evaluate the in vitro performance of the initial prototype of our paediatric continuous-flow total artificial heart. The paediatric continuous-flow total artificial heart pump was downsized from the adult continuous-flow total artificial heart configuration by a scale factor of 0.70 (1/3 of total volume) to enable implantation in infants. System performance of this prototype was evaluated using the continuous-flow total artificial heart mock loop set to mimic paediatric circulation. We generated maps of pump performance and atrial pressure differences over a wide range of systemic vascular resistance/pulmonary vascular resistance and pump speeds. Performance data indicated left pump flow range of 0.4-4.7 l/min at 100 mmHg delta pressure. The left/right atrial pressure difference was maintained within ±5 mmHg with systemic vascular resistance/pulmonary vascular resistance ratios between 1.4 and 35, with/without pump speed modulation, verifying expected passive self-regulation of atrial pressure balance. The paediatric continuous-flow total artificial heart prototype met design requirements for self-regulation and performance; in vivo pump performance studies are ongoing.

Pump speed modulations and sub-maximal exercise tolerance in left ventricular assist device recipients: A double-blind, randomized trial

The effect of pump speed increase on sub-maximal exercise tolerance, corresponding to activities of daily living (ADLs), is unknown. The aim of this study was to determine the effects of increasing pump speed during exercise at a sub-maximal level below anaerobic threshold (AT). Patients each completed 3 exercise sessions on an ergometer cycle. On Day 1 workload at AT was defined. On Day 2 of the study, 2 sub-maximal tests at a workload below AT were undertaken: one at fixed baseline pump speed (Speedbase) and the other with baseline pump speed + 800 rpm (Speedinc). The sequence of the 2 sub-maximal tests was determined by randomization. Both patient and physician were blinded to the sequence. Exercise duration, oxygen consumption (VO2) and rate of perceived exertion (RPE), using the Borg scale (score 6 to 20), were recorded. Nineteen patients (all with a HeartMate II ventricular assist device) completed 57 exercise tests. Baseline pump speed was 9,326 ± 378 rpm. At AT, workload was 63 ± 26 W (25 to 115 W) and VO2 was 79 ± 14% of maximum. Exercise duration improved by 106 ± 217 seconds (~13%) in Speedinc compared with Speedbase (837 ± 358 vs 942 ± 359 seconds; p = 0.048). The RPE was 13.2 ± 2.5 in Speedbase vs 12.7 ± 2.4 in Speedinc (p = 0.2). Increasing pump speed by 800 rpm during sustained, low-intensity physical activity is safe and prolongs exercise duration in patients supported with a HeartMate II device. Automated pump speed increase during light exercise may contribute to improved quality of life by facilitating ADLs.

Exercise physiology in chronic mechanical circulatory support patients: vascular function and beyond.

The majority of patients currently implanted with left ventricular assist devices have the expectation of support for more than 2 years. As a result, survival alone is no longer a sufficient distinctive for this technology, and there have been many studies within the last few years examining functional capacity and exercise outcomes. Despite strong evidence for functional class improvements and increases in simple measures of walking distance, there remains incomplete normalization of exercise capacity, even in the presence of markedly improved resting hemodynamics. Reasons for this remain unclear. Despite current pumps being run at a fixed speed, it is widely recognized that pump outputs significantly increase with exercise. The mechanism of this increase involves the interaction between preload, afterload, and the intrinsic pump function curves. The role of the residual heart function is also important in determining total cardiac output, as well as whether the aortic valve opens with exercise. Interactions with the vasculature, with skeletal muscle blood flow and the state of the autonomic nervous system are also likely to be important contributors to exercise performance. Further studies examining optimization of pump function with active pump speed modulation and options for optimization of the overall patient condition are likely to be needed to allow left ventricular assist devices to be used with the hope of full functional physiological recovery.

(327) - Electrical Remodeling After Continuous-Flow Left Ventricular Assist Device Implantation

s S129 Results: Figure shows representative waveforms of pump speed, AoP, and pump flow with sinusoidal pump speed modulations of 0%, ±15% and ±25%. The AoP pulse pressure significantly increased to 12.7 mm Hg and 17.7 mmHg with ±15% and ±25% speed modulations, respectively (Table). There were no changes in the mean AoP, mean pump flow, or left atrial pressure. Conclusion: The feasibility to generate pressure pulsatility by pump speed modulation with the CFTAH was validated. This unique platform is suitable for evaluating the physiologic impact of pulsatility and allows determination of the best speed modulations in term of magnitude, frequency, and profiles.

(328) - Generating Pulsatility by Pump Speed Modulation with Continuous-Flow Total Artificial Heart in Awake Calves

(328) - Generating Pulsatility by Pump Speed Modulation with Continuous-Flow Total Artificial Heart in Awake Calves