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Fontan circulatory inefficiency can be addressed by replacing the missing subpulmonary power source to reverse the Fontan paradox. An implantable cavopulmonary assist device is described that will simultaneously reduce systemic venous pressure and increase pulmonary arterial pressure, improving preload and cardiac output, in a univentricular Fontan circulation on a long-term basis. A rotary blood pump that was based on the von Karman viscous pump was designed for implantation into the total cavopulmonary connection (TCPC). It will impart modest pressure energy to augment Fontan flow without risk of obstruction. In the event of rotational failure, it is designed to default to a passive flow diverter. Pressure-flow performance was characterized in vitro in a Fontan mock circulatory loop with blood analog. The pump performed through the fully specified operating range, augmenting flow in all 4 directions of the TCPC. Pressure rise of 6 to 8 mm Hg was readily achieved, ranging to 14 mm Hg at highest speed (5600 rpm). Performance was consistent across a wide range of cardiac outputs. In stalled condition (0 rpm), there was no discernible pressure loss across the TCPC. A blood pump technology is described that can reverse the Fontan paradox and may permit a surgical strategy of long-term biventricular maintenance of a univentricular Fontan circulation. The technology is intended for Fontan failure in which right-sided circulatory inefficiencies predominate and ventricular systolic function is preserved. It may also apply before clinical Fontan failure as health maintenance to preempt the progression of Fontan disease. [ABSTRACT FROM AUTHOR]

• A control system to enhance vascular pulsatility for rotary blood pump was proposed. • Switching two differential pump speed setpoints to raise vascular pulsatility. • The proposed control algorithm was only based on intrinsic pump speed measurements. • This algorithm augmented vascular pulsatility, provided flow rates, avoided suction. Continuous flow rotary blood pumps (RBP) operating clinically at constant rotational speeds cannot match cardiac demand during varying physical activities, are susceptible to suction, diminish vascular pulsatility, and have an increased risk of adverse events. A sensorless, physiologic feedback control strategy for RBP was developed to mitigate these limitations. The proposed algorithm used intrinsic pump speed to obtain differential pump speed (Δ RPM). The proposed gain-scheduled proportional-integral controller, switching of setpoints between a higher pump speed differential setpoint (Δ RPM Hr) and a lower pump speed differential setpoint (Δ RPM Lr), generated pulsatility and physiologic perfusion, while avoiding suction. The switching between Δ RPM Hr and Δ RPM Lr setpoints occurred when the measured Δ RPM reached the pump differential reference setpoint. In-silico tests were implemented to assess the proposed algorithm during rest, exercise, a rapid 3-fold pulmonary vascular resistance increase, rapid change from exercise to rest, and compared with maintaining a constant pump speed setpoint. The proposed control algorithm augmented aortic pressure pulsatility to over 35 mmHg during rest and around 30 mmHg during exercise. Significantly, ventricular suction was avoided, and adequate cardiac output was maintained under all simulated conditions. The performance of the sensorless algorithm using estimation was similar to the performance of sensor-based method. This study demonstrated that augmentation of vascular pulsatility was feasible while avoiding ventricular suction and providing physiological pump outflows. Augmentation of vascular pulsatility can minimize adverse events that have been associated with diminished pulsatility. Mock circulation and animal studies would be conducted to validate these results. [ABSTRACT FROM AUTHOR]

Background Ex vivo lung perfusion (EVLP) has the potential to increase the donor pool for lung transplantation by facilitating resuscitation and extended evaluation of marginal organs. Current EVLP methodology employs continuous flow (CF) pumps that produce non-pulsatile EVLP hemodynamics. In this feasibility study, we tested the hypothesis that a pulsatile flow (PF) pump will provide better EVLP support than a CF pump through delivery of physiologic hemodynamics. Methods Porcine lungs were supported in an EVLP model by centrifugal CF (n = 3) or PF (n = 4) left ventricular assist devices. Lungs were ventilated at 4 to 5 mL/kg, 0.21 fraction of inspired oxygen (FiO 2 ), and perfused with an acellular, albumin-based solution corrected for osmolarity, acid-base balance, and carbon dioxide pressure (≤20 hours at 30 ° C) for a minimum of 12 hours support. Prostaglandin E 1 and 30% albumin were infused continuously. Hemodynamic, respiratory, and blood gas parameters were continuously monitored and digitally recorded hourly. Parenchymal biopsies were used for quantification of wet to dry weight ratio. Results All lungs maintained function in the EVLP circuit for a minimum of 12 hours (mean 14.7 ± 1 hours) and demonstrated minimal edema formation. The PF EVLP produced higher pulsatility as demonstrated by greater energy equivalent pressure and surplus hemodynamic energy compared with CF EVLP ( p < 0.05). There were no statistically significant differences in pulmonary impedance, arterial partial pressure of oxygen/fraction of inspired oxygen, wet to dry weight ratio, and peak airway pressure between CF and PF EVLP. Conclusions The CF and PF EVLP systems successfully maintained lungs 12+ hours using a modified Steen perfusate (XVIVO Perfusion, Inc, Goteborg, Sweden); however, there were no statistically significant differences between CF and PF groups despite higher pulsatility, suggesting that PF may not offer immediate benefits over CF for prolonged ex vivo lung preservation. [ABSTRACT FROM AUTHOR]

Background Rotary blood pumps operate at a constant speed (rpm) that diminishes vascular pulsatility and variation in ventricular end-systolic and end-diastolic volumes, which may contribute to adverse events, including aortic insufficiency and gastrointestinal bleeding. In this study, pump speed modulation algorithms for generating pulsatility and variation in ventricular end-systolic and end-diastolic volumes were investigated in an ischemic heart failure (IHF) bovine model ( n = 10) using a clinically implanted centrifugal-flow left ventricular assist device (LVAD). Methods Hemodynamic and hematologic measurements were recorded during IHF baseline, constant pumps speeds, and asynchronous (19–60 cycles/min) and synchronous (copulse and counterpulse) pump speed modulation profiles using low relative pulse speed (±25%) of 3,200 ± 800 rpm and high relative pulse speed (±38%) of 2,900 ± 1,100 rpm. End-organ perfusion, hemodynamics, and pump parameters were measured to characterize pulsatility, myocardial workload, and LVAD performance for each speed modulation profile. Results Speed modulation profiles augmented aortic pulse pressure, surplus hemodynamic energy, and end-organ perfusion ( p < 0.01) compared with operation at constant speed. Left ventricular external work and myocardial oxygen consumption were significantly reduced compared with IHF baseline ( p < 0.01) but at the expense of higher LVAD power consumption. Conclusions Pump speed modulation increases pulsatility and improves cardiac function and end-organ perfusion, but the asynchronous mode provides the technologic advantage of sensorless control. Investigation of asynchronous pump speed modulation during long-term support is warranted to test the hypothesis that operating an LVAD with speed modulation will minimize adverse events in patients supported by an LVAD that may be associated with long-term operation at a constant pump speed. [ABSTRACT FROM AUTHOR]

Objective: The anatomic and physiologic constraints for pediatric cavopulmonary assist differ markedly from adult Fontan circulations owing to smaller vessel sizes and risk of elevated pulmonary resistance. In this study, hemodynamic and hemolysis performance of a catheter-based viscous impeller pump (VIP) to power the Fontan circulation is assessed at a pediatric scale (∼15 kg) and performance range (0-30 mm Hg). Methods: Computer simulation and mock circulation studies were conducted to assess the hydraulic performance, acute hemodynamic response to different levels VIP support, and the potential for vena caval collapse. Computational fluid dynamics simulations were used to estimate VIP hydraulic performance, shear rates, and potential for hemolysis. Hemolysis was quantified in a mock loop with fresh bovine blood. Results: A VIP augmented 4-way total cavopulmonary connection flow at pediatric scales and restored systemic pressures and flows to biventricular values, without causing flow obstruction or suction. VIP generated flows up to 4.1 L/min and pressure heads of up to 38 mm Hg at 11,000 rpm. Maximal shear rate was 160 Pa, predicting low hemolysis risk. Observed hemolysis was low with plasma free hemoglobin of 11.4 mg · dL−1 · h−1. Conclusions: A VIP will augment Fontan cavopulmonary flow in the proper pressure and flow ranges, with low hemolysis risk under more stringent pediatric scale and physiology compared with adult scale. This technology may be developed to simultaneously reduce systemic venous pressure and improve cardiac output after stage 2 or 3 Fontan repair. It may serve to compress surgical staging, lessening the pathophysiologic burden of repair. [ABSTRACT FROM AUTHOR]

Objective: An ectopic coronary artery that courses between the aortic root and the pulmonary trunk may lead to sudden cardiac death, especially in athletes. It has been speculated that during exercise, compression of the coronary artery between the great vessels may impair coronary blood flow and produce myocardial ischemia and fatal arrhythmia. However, this hypothesis cannot be tested in humans, and little experimental data exist to explain this phenomenon. To this end, in a calf with an anomalous left coronary artery that coursed from the right sinus of Valsalva between the great vessels, we assessed for myocardial ischemia during pharmacologically induced tachycardia and hypertension. Methods: We identified a juvenile male calf (103 kg) with an anomalous left coronary artery from the right sinus of Valsalva that coursed between the great vessels. Via thoracotomy, the animal was instrumented for hemodynamic measurements. Intravenous dobutamine increased heart rate and myocardial metabolic demands. Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. Fluorescent-labeled microspheres were used to map regional myocardial blood flow, and hemodynamics were recorded during each condition. Masson’s trichrome staining for fibrosis, wheat-germ agglutinin staining for myocyte size, terminal deoxynucleotidyl transferase dUTP nick end-label staining for apoptosis, and isolectin-B4 staining for capillary density were performed. Results: For the first time, empiric data documented that an ectopic coronary artery produced myocardial ischemia during elevated myocardial metabolic demands. Left coronary artery resistance increased in a cardiac cycle–dependent pattern that was consistent with systolic compression between the great vessels. Increased cardiac fibrosis, myocyte hypertrophy, cardiac apoptosis, and capillary density indicated that regional ischemic, inflammatory-mediated myocardial remodeling was present. Conclusions: These findings confirm the proposed mechanism of sudden death and support early surgical repair of coronary arteries that course between the aortic root and the pulmonary trunk. [Copyright &y& Elsevier]

Background: Left ventricular assist devices are increasingly used to treat patients with advanced and otherwise refractory heart failure as bridge to transplant or destination therapy. We evaluated a new miniaturized left ventricular assist device that requires minimal surgery for implantation, potentially allowing implantation in earlier stage heart failure. Methods: HeartWare (Miami Lakes, Fla) developed transapical miniaturized ventricular assist device. Acute (n = 4), 1-week (n = 2), and 30-day (n = 4) bovine model experiments evaluated hemodynamic efficacy and biocompatibility of the device, which was implanted through small left thoracotomy with single insertion at apex of left ventricle without cardiopulmonary bypass. The device outflow cannula was positioned across the aortic valve. The international normalized ratio was maintained between 2.0 and 2.5 with warfarin. Hemodynamic, echocardiographic, fluoroscopic, hematologic, and blood chemistry measurements were evaluated. Results: The device was successfully implanted through the left ventricular apex in all 10 animals. The device was operated at 15,000 ± 1000 rpm (power consumption, 3.5–6.0 W). The device maintained normal end-organ perfusion with no significant hemolysis (0–30 mg/dL). There were no pump failures or device-related complications. At autopsy, no abnormalities were seen in endocardium, aortic valve leaflets, or aortic root. There was no evidence of thromboembolism or abnormalities in any peripheral end organs. Conclusions: We successfully demonstrated feasibility of a novel intraventricular assist device that can be completely implanted through left ventricular apex. This transapical surgical approach eliminates needs for sternotomy, device pocket, cardiopulmonary bypass, ventricular coring, and construction of an outflow graft anastomosis. [ABSTRACT FROM AUTHOR]

Since the Fontan/Kreutzer procedure was introduced, evolutionary clinical advances via a staged surgical reconstructive approach have markedly improved outcomes for patients with functional single ventricle. However, significant challenges remain. Early stage mortality risk seems impenetrable. Serious morbidities – construed as immutable consequences of palliation – have hardly been addressed. Late functional status is increasingly linked to pathophysiologic consequences of prior staged procedures. As more single-ventricle patients survive into adulthood, Fontan failure is emerging as an intractable problem for which there is no targeted therapy. Incremental solutions to address these ongoing problems have not had a measurable impact. Therefore, a fundamental reconsideration of the overall approach is reasonable and warranted. The ability to provide a modest pressure boost (2 to 6 mmHg) to existing blood flow at the total cavopulmonary connection can effectively restore more stable biventricular status. This would impact not only treatment of late Fontan failure, but also facilitate early surgical repair. A realistic means to provide such a pressure boost has never been apparent. Recent advances are beginning to unravel the unique challenges that must be addressed to realize this goal, with promise to open single-ventricle palliation to new therapeutic vistas. [ABSTRACT FROM AUTHOR]

Background: Advanced therapies for heart failure (HF), such as mechanical circulatory support (MCS) devices and xenotransplantation, are usually tested in bovine and porcine models. This approach assumes a priori that animal (patho)physiology will closely match that of humans. Systemic aortic input impedance (ZART) is an important physiologic determinant of left ventricular (LV) performance. We tested the hypothesis that ZART is lower in bovine and porcine than in humans with normal or failing hearts. Methods: High-fidelity aortic pressure and flow waveforms were recorded intra-operatively at native and paced heart rates of 100 beats per minute (bpm) in adult human patients with normal LV function (n = 13) or end-stage HF (n = 15), and normal calves (n = 10) and pigs (n = 18). Fast Fourier transformation was used to calculate ZART, and arterial resistance and compliance were estimated using a 4-element Windkessel model. Results: Humans with HF had greater ZART than those with normal LV function, characterized by higher resistance (1.16 ± 0.12 vs 1.00 ± 0.10 mm Hg·s/ml, p < 0.05) and lower compliance (1.53 ± 0.21 vs 1.88 ± 0.33 ml·mm Hg, p < 0.05). Healthy calves and pigs had significantly lower resistance (calf: 0.63 ± 0.07 mm Hg·s/ml; pig: 0.90 ± 0.07 mm Hg·s/ml) and higher compliance (calf: 2.79 ± 0.37 ml·mm Hg; pig: 2.80 ± 0.64 ml·mm Hg) when compared to humans (p < 0.05) with normal or failing hearts. Conclusions: ZART is significantly lower in calves and pigs than in humans with or without HF. This finding has important implications for the pre-clinical testing of MCS devices and xenotransplants, which are usually examined in bovine and porcine models, respectively. Specifically, these therapies may respond differently in humans than animals due to non-equivalence of systemic after-load. [Copyright &y& Elsevier]

Objective: We sought to investigate differences in indices of pulsatility between patients with normal ventricular function and patients with heart failure studied at the time of implantation with continuous-flow or pulsatile-flow left ventricular assist devices. Methods: Eight patients with normal ventricular function and 22 patients with heart failure were studied. A high-fidelity aortic and left ventricular pressure catheter was inserted retrograde through the aortic valve into the left ventricle, and transit-time flow probes were placed on the aorta and device outflow graft. Hemodynamic waveforms were recorded at native heart rate before cardiopulmonary bypass and over a range of device flow rates controlled by adjusting beat rate or rpm. These data were used to calculate vascular input impedance and 2 indices of vascular pulsatility: energy-equivalent pressure and surplus hemodynamic energy. Results: At low support levels, pulsatile support restored surplus hemodynamic energy to within 2.5% of normal values, whereas continuous support diminished surplus energy by more than 93%. At high support levels, pulsatile support augmented surplus energy by 49% over normal values, whereas continuous support further diminished surplus energy by 97%. Pulsatile support diminished vascular impedance from baseline failure values, whereas continuous support increased impedance. Vascular impedances at baseline for patients undergoing pulsatile and continuous support and during pulsatile support revealed normal vascular compliance, whereas impedance during continuous support indicated a loss of compliance (or “stiffening”) of the vasculature. Conclusion: These results suggest that selection of device type and flow rate can influence vascular pulsatility and input impedance, which might affect clinical outcomes. [Copyright &y& Elsevier]

• A new control algorithm for cavopulmonary pump in Fontan circulation was proposed. • Switching two cavopulmonary head setpoints to raise pulmonary vascular pulsatility. • The cavopulmonary head was estimated only with intrinsic pump speed measurements. • This method augmented pulmonary vascular pulsatility and provided needed flow rates. Fontan 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. CPAD 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 (CPPH Hr / CPPH Lr) 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. The 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. The 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. [ABSTRACT FROM AUTHOR]

• A novel suction index based control algorithm for rotary blood pumps was developed. • The suction index was extracted from the intrinsic pump speed measurements. • The SI control algorithm does not require a model, or pressure or flow sensors. • Blood pump flow matched perfusion demand for rest and exercise. • Suction was avoided for all test conditions Rotary blood pumps (RBP) are long-term mechanical circulatory support devices that support a failing heart by pumping blood. Ventricular collapse and suction, which can lead to myocardial damage and arrhythmias, is a significant risk factor during RBP support. The RBP also needs to maintain pump flow to match perfusion demand over a wide range of physiologic conditions. We have developed a novel sensorless control algorithm to maintain physiologic perfusion while avoiding ventricular suction, using a suction index (SI) extracted from the intrinsic pump speed measurements. The objective of the proposed control algorithm is to maintain an SI setpoint. Using nonlinear mathematical models of a human circulatory system and a RBP, efficacy and robustness of the proposed algorithm with 2% RPM measurement were tested in-silico by comparing it to differential pump speed control, differential pump pressure control, constant speed control, and mean aortic pressure control during (1) rest and exercise conditions, (2) a rapid eight-fold increase in pulmonary vascular resistance for rest and exercise, and (3) transition from exercise to rest. The proposed control algorithm provided physiologic perfusion while simultaneously preventing ventricular suction for all test conditions. The performance of the proposed control algorithm was superior to other tested control strategies in avoiding suction. Maintaining a reference SI effectively provided physiologic perfusion and prevented ventricular suction. The proposed SI control approach can meet physiologic circulatory demand and avoid suction in RBP without requiring the use of unreliable pressure or flow sensors or a pump model. [ABSTRACT FROM AUTHOR]

• A new sensorless physiologic control algorithm for the Fontan pump was developed. • A cavopulmonary pressure head was proposed to provide physiologic perfusion. • The approach uses only intrinsic pump parameters and does not need external sensors. • The proposed algorithm maintained physiologic perfusion while avoiding suction. Mechanical circulatory support devices using continuous flow blood pump technologies are currently being developed to provide cavopulmonary support in patients with Fontan circulation. While cavopulmonary support can functionally replace the missing native right ventricle and biventricularize the Fontan circulation, there is a need for the pump to adapt to variable physiologic demands. A constant pump speed limits the ability to provide sufficient physiologic perfusion over a range of physiologic conditions. To address this challenge, a physiologic control algorithm for a Fontan pump was developed. The proposed algorithm uses a gain-scheduled, proportional-integral controller that generates a user defined cavopulmonary pressure head (CPPH = pulmonary artery pressure - vena caval pressure), to provide physiologic pressure rise while avoiding suction. The approach uses only intrinsic pump parameters and does not require the use of pressure or flow sensors. Performance and robustness of the sensorless control algorithm was quantified in-silico by simulating the following conditions: (1) Directly measured CPPH with pressure sensors; (2) CPPH estimation using the intrinsic pump measurement of pump speed and extended Kalman filter (EKF); (3) constant speed control algorithm; and (4) rapid four-fold increase in vena caval resistance (VCR) for (1) to (3). The results demonstrated that the sensorless control algorithm maintained physiologic perfusion while simultaneously preventing vena caval suction without the need for pressure sensors. The proposed algorithm was superior to the constant speed control strategy for physiologic perfusion and suction prevention, and warranted further investigation in vitro and in-vivo. [ABSTRACT FROM AUTHOR]

Continuous-flow ventricular assist devices (CVADs) have gained widespread use as an effective clinical therapy for patients with advanced-stage heart failure. Axial and centrifugal CVADs have been successfully used as bridge-to-transplant and destination therapy. CVADs are smaller, more reliable, and less complex than the first-generation pulsatile-flow ventricular assist devices. Despite their recent clinical success, arteriovenous malformations, gastrointestinal bleeding, hemorrhagic strokes, aortic valve insufficiency, and valve fusion have been reported in heart failure patients supported by CVADs. It has been hypothesized that diminished arterial pressure and flow pulsatility delivered by CVAD may be a contributing factor to these adverse events. Subsequently, the clinical significance of vascular pulsatility continues to be highly debated. Studies comparing pulsatile-flow and continuous-flow support have presented conflicting findings, largely due to variations in device operation, support duration, and the criteria used to quantify pulsatility. Traditional measurements of pulse pressure and pulsatility index are less effective at quantifying pulsatility for mechanically derived flows, particularly with the growing trend of CVAD speed modulation to achieve various pulsatile flow patterns. Kinetic measurements of energy equivalent pressure and surplus hemodynamic energy can better quantify pulsatile energies, yet technologic and conceptual challenges are impeding their clinical adaption. A review of methods for quantifying vascular pulsatility and their application as a research tool for investigating physiologic responses to CVAD support are presented. [ABSTRACT FROM AUTHOR]

Graphical Abstract Image, graphical abstract BACKGROUND Continuous-flow ventricular assist devices (CF-VADs) produce non-physiologic flow with diminished pulsatility, which is a major risk factor for development of adverse events, including gastrointestinal (GI) bleeding and arteriovenous malformations (AVMs). Introduction of artificial pulsatility by modulating CF-VAD flow has been suggested as a potential solution. However, the levels of pulsatility and frequency of CF-VAD modulation necessary to prevent adverse events are currently unknown and need to be evaluated. METHODS The purpose of this study was to use human aortic endothelial cells (HAECs) cultured within an endothelial cell culture model (ECCM) to: (i) identify and validate biomarkers to determine the effects of pulsatility; and (ii) conclude whether introduction of artificial pulsatility using flow-modulation approaches can mitigate changes in endothelial cells seen with diminished pulsatile flow. Nuclear factor erythroid 2–related factor 2 (Nrf-2)–regulated anti-oxidant genes and proteins and the endothelial nitric oxide synthase/endothelin-1 (eNOS/ET-1) signaling pathway are known to be differentially regulated in response to changes in pulsatility. RESULTS Comparison of HAECs cultured within the ECCM (normal pulsatile vs CF-VAD) with aortic wall samples from patients (normal pulsatile [ n = 5] vs CF-VADs [ n = 5]) confirmed that both the Nrf-2–activated anti-oxidant response and eNOS/ET-1 signaling pathways were differentially regulated in response to diminished pulsatility. Evaluation of 2 specific CF-VAD flow-modulation protocols to introduce artificial pulsatility, synchronous (SYN, 80 cycles/min, pulse pressure 20 mm Hg) and asynchronous (ASYN, 40 cycles/min, pulse pressure 45 mm Hg), suggested that both increased expression of Nrf-2–regulated anti-oxidant genes and proteins along with changes in levels of eNOS and ET-1 can potentially be minimized with ASYN and, to a lesser extent, with SYN. CONCLUSIONS HAECs cultured within the ECCM can be used as an accurate model of large vessels in patients to identify biomarkers and select appropriate flow-modulation protocols. Pressure amplitude may have a greater effect in normalizing anti-oxidant response compared with frequency of modulation. [ABSTRACT FROM AUTHOR]

Background: Direct measurement of blood flow output has been incorporated into ventricular assist devices (VADs), but long-term reliability of the additional device components has raised concerns regarding sensor drift and failure. As an alternative approach, the HeartMate II axial VAD (Thoratec Corp, Pleasanton, CA) estimates device flow output from power consumption and rotational speed of the device motor. This study evaluated the accuracy of HeartMate II flow estimation at the time of implantation. Methods: In 20 patients, intraoperative blood flow measurement of the HeartMate II flow estimator was compared with flow values obtained with an ultrasonic flow probe placed around the device outflow graft. Estimated and measured VAD flow data were simultaneously recorded and digitally stored while the device motor speed varied from 7,800 to 11,000 rpm and while achieving device flow outputs of 2 to 7 liters/min. Estimated and measured flows were compared using linear regression analyses and root mean square error. Results: HeartMate II flow estimation (FE) demonstrated a linear correlation with ultrasonic flow probe (FP) measurements: FE = 0.74 FP + 0.99 (R 2 = 0.56, p = 0.0001). A root mean square error of 0.8 liters/min was observed between flow estimation and direct flow measurement and suggests a 15% to 20% difference at flows of 4 of 6 liters/min. Conclusions: These results suggest that HeartMate II flow estimation may be used to provide directional information for trend purposes rather than absolute values of device blood flow output. Patient management should include but not be limited to this information. [Copyright &y& Elsevier]

The circadian rhythm of varying blood pressure and heart rate is attenuated or absent in patients with severe heart failure. In 28 patients supported by a left ventricular assist device (LVAD) for at least 30 days, a restoration of the circadian rhythm was demonstrated by a consistent nocturnal decrease, and then increase, of the LVAD flow while at a constant LVAD speed. The return of the circadian rhythm has implications for cardiac recovery, and the observation indicates that the continuous-flow LVAD has an intrinsic automatic response to physiologic demands. [Copyright &y& Elsevier]