Rotary left ventricular assist devices (LVADs) show weaker response to preload and greater response to afterload than the native heart. This may lead to ventricular suction or pulmonary congestion, which can be deleterious to the patient's recovery. A physiological control system which optimizes responsiveness of LVADs may reduce adverse events. This study compared eight physiological control systems for LVAD support against constant speed mode. Pulmonary (PVR) and systemic (SVR) vascular resistance changes, a passive postural change and exercise were simulated in a mock circulation loop to evaluate the controller's ability to prevent suction and congestion and to increase exercise capacity. Three active and one passive control systems prevented ventricular suction at high PVR (500 dyne s cm(-5)) and low SVR (600 dyne s cm(-5)) by decreasing LVAD speed (by 200-515 rpm) and by increasing LVAD inflow cannula resistance (up to 1000 dyne s cm(-5)) respectively. These controllers increased LVAD preload sensitivity (to 0.196-2.415 L min(-1) mmHg(-1)) compared to the other control systems and constant speed mode (0.039-0.069 L min(-1) mmHg(-1)). The same three active controllers increased pump speed (600-800 rpm) and thus LVAD flow by 4.5 L min(-1) during exercise which increased exercise capacity. Physiological control systems that prevent adverse events and/or increase exercise capacity may help improve LVAD patient conditions.

Extracorporeal membrane oxygenation (ECMO) is used in critical care to manage patients with severe respiratory and cardiac failure. ECMO brings blood from a critically ill patient into contact with a non-endothelialized circuit which can cause clotting and bleeding simultaneously in this population. Continuous systemic anticoagulation is needed during ECMO. The membrane oxygenator, which is a critical component of the extracorporeal circuit, is prone to significant thrombus formation due to its large surface area and areas of low, turbulent, and stagnant flow. Various surface coatings, including but not limited to heparin, albumin, poly­(ethylene glycol), phosphorylcholine, and poly­(2-methoxyethyl acrylate), have been developed to reduce thrombus formation during ECMO. The present work provides an up-to-date overview of anti-thrombogenic surface coatings for ECMO, including both commercial coatings and those under development. The focus is placed on the coatings being developed for oxygenators. Overall, zwitterionic polymer coatings, nitric oxide (NO)-releasing coatings, and lubricant-infused coatings have attracted more attention than other coatings and showed some improvement in in vitro and in vivo anti-thrombogenic effects. However, most studies lacked standard hemocompatibility assessment and comparison studies with current clinically used coatings, either heparin coatings or nonheparin coatings. Moreover, this review identifies that further investigation on the thrombo-resistance, stability and durability of coatings under rated flow conditions and the effects of coatings on the function of oxygenators (pressure drop and gas transfer) are needed. Therefore, extensive further development is required before these new coatings can be used in the clinic.

Controlled and repeatable in vitro evaluation of cardiovascular devices using a mock circulation loop (MCL) is essential prior to in vivo or clinical trials. MCLs often consist of only a systemic circulation with no autoregulatory responses and limited validation. This study aimed to develop, and validate against human data, an advanced MCL with systemic, pulmonary, cerebral, and coronary circulations with autoregulatory responses. The biventricular MCL was constructed with pneumatically controlled hydraulic circulations with Starling responsive ventricles and autoregulatory cerebral and coronary circulations. Hemodynamic repeatability was assessed and complemented by validation using impedance cardiography data from 50 healthy humans. The MCL successfully simulated patient scenarios including rest, exercise, and left heart failure with and without cardiovascular device support. End-systolic pressure-volume relationships for respective healthy and heart failure conditions had slopes of 1.27 and 0.54 mm Hg mL −1 (left ventricle), and 0.18 and 0.10 mm Hg mL −1 (right ventricle), aligning with the literature. Coronary and cerebral autoregulation showed a strong correlation (R 2 : .99) between theoretical and experimentally derived circuit flow. MCL repeatability was demonstrated with correlation coefficients being statistically significant (P < .05) for all simulated conditions while MCL hemodynamics aligned well with human data. This advanced MCL is a valuable tool for inexpensive and controlled evaluation of cardiovascular devices.

Preventing ventricular suction and venous congestion through balancing flow rates and circulatory volumes with dual rotary ventricular assist devices (VADs) configured for biventricular support is clinically challenging due to their low preload and high afterload sensitivities relative to the natural heart. This study presents the in vivo evaluation of several physiological control systems, which aim to prevent ventricular suction and venous congestion. The control systems included a sensor-based, master/slave (MS) controller that altered left and right VAD speed based on pressure and flow; a sensor-less compliant inflow cannula (IC), which altered inlet resistance and, therefore, pump flow based on preload; a sensor-less compliant outflow cannula (OC) on the right VAD, which altered outlet resistance and thus pump flow based on afterload; and a combined controller, which incorporated the MS controller, compliant IC, and compliant OC. Each control system was evaluated in vivo under step increases in systemic (SVR ∼1400-2400 dyne/s/cm(5) ) and pulmonary (PVR ∼200-1000 dyne/s/cm(5) ) vascular resistances in four sheep supported by dual rotary VADs in a biventricular assist configuration. Constant speed support was also evaluated for comparison and resulted in suction events during all resistance increases and pulmonary congestion during SVR increases. The MS controller reduced suction events and prevented congestion through an initial sharp reduction in pump flow followed by a gradual return to baseline (5.0 L/min). The compliant IC prevented suction events; however, reduced pump flows and pulmonary congestion were noted during the SVR increase. The compliant OC maintained pump flow close to baseline (5.0 L/min) and prevented suction and congestion during PVR increases. The combined controller responded similarly to the MS controller to prevent suction and congestion events in all cases while providing a backup system in the event of single controller failure.

The low preload and high afterload sensitivities of rotary ventricular assist devices (VADs) may cause ventricular suction events or venous congestion. This is particularly problematic with rotary biventricular support (BiVAD), where the Starling response is diminished in both ventricles. Therefore, VADs may benefit from physiological control systems to prevent adverse events. This study compares active, passive and combined physiological controllers for rotary BiVAD support with constant speed mode. Systemic (SVR) and pulmonary (PVR) vascular resistance changes and exercise were simulated in a mock circulation loop to evaluate the capacity of each controller to prevent suction and congestion and increase exercise capacity. All controllers prevented suction and congestion at high levels of PVR (900 dynes s cm(-5)) and SVR (3000 dynes s cm(-5)), however these events occurred in constant speed mode. The controllers increased preload sensitivity (0.198-0.34 L min(-1) mmHg(-1)) and reduced afterload sensitivity (0.0001-0.008 L min(-1) mmHg(-1)) of the VADs when compared to constant speed mode (0.091 and 0.072 L min(-1) mmHg(-1) respectively). The active controller increased pump speeds (400-800 rpm) and pump flow by 2.8 L min(-1) during exercise, thus increasing exercise capacity. By reducing suction and congestion and by increasing exercise capacity, the control systems presented in this study may help increase quality of life of VAD patients.

The high cost of ventricular assist devices results in poor cost‐effectiveness when used as a short‐term bridging solution, thus a low‐cost alternative is desirable. The present study aimed to develop an intraventricular balloon pump (IVBP) for short‐term circulatory support, and to evaluate the effect of balloon actuation timing on the degree of cardiac support provided to a simulated in vitro severe heart failure (SHF) patient. A silicone IVBP was designed to avoid contact with internal left ventricular (LV) features (ie, papillary muscles, chordae, aortic, and mitral valves) based on LV computed tomography data of 10 SHF patients with dilated cardiomyopathy. The hemodynamic effects of varying balloon inflation and deflation timing parameters (inflation duty [D] and end‐inflation point [σ]) were evaluated in a purpose‐built systemic mock circulatory loop. Three IVBP actuation timing categories were defined: co‐, transitional, and counterpulsation. Compared to the SHF baseline, co‐pulsation increased aortic flow from 3.5 to 5.2 L/min, mean arterial pressure from 72.1 to 94.8 mmHg and ejection fraction from 14.4% to 21.5%, while mean left atrial pressure decreased from 14.6 to 10 mmHg. Transitional and counterpulsation resulted in a double ventricular pulse and extended the duration of increased ventricular pressure, potentially impeding diastolic filling and coronary perfusion. This in vitro study showed the IVBP could restore the hemodynamic balance of a simulated SHF patient with dilated cardiomyopathy to healthy levels.

Due to a shortage of donor hearts, rotary left ventricular assist devices (LVADs) are used to provide mechanical circulatory support. To address the preload insensitivity of the constant speed controller (CSC) used in conventional LVADs, we developed a preload-based Starling-like controller (SLC). The SLC emulates the Starling law of the heart to maintain mean pump flow () with respect to mean left ventricular end diastolic pressure (PLVEDm) as the feedback signal. The SLC and CSC were compared using a mock circulation loop to assess their capacity to increase cardiac output during mild exercise while avoiding ventricular suction (marked by a negative PLVEDm) and maintaining circulatory stability during blood loss and severe reductions in left ventricular contractility (LVC). The root mean squared hemodynamic deviation (RMSHD) metric was used to assess the clinical acceptability of each controller based on pre-defined hemodynamic limits. We also compared the in-silico results from our previously published paper with our in-vitro outcomes. In the exercise simulation, the SLC increased by 37%, compared to only 17% with the CSC. During blood loss, the SLC maintained a better safety margin against left ventricular suction with PLVEDm of 2.7 mmHg compared to -0.1 mmHg for CSC. A transition to reduced LVC resulted in decreased mean arterial pressure (MAP) and with CSC, whilst the SLC maintained MAP and . The results were associated with a much lower RMSHD value with SLC (70.3%) compared to CSC (225.5%), demonstrating improved capacity of the SLC to compensate for the varying cardiac demand during profound circulatory changes. In-vitro and in-silico results demonstrated similar trends to the simulated changes in patient state however the magnitude of hemodynamic changes were different, thus justifying the progression to in-vitro evaluation.

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