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.