(C.J.W); frank.pigula@ulp.org (F.A.P.) Overline: Cardiovascular diseaseOne Sentence Summary: A soft robotic sleeve modeled on the structure of the human heart assists cardiovascular function in an ex vivo and in vivo porcine model of heart failure. Abstract:There is much interest in form-fitting, low modulus, implantable devices or soft robots that can mimic or assist in complex biological functions such as the contraction of heart muscle. Here we present a soft robotic sleeve that is implanted around the heart and actively compresses and twists to act as a cardiac ventricular assist device. The sleeve does not contact blood, obviating the need for anticoagulation therapy or blood thinners, and reduces complications with current ventricular assist devices such as clotting and infection. Our approach used a biologically inspired design to orient individual contracting elements or actuators in a layered helical and circumferential fashion, mimicking the orientation of the outer two muscle layers of the mammalian heart. The resulting implantable soft robot mimicked the form and function of the native heart, with a stiffness value of the same order of magnitude as native heart tissue. We demonstrated feasibility of this soft sleeve device for supporting heart function in a porcine model of acute heart failure. The soft robotic sleeve can be customized to patient-specific needs and may have the potential to act as a bridge to transplant for patients with heart failure.

Previous soft robotic ventricular assist devices have generally targeted biventricular heart failure and have not engaged the interventricular septum that plays a critical role in blood ejection from the ventricle. We propose implantable soft robotic devices to augment cardiac function in isolated left or right heart failure by applying rhythmic loading to either ventricle. Our devices anchor to the interventricular septum and apply forces to the free wall of the ventricle to cause approximation of the septum and free wall in systole and assist with recoil in diastole. Physiological sensing of the native hemodynamics enables organ-in-the-loop control of these robotic implants for fully autonomous augmentation of heart function. The devices are implanted on the beating heart under echocardiography guidance. We demonstrate the concept on both the right and the left ventricles through in vivo studies in a porcine model. Different heart failure models were used to demonstrate device function across a spectrum of hemodynamic conditions associated with right and left heart failure. These acute in vivo studies demonstrate recovery of blood flow and pressure from the baseline heart failure conditions. Significant reductions in diastolic ventricle pressure were also observed, demonstrating improved filling of the ventricles during diastole, which enables sustainable cardiac output.

Soft robotic devices have significant potential for medical device applications that warrant safe synergistic interaction with humans. This article describes the optimization of an implantable soft robotic system for heart failure whereby soft actuators wrapped around the ventricles are programmed to contract and relax in synchrony with the beating heart. Elastic elements integrated into the soft actuators provide recoiling function so as to aid refilling during the diastolic phase of the cardiac cycle. Improved synchronization with the biological system is achieved by incorporating the native ventricular pressure into the control system to trigger assistance and synchronize the device with the heart. A three-state electro-pneumatic valve configuration allows the actuators to contract at different rates to vary contraction patterns. An in vivo study was performed to test three hypotheses relating to mechanical coupling and temporal synchronization of the actuators and heart. First, that adhesion of the actuators to the ventricles improves cardiac output. Second, that there is a contraction-relaxation ratio of the actuators which generates optimal cardiac output. Third, that the rate of actuator contraction is a factor in cardiac output.