The treatment of single functional ventricle is indisputably a significant healthcare challenge. It is the leading cause of death from any birth defect in the first year of life. Those who survive through completion of Fontan repair have chronic circulatory inefficiency and a lifelong risk of failure for which there is no preventive therapy. As more survivors reach adulthood, late Fontan failure and attrition has become a public health concern. As a clear reflection of its palliative nature, survival 30 years after Fontan is 43-70%. In a univentricular Fontan circulation, the vena cavae are connected directly to the pulmonary artery, placing the systemic and pulmonary circulations in a stable series arrangement. But, there is no subpulmonary power source to pump blood through the lungs. As a result, systemic venous pressure is pathologically elevated and preload to the single ventricle is reduced; combined, these factors form the basis of the Fontan paradox. Survivors are trapped for the remainder of their lives in a syndromic cycle of chronic debilitating disease that has no known solution. We have theorized that a means to replace the missing subpulmonary power source by modestly augmenting existing Fontan cavopulmonary flow (~6-8 mmHg) will address these problems. By replacing what is missing, the Fontan circulation can be reversed to a more stable two-ventricle physiology, producing physiologic cure. The biomechanical parameters for a blood pump to function in the complex 4-way flow anatomy of a cavopulmonary connection are markedly dissimilar to any other circulatory assist application: No such pump currently exists. We hypothesize that an anatomically-specific pump, based on the von Karman viscous pump, is an optimal solution to assist cavopulmonary flow. A single impeller will provide low-pressure, high-volume cavopulmonary blood flow augmentation in 4 opposing directions with no risk of venous pathway obstruction. In the event of rotational failure, the pump will default to serve as a relatively innocuous passive flow diverter in an unsupported Fontan. To develop this breakthrough innovation, our specific aims are to: 1) perform electromechanical optimization of a Fontan viscous pump; 2) perform biocompatibility optimization of a Fontan viscous pump via hemolysis and thrombogenicity studies; 3) perform durability and chronic in vivo testing of a Fontan viscous pump in an animal model of Fontan circulation. We will accomplish these aims by intersecting expertise in computational fluid dynamics; hydraulics; electromagnetics; rotordynamics; tribology; in vitro mock loop testing; thrombogenicity testing; and in vivo studies. Pilot data in an advanced prototype demonstrate compelling feasibility of this technology to improve circulatory status by permanently reversing the Fontan paradox. A permanently implantable Fontan blood pump will usher in a new era in single ventricle care. By simply replacing what is missing, it will enable the ultimate exit strategy for single ventricle heart disease: biventricular health.
We seek to develop an implantable blood pump that will permanently reverse the univentricular Fontan circulation. By replacing the missing subpulmonary power source, a normal two-ventricle circulation will be restored. It will prevent the progression of chronic Fontan disease, and substantially improve quality and duration of life for decades.
