Cavopulmonary Assist to Reverse the Fontan

毫无疑问，单功能脑室的治疗是一个重大的医疗挑战。它是领先的 出生第一年因任何出生缺陷而死亡的原因。那些通过完成方坦而幸存下来的人 修复具有慢性循环低效和终生失败的风险，没有预防性治疗。 随着越来越多的幸存者成年，晚期方坦衰竭和磨损已成为一个公共卫生问题。作为一名 清楚地反映出其姑息性质，方坦术后30年存活率为43-70%。在单室Fontan中 循环中，腔静脉直接连接到肺动脉，将全身和肺 在稳定的系列安排中的环流。但是，没有肺下动力源来泵血。 通过肺部。其结果是，全身静脉压病理性升高，并预加负荷至单侧。 脑室减少；这些因素结合在一起，形成了方坦悖论的基础。幸存者被困在 他们的余生处于慢性衰弱疾病的综合征循环中，没有已知的解决方案。 我们已经提出了一种方法来替换丢失的肺下电源，方法是适度增加 现有的Fontan腔静脉肺动脉流(~6-8 mm Hg)将解决这些问题。通过替换缺失的内容， Fontan循环可以逆转为更稳定的双心室生理，产生生理学治愈。 血泵在心脏复杂四向流解剖中作用的生物力学参数 腔-肺连接明显不同于任何其他循环辅助应用：没有这样的泵 目前存在。我们假设，在冯·卡曼粘性泵的基础上， 是辅助腔肺血流的最佳方案。单个叶轮将提供低压、大流量 4个相反方向的腔肺血流量增加，无静脉通路阻塞的风险。 如果发生旋转故障，泵将默认充当相对无害的被动流量分流装置。 无人支持的方坦。为了发展这一突破性的创新，我们的具体目标是：1)执行 Fontan粘性泵的机电优化2)Fontan的生物相容性优化 通过溶血和血栓形成研究的粘性泵；3)执行耐用性和长期体内测试 Fontan循环动物模型中的Fontan粘性泵。我们将通过交叉来实现这些目标 计算流体动力学专业知识；水力学；电磁学；旋转动力学；摩擦学；体外模拟 循环试验；血栓形成试验；以及活体研究。高级原型中的试验数据演示了 这项技术通过永久逆转Fontan改善循环状况的令人信服的可行性 自相矛盾。可永久植入的Fontan血泵将开启单心室护理的新纪元。通过 简单地取代缺失的东西，它将使单心室心脏病的最终退出策略成为可能： 两个心室的健康。

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.