Cavopulmonary Assist to Reverse the Fontan

单功能心室的治疗无疑是一个重大的医疗挑战。它是领先的 出生后第一年内任何出生缺陷导致的死亡原因。那些在丰唐完工后幸存下来的人 修复具有慢性循环效率低下和终生失败的风险，对此没有预防性治疗。 随着越来越多的幸存者进入成年，晚期Fontan失败和自然减员已成为一个公共卫生问题。作为 Fontan术后30年生存率为43- 70%，这清楚地反映了其姑息性的性质。单心室Fontan 在循环中，腔静脉直接连接到肺动脉，将体循环和肺循环放置在腔静脉中。 在一个稳定的系列安排循环。但是，没有肺下动力源来泵送血液 穿过肺部结果，全身静脉压病理性升高，并预加载到单个 心室缩小;结合起来，这些因素形成了Fontan悖论的基础。幸存者被困在 他们的余生都在慢性衰弱疾病的综合征循环中度过，这种疾病没有已知的解决方案。 我们已经从理论上证明，通过适度增加肺动脉压来替代缺失的肺下电源的方法 现有的Fontan腔静脉血流（~6-8 mmHg）将解决这些问题。通过替换缺失的部分， Fontan循环可以逆转为更稳定双心室生理学，产生生理学治愈。 血泵在复杂的四向血流解剖结构中发挥作用的生物力学参数 腔静脉连接与任何其他循环辅助应用明显不同：无此类泵 目前存在。我们假设，一个解剖学上特定的泵，基于冯卡门粘性泵， 是辅助空腔流动的最佳解决方案。一个单一的叶轮将提供低压，高容量 4个相反方向的腔静脉血流量增加，没有静脉通路阻塞的风险。 在旋转故障的情况下，泵将默认用作相对无害的被动分流器， 一个不受支持的方丹为了开发这一突破性创新，我们的具体目标是：1）执行 Fontan粘性泵的机电优化; 2）Fontan粘性泵的生物相容性优化 粘性泵通过溶血和血栓形成研究; 3）进行耐久性和慢性体内测试， Fontan循环动物模型中的Fontan粘性泵。我们要实现这些目标， 计算流体动力学;水力学;电磁学;转子动力学;摩擦学;体外模拟 环测试;血栓形成性测试;和体内研究。先进原型中的试验数据表明， 该技术通过永久逆转Fontan改善循环状态的令人信服的可行性 悖论永久植入式Fontan血泵将开创单心室护理的新时代。通过 简单地取代缺失的部分，它将使单心室心脏病的最终退出策略成为可能： 双心室健康

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.