Why Total Artificial Hearts Fail: Hemocompatibility, Infection, and the Biological Limits of Durable Cardiac Replacement

Total artificial hearts (TAHs) can restore hemodynamics in refractory biventricular failure, yet truly durable long-term support remains difficult to achieve. This editorial examines more than five decades of TAH development, beginning with the first human implantation in 1969, and highlights recurring constraints that continue to limit performance across platforms. These include hemocompatibility problems that can drive both thrombosis and bleeding, chronic infection risk from permanent percutaneous interfaces and biofilm formation, physiologic mismatch from loss of native autoregulation and cardio-renal/endocrine signaling, immune and inflammatory activation related to foreign surfaces and recurrent infection, and persistent challenges in patient selection. Together, these patterns suggest that replacing pump output alone does not replace the heart as an integrated endocrine, immunologic, and neurohumoral organ. Recognizing these limits is essential for realistic counseling and for directing innovation toward improved blood-contacting surfaces, fully implantable energy delivery, smarter closed-loop control, and hybrid biologic-mechanical strategies.