RESUMO
A rather long and extensive experience with tissue reconstruction in patients with mitral valve disease, and a much less extensive one with oartic lesions, has convinced us of the superiority of the presented techniques of reconstruction, and of the preferability of fascia lata over all other tissues so far tried for this purpose. Despite an early increment of shrinkage of the order of about 30% of each linear measurement, late studies of fascia lata removed from reconstructed valves after several years (over five) indicate no loss of cellularity and no measurable loss of tissue strength or flexibility. Late calcification was not observed in any of our baboons, although it appears to be a consistent development in dogs. It has been seen in only one patient (after four years) to date. It is now believed that we can offer prolonged clinical benefit approaching actural "cure" to many of the younger patients who otherwise would have no recourse but to prosthetic palliation. It is true that recently Willen, Dubiel and Johansson (50, 51), Gersbach and Wegmann (52), and Senning and Rothlin (53) have demonstrated that repetitive deposits of fibrin upon the surfaces of fascia lata implanted within the cardiovascular chambers lead to progressive encapsulation with organizing connective tissue (scar). At some time period following surgery, closer to 10 years than to 5, degeneration of the fascia takes place, presumably due to "strangulation" by the organized exudate which interrupts the "normal" mechanism of its nutrition which is based upon diffusion from the flowing blood. The recent contributions of Sullivan, Harken and Gorlin (54), Weily and Genton (55), and Harker and Slicter (56) to our understanding of the role of the platelets in initiating such fibrinous deposition now provide us with a way to prevent such late degeneration of valves made of fascia lata. The regular administration of platelet dispersing agents (aspirin, Persantin, or inderol) in ordinary therapeutic dosage would seem to be completely protective. Undoubtedly, anticoagulant therapy would be equally effective. However, the permanent maintenance of a proper level of "anti-coagulation" such as is usually deemed necessary following implantation of a prosthetic heart valve is a heavy psychological and biological burden for a patient to bear. Many such individuals live precariously between the risks of thromboembolism and the risks of hemorrhage. Thromboembolism really only represents a farther point along the spectrum of the readiness of fibrin accumulation following initial platelet aggregation and deposition. Since frank thromboembolism appears "never" to follow intracardiac implantation of fascia lata, it would seem that platelet dispersive therapy sould suffice in such cases.
