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Implanted biomaterials are often inevitably attacked by the bacterial infection. So far this problem has not been sufficiently explained and solved. It represents an 'evergreen' in the artificial heart research. Infection of biomaterials is a completely new clinical entity that profoundly differs from the common clinical course of various kinds of infections and their treatment. These infections are persistent; they resist host defense mechanisms and antibiotic therapy because the nature of these microorganisms has changed due to their protection by the biofilm of some bacteria on the surfaces of implanted biomaterials. In our 66 long-term experiments with total artificial heart (TAH) in 25 animals, the infection and sepsis were the main causes of death. The different organs, attacked by the bacterial and septic complications, varied from case to case as the predominant organs, the function of which ceased to be compatible with further survival. The main foci where the infection started were also very variable. The artificial hearts used in these 25 calves were predominantly of TNS-BRNO-VII type (19 animals), TNS-BRNO-II type (4 animals) and of ROSTOCK TAH type (2 animals). The decrease of the immune defense in the TAH recipients of different intensity was evident during the course of infectious process and simultaneously, the virulence and resistance of the microorganisms against antibiotics substantially increased. The activity of the infectious agents was often combined with increased blood coagulation and thrombi formation. In 5 calves hemolytic and hemorrhagic episodes were observed, and in 15 calves without simultaneous anti-calcification treatment, a primary calcification of driving diaphragms was observed. A common dystrophic calcification sometimes complicated septic thrombogenesis. The tactics of the antibiotic therapy differed according to the results of hemocultivation tests and body temperature and was often supported by the stimulation of the immune resistance. In 2 cases we used the coating of blood chamber and driving diaphragm with albumin and hydrophilic polyurethane in order to show whether this changed surface will influence positively or negatively the bacterial seeding on the biomaterial surface. We assume the infections in the TAH recipients to be a multi-factorial process, and therefore the prevention and therapy ought to be also multi-factorial. We tried to respect this approach and we were able to increase the survival from 39 to 293 days.
