Recent efforts in artificial heart research in Czechoslovakia.

The authors present basic information about the technical development of the total artificial heart (TAH) and TAH drivers. Long-term experiments, in which the TAH TNS-Brno-II and VII and the Rostock hearts were implanted, are described. Long-term experiments were dedicated to analysis of specific pathophysiologic problems (venous hypertension, thrombogenesis, and calcification) in order to increase survival rates. Thrombogenesis has been partially solved in the TNS-BRNO-VII device by optimal TAH construction using an asymmetric driving diaphragm, the undulating motion of which produced excellent results. Two methods for prevention of increase in central venous pressure (CVP) are verified: administration of antihypertensive drugs and atrial electrical stimulation. Of 155 calves studied, 50 long-term experiments in calves and one in a goat were done. The survival of these animals extended from 31 to 293 days of pumping (average survival, 116.9 days). To prevent driving diaphragm calcification, we have incorporated exogenic inhibitors of calcification into the diaphragm biomaterial (polyurethane). A unique long-term experiment with intrathoracic TAH implantation in the goat is also described. In addition clinical use of the TAH as a bridge to transplantation is discussed. Parallel research with the left ventricular assist device (LVAD) system was studied experimentally, and twice used in patients. The TAH TNS-BRNO-VII/80/clin/ was used in four patients. It worked faultlessly for 22 hours to 10 days. More precise and specific indications for TAH implantation when used as a bridge to transplantation are needed.

Therapy of venous hypertension in calves with total artificial heart (TAH).

Vasomotor disregulation, preponderantly expressed by a pathological increase of central venous pressure (CVP) in calves with total artificial heart (TAH), starts to be evident from about the 50th day of pumping. The main cause of this state is an imbalance in cardiac receptor areas. Ventricular vasodepressor mechanisms are eliminated with the ventricular tissue, which is replaced by the artificial blood pump. In the stumps of both atria, which remain in situ, all neural elements disappear immediately after TAH implantation, but within two months they are fully regenerated. Regenerated atrial receptors are the starting points of afferent neural stimuli, which in the vasomotor center of the brainstem, increase the activity of the vasoconstricting functional component. A general tendency to vasoconstriction, now not well counterbalanced, increases, and the progressive venous hypertension causes loss of liver function and morphology. Two therapeutic approaches were tried: afferent therapy by atrial electrical stimulation, and efferent therapy by the administration of antihypertensives. Both kinds of this therapy were sufficiently effective in reducing CVP, protecting the liver, and prolonging average survival.