Heat Dissipation from Artificial Hearts: Characterizing Tissue Responses and Defining Safe Levels

Summary

Mechanical artificial hearts generate heat, imposing unprecedented biomedical problems. Experiments were conducted in calves to study the effects of chronic heating and the mechanisms of the adaptation response, and to determine the safe levels for device-tissue interfacial temperatures. Electric heat sources which dissipated three different levels of constant heat flux (0.04, 0.06, or 0.08 W/cm²) were implanted adjacent to lung and muscle for up to seven weeks. The tissue temperatures were continuously monitored at the heater surface and 1, 3, and 7 mm from the surface. Correlating the local tissue temperatures with histologic features, the safe upper limit was identified to be 43°C, or 4°C above the body temperature. There were significant differences in tissue temperatures between the lung and muscle at all distances and with all three fluxes (P = 0.0001), reflecting a higher blood perfusion in the lung tissue. With the highest heat flux of 0.08 W/cm², and the resultant initial surface temperature of 42.8°C ± 0.9°C, the lung showed no sign of tissue damage or necrosis, while the muscle, with a surface temperature of 45.3°C ± 2.2°C, was necrotic to a distance of 18.1mm and 3.0mm from the surface at 2 and 4 weeks, respectively. By the seventh week this muscle necrosis was totally replaced by fibrosis. Gradual decreases in the surface temperatures with the two higher heat fluxes and enhanced angiogenesis have suggested that the tissues adapt to chronic heating by increased perfusion. The expression of heat shock proteins by the tissue repair cells in the tissue capsule also suggests that cellular adaptation to heating is occurring.