Changes in Total Artificial Heart Driving Diaphragms After Long-Term Pumping

Summary

During long-term pumping, the material of which driving diaphragms (DD) in total artificial hearts are constructed is subjected to many factors that limit its durability and functional capacity. Severe mechanical stress, various physical factors, temperature changes of the material, a long contact with blood, and possibly, even immune reactions between the diaphragm material and the immunological defense system of the organism must be considered.

The first reaction between the diaphragm surface and the blood components of the host organism is protein adsorption on the diaphragm surface. The procoagulant pathway is thus activated and thrombi created by this pathway grow as a primarily induced process and then become a biological skeleton for the anchoring and further growth of calcified deposits (CD). This type of calcification is dystrophic a secondary process, and it thus escapes from the regulatory processes that govern the mechanisms of calcification. At least in the initial period of pumping, experimental animals are treated with anticoagulant and antiplatelet agents. The pro-coagulant pathway may thus be more or less suppressed, becoming subsumed by the increased tendency to calcification. The protein and the phospholipid layer become a receptive field for calcifying nuclei. This process is then regulated by the specific regulatory mechanisms of calcification. Under these conditions, the thrombotization of calcified deposits is a secondary process.

The study of calciphylaxis has revealed the possibility of extending experimental calcification heterotopically to various organs and tissues. Such an ectopic calcifying organ in our experiments could be the driving diaphragm. From studying the phenomenon of calciphylaxis, we know that repeated administration of the same challenger that induce calciphylactic calcification after one dose during the so-called critical period can, on the other hand, block the calcifying process. This phenomenon is presumed to represent reversed calciphylaxis.

We have used this experience of reversed calciphylaxis and have administered systemically in repeated doses, a well known calciphylactic challenger, colloidal solution of iron — ferrisaccharate — to 13 of our experimental long-surviving calves. In comparison with untreated animals, we achieved either total or partial prevention of calcification in the majority of treated calves. We presume that the so-called endogenous inhibitors of calcification were stimulated by this treatment. For direct comparison, we examined 13 untreated calves. We also studied the DD in another 40 long-surviving calves and in 12 short surviving animals not treated with iron for up to 30 days of pumping. We assume the systemic factors, i.e., the internal metabolism of calcific promoters and inhibitors as the decisive factors in the calcifying process, whereas the local mechanical and physicochemical factors are so-called supporting, but not decisive, factors.