Electron microscopic study of driving diaphragms in long-term survival with a total artificial heart

A driving diaphragm in the long-term working total artificial heart (TAH) is under serious mechanical stress, and the long steady contact with blood causes changes to the diaphragm's surface. These changes can be influenced either by local or systemic interventions. In our study, we tried to follow the development of changes to the diaphragm's surface comparing the samples of diaphragms of long (over 30 days) and short (under 30 days) surviving calves and the effect of some preventive measures as well. We could confirm the presence of two types of calcification: a dystrophic calcification affecting primarily formed thrombi and necrotic tissue, and a primary type of calcification that begins in the form of calcifying nuclei on the protein layer of the polyurethane surface that is later on extensively covered with a fibrin network and blood cells. The calcified deposits caused mechanical damage or were the source of microembolization to the vital organs. A clotting mechanism occurs at the same time as the calcifying process from the beginning, often forming a fibrin network in and over the calcified deposits. An attempt at prevention was made by systemic administration of colloidal iron solution, Ferrum Lek (ferri saccharate in a stable colloidal form), based on the concept of the so-called reversed calciphylaxis.