Thromboembolic and infectious complications of total artificial heart implantation.
Ward R A,Wellhausen S R,Dobbins J J,Johnson G S,DeVries W C
Annals of the New York Academy of Sciences
Thromboembolic and infectious events were found to be major complications of long-term total artificial heart implantation in two patients. Similar complications have been reported in other patients, as well as in animal studies. The thromboembolic events and the infectious complications appear to be interrelated. On the one hand, thrombi located on the valves and at the vascular anastomoses of the artificial heart were found to be infected at autopsy; such infections are known to exacerbate formation of thromboemboli. On the other hand, the generation of microthrombi may have contributed to the RES blockade seen in our patients. We hypothesize that this RES blockade led to a progressive decrease in lymphoid system function and impaired the patients' capacity to clear microorganisms from the circulation. These phenomena arose, in part, from the design of the artificial heart and were exacerbated by associated therapy, such as blood transfusions. Our data suggest several measures that might be taken in order to reduce the severity of both the thrombogenic and infectious complications. Improved anticoagulation regimens, which increase the ability of the physician to maintain the proper balance between thrombotic and hemorrhagic potential, are needed. This may require not only improved methods of monitoring anticoagulation and predicting changes in the effectiveness of various agents as other events supervene, but also new anticoagulant and antithrombotic drugs, for example, low molecular weight heparins and prostacyclin derivatives. It is also clear that the design of the artificial heart should be modified in order to improve fluid dynamics so that they will approximate as closely as possible those of the natural heart. This includes redesigning the mounting of the valves to eliminate crevices and discontinuities that allow stagnant flow and predispose to thrombus formation as well as imposing a dP/dt that minimizes shear-related hemolysis, thereby minimizing the need for blood transfusions. Prevention of infections presents a more difficult problem. Transcutaneous lines (regardless of their use) are an obvious route for infection, and attention should be given to minimizing the number and length of use of monitoring lines. However, until a totally implantable drive system is available, the drive lines will remain a potential avenue for the introduction of infections. The risk may be minimized by rigorous attention to care of the exit sites and by improved designs that will provide a better mechanical barrier by, for example, enhancing epithelial ingrowth into the materials of the drive line.(ABSTRACT TRUNCATED AT 250 WORDS)
Inflammatory mediated chronic anemia in patients supported with a mechanical circulatory assist device.
Pierce Christopher N,Larson Douglas F,Arabia Francisco A,Copeland Jack G
The journal of extra-corporeal technology
It is widely accepted and clinically anticipated that the patient implanted with a mechanical circulatory assist device (MCAD) will develop a state of chronic anemia that will last throughout the duration of MCAD support. Large-scale hemolysis mediated by the high sheer stress transmitted to the erythrocytes (RBCs) from the mechanical action of most MCAD systems is the accustomed mechanism responsible for this anemic status. MCAD patients exhibiting chronic anemia require frequent blood transfusions placing the patients at a high infectious risk to maintain an acceptable hematocrit. It is also acknowledged that the biomaterial interaction of the MCAD with the immune system precipitates a chronic inflammatory state in this patient population. Taken together, we hypothesize that inflammatory mediation of the erythropoiesis pathway at multiple sites-limiting the replacement of lysed RBCs-dictates the extent of chronic anemia in MCAD patients more than mechanical trauma to the blood. Hematological parameters were retrospectively analyzed for 78 patients implanted with a mechanical circulatory assist device for greater than 30 days at the University of Arizona Health Sciences Center between the years 1996 to 2002. Analysis demonstrates that the rate of hemolysis slows after MCAD implantation, marked by a progressively decreasing plasma hemoglobin concentration. In addition, the absolute reticulocyte count, a marker of juvenile RBC production, increases and remains above maximum normal values after MCAD implantation. Furthermore, the mean cell hemoglobin concentration indicates sufficient substrate for RBC development and maturation. However, hematocrit, a conventional marker of anemia, drops and remains below minimum normal value throughout the measured time period. A state of anemia in the MCAD supported patient results initially from the effect of hemolysis associated with the mechanical action of the MCAD, then chronically persists as the result of another undetermined mechanism. Given the state of chronic inflammation in the patient population, immunological activation most likely limits the full production of RBCs to their mature state.