Brain and Spinal Cord Lesions with Long-Term Total Artificial Heart Pumping

Summary

Animals surviving for extended periods with a total artificial heart (TAH) device sometimes experience central nervous system (CNS) complications. These are caused by the hypoperfusion of the CNS for various reasons; by microthromboembolization, which is manifested either by the emboli from a primary thrombotic formation or by calcified emboli; or by central nervous hemorrhages, owing to various causes. The central nervous system can be threatened by hypoperfusion, which may be caused particularly by a mechanical obstruction in the input or output tract of the pump, or by inadequate pumping. Clinically, peripheral spinal paralysis with a histological picture of tigrolysis of the ganglionic cells in the brain and spinal cord and encephalomalacia are frequent findings in these cases. Prevention in these cases can partially depend on proper TAH construction and adequate control and driving. Thromboembolic complications affecting the central nervous system can cause immediate termination of an experiment, if the thromboemboli affect the brain-stem centers. If other parts of the brain are impaired, then for some time this situation can be compatible with life; the animal is mostly hemiplegic before it expires after a few days. From the point of pathogenesis we can differentiate the thrombi caused directly by noncompatible thrombogenic material from those caused by incompatible pump construction resulting in “dead areas” where the bloodstream stagnates and thrombi are formed, or from septic thrombi caused by infection in the animal. On the other hand, the thrombus may be calcified (so-called secondary dystrophic calcification) or the driving diaphragm may be affected by “primary calcification.” The prevention of simple thromboembolism may be achieved by adequate TAH construction, by the use of nonthrombogenic material, and by avoiding infection, whereas the prevention of primary calcification may be attained by a special anticalcification treatment. Hemorrhagic lesions affecting the CNS are caused by inadequate anticoagulation and antiaggregation therapy, or by idiopathic endogenous disturbances of coagulation based on septic states or hepatic disturbances caused mostly by an increase in central venous pressure. A solution to the prevention of all possible causes of central nervous disturbance in TAH patients is necessary before its use becomes a clinical reality.