Twelve patients with symptomatic aortic valve disease and 12 patients with aortic ball-valve prostheses were studied for evidence of traumatic hemolysis. Low or absent haptoglobins suggesting an accelerated rate of red cell destruction were found in 3 of the 12 patients with diseased valves and 11 of the 12 patients with ball-valve prostheses.
Two patients with diseased valves and three patients with ball-valve prostheses had hemosiderinuria. All but one of these had increased 24-hr urine iron excretions. Of the five patients with hemosiderinuria, two had severe hemolysis with iron deficiency anemia secondary to urinary iron loss. One of these patients had a prosthetic aortic valve. The other had severe aortic stenosis. In the remaining three patients, hemolysis was minimal. In all patients studied there was a marked diurnal variation in urinary iron levels with significantly greater amounts of iron being excreted during periods of activity than during periods of rest. Ferrokinetic and chromium survival studies indicated hemolysis by random destruction of red cells of all ages in three patients. Fourteen and one half percent of the injected dose of radioactive iron was recovered in the form of hemoglobin and hemosiderin from the urine of one patient.
It is concluded that mechanical hemolysis can result in iron deficiency anemia in patients with aortic valve disease as well as in those with prosthetic aortic ball valves. Hemolysis occurs by random destruction of cells of all ages rather than as a consequence of cell aging in such patients. Because urinary iron loss may occur with minimal hemolysis, urines should be examined for hemosiderin in all such patients with anemia, fragmented red cells, and decreased serum haptoglobins.