Intravascular hemolysis in the late course of aortic valve

The degree of intravascular hemolysis was evaluated in 315 patients in the late course of aortic valve replacement. Starr-Edwards aortic ball valves of series 2300 caused significantly more hemolysis than did those of series 1200, as estimated from the serum lactate dehydrogenase levels. Smaller valves of series 2300 caused a higher degree of hemolysis than did the larger ones. Aortic disc valves induced a more moderate red cell destruction than did the ball valves, the Lillehei-Kaster significantly more than the Bjørk-Shiley prostheses. Crushing of red cells is thought to be a more important cause of hemolysis than shearing forces in turbulent blood. Hemolytic anemia represented a problem only in some patients with Starr-Edwards valve type 2300, although iron substitution was necessary also in some with other prostheses, since the hemoglobin-binding capacity of haptoglobin was exceeded in several patients. Valvular or paravalvular leakage was associated with stronger hemolysis in some patients, and should be suspected whenever the rate of red cell destruction increases. Longstanding intravascular hemolysis did not seriously affect renal function.