MECHANISMS OF HEMOLYSIS WITH MITRAL PROSTHETIC REGURGITATION - STUDY USING TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND FLUID DYNAMIC SIMULATION

Objectives. The aims of this study were to define the hydrodynamic mec hanisms involved in the occurrence of hemolysis in prosthetic mitral v alve regurgitation and to reproduce them in a numeric simulation model in order to estimate peak shear stress. Background. Although in vitro studies have demonstrated that shear stresses >3,000 dynes/cm(2) are associated with significant erythrocyte destruction, it is not known w hether these values can occur in vivo in conditions of abnormal prosth etic regurgitant flow. Methods. We studied 27 patients undergoing reop eration for significant mitral prosthetic regurgitation, 16 with and 1 1 without hemolysis. We classified the origin and geometry of the regu rgitant jets by using transesophageal echocardiography. By using the p hysical and morphologic characteristics defined, several hydrodynamic patterns were simulated numerically to determine shear rates. Results. Eight (50%) of the 16 patients with hemolysis had paravalvular leaks and the other 8 had a jet with central origin, in contrast to 2 (18%) and 9 (82%), respectively, of the 11 patients without hemolysis (p = 0 .12, power 0.38). Patients with hemolysis had patterns of how fragment ation (n = 2), collision (n = 11) or rapid acceleration (n = 3), where as those without hemolysis had either free jets (n = 7) or slow decele ration (n = 4) (p < 0.001, power 0.99). Numeric simulation demonstrate d peak shear rates of 6,000, 4,500, 4,500, 925 and 950 dynes/cm(2) in these five models, respectively. Conclusions. The distinct patterns of regurgitant flea seen in these patients with mitral prosthetic hemoly sis were associated with rapid acceleration and deceleration or high p eak shear rates, or both. The nature of the flea disturbance produced by the prosthetic regurgitant lesion and the resultant increase in she ar stress are more important than the site of origin of the flow distu rbance in producing clinical hemolysis.