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J Am Coll Cardiol, 1996; 27:399-406 © 1996 by the American College of Cardiology Foundation |
Department of Cardiology, Cleveland Clinic Foundation, Ohio 44195, USA.
OBJECTIVES. The aims of this study were to define the hydrodynamic mechanisms involved in the occurrence of hemolysis in prosthetic mitral valve 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/cm2 are associated with significant erythrocyte destruction, it is not known whether these values can occur in vivo in conditions of abnormal prosthetic regurgitant flow. METHODS. We studied 27 patients undergoing reoperation for significant mitral prosthetic regurgitation, 16 with and 11 without hemolysis. We classified the origin and geometry of the regurgitant jets by using transesophageal echocardiography. By using the physical 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 flow fragmentation (n = 2), collision (n = 11) or rapid acceleration (n = 3), whereas those without hemolysis had either free jets (n = 7) or slow deceleration (n = 4) (p < 0.001, power 0.99). Numeric simulation demonstrated peak shear rates of 6,000, 4,500, 4,500, 925 and 950 dynes/cm2 in these five models, respectively. CONCLUSIONS. The distinct patterns of regurgitant flow seen in these patients with mitral prosthetic hemolysis were associated with rapid acceleration and deceleration or high peak shear rates, or both. The nature of the flow disturbance produced by the prosthetic regurgitant lesion and the resultant increase in shear stress are more important than the site of origin of the flow disturbance in producing clinical hemolysis.
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