OBJECTIVES: We sought to determine, using serial echocardiography, the hydrodynamic mechanisms involved in the occurrence of hemolysis after mitral valve repair. BACKGROUND: Recently, fluid dynamic simulation models have identified distinct patterns of mitral regurgitant flow disturbances in patients with mitral prosthetic hemolysis that were associated with high shear stress and may therefore produce clinical hemolysis. Rapid acceleration, fragmentation, and collision jets were associated with high shear stress and hemolysis whereas slow deceleration and free jets were not. METHODS: We reviewed serial echocardiographic studies of 13 consecutive patients with hemolytic anemia after mitral valve repair who were referred for mitral reoperation between January 1985 and December 1996 (group 1). Thirteen patients undergoing reoperation for mitral regurgitation after mitral valve repair but without hemolysis served as controls (group 2). RESULTS: The mitral regurgitant jet was central in origin in 12 group 1 patients and 9 group 2 patients (Fisher exact test, p= 0.3). The other patients had para-ring regurgitation. Group 1 patients had collision (n=11), rapid acceleration (n=2) or fragmentation (n=1) jets whereas group 2 patients had slow deceleration (n=11) or free jets (n=2) (Fisher exact test, p < 0.0001). One patient with hemolysis had both collision and rapid acceleration jets. The "culprit" jet could be identified on the postbypass transesophageal echocardiography (TEE) study in only 1 patient at the time of initial mitral repair. Twelve group 1 patients underwent reoperation, with subsequent resolution of hemolysis in all patients. At reoperation, the initial repair was found to be intact in 8 (67%) patients. CONCLUSION: Distinct patterns of flow disturbance associated with high shear stress were identified by color Doppler imaging in patients with hemolysis after mitral valve repair. The majority (92%) of these color flow disturbances were not present during intraoperative postbypass TEE study after initial mitral repair and subsequently developed in the early postoperative period.
OBJECTIVES: We sought to determine, using serial echocardiography, the hydrodynamic mechanisms involved in the occurrence of hemolysis after mitral valve repair. BACKGROUND: Recently, fluid dynamic simulation models have identified distinct patterns of mitral regurgitant flow disturbances in patients with mitral prosthetic hemolysis that were associated with high shear stress and may therefore produce clinical hemolysis. Rapid acceleration, fragmentation, and collision jets were associated with high shear stress and hemolysis whereas slow deceleration and free jets were not. METHODS: We reviewed serial echocardiographic studies of 13 consecutive patients with hemolytic anemia after mitral valve repair who were referred for mitral reoperation between January 1985 and December 1996 (group 1). Thirteen patients undergoing reoperation for mitral regurgitation after mitral valve repair but without hemolysis served as controls (group 2). RESULTS: The mitral regurgitant jet was central in origin in 12 group 1 patients and 9 group 2 patients (Fisher exact test, p= 0.3). The other patients had para-ring regurgitation. Group 1 patients had collision (n=11), rapid acceleration (n=2) or fragmentation (n=1) jets whereas group 2 patients had slow deceleration (n=11) or free jets (n=2) (Fisher exact test, p < 0.0001). One patient with hemolysis had both collision and rapid acceleration jets. The "culprit" jet could be identified on the postbypass transesophageal echocardiography (TEE) study in only 1 patient at the time of initial mitral repair. Twelve group 1 patients underwent reoperation, with subsequent resolution of hemolysis in all patients. At reoperation, the initial repair was found to be intact in 8 (67%) patients. CONCLUSION: Distinct patterns of flow disturbance associated with high shear stress were identified by color Doppler imaging in patients with hemolysis after mitral valve repair. The majority (92%) of these color flow disturbances were not present during intraoperative postbypass TEE study after initial mitral repair and subsequently developed in the early postoperative period.
Authors: Vasilis C Babaliaros; Adam B Greenbaum; Jaffar M Khan; Toby Rogers; Dee Dee Wang; Marvin H Eng; William W O'Neill; Gaetano Paone; Vinod H Thourani; Stamatios Lerakis; Dennis W Kim; Marcus Y Chen; Robert J Lederman Journal: JACC Cardiovasc Interv Date: 2017-04-24 Impact factor: 11.195