emolytic anemia is uncommon after mitral valve repair and only a few cases have been reported. Although it is thought that rapid acceleration, fragmentation and collision of mitral regurgitation jets may be associated with high shear stress and cause hemolysis, 1,2 the precise mechanisms are not understood. In addition, the course of severe hemolysis after mitral valve repair has not been established, although in most cases the hemolysis improves with reoperation. [2][3][4][5][6][7][8][9][10][11] We report a patient who developed a severe hemolytic anemia after mitral valve repair that was reduced without the need for reoperation.
Case ReportA 60-year-old man suffered from shortness of breath because of severe mitral regurgitation secondary to the prolapse of the posterior mitral leaflet. Transthoracic echocardiography revealed severe mitral regurgitation filling the whole left atrium from the medial scallop of the posterior mitral leaflet. The dimension of the left atrium in systole phase and the left ventricle in diastole was 53 mm and 58 mm, respectively. Surgery was performed under cardiopulmonary bypass, in mild hypothermia. Myocardial protection was afforded with cold crystalloid cardioplegia. A left paraseptal atriotomy was performed. The prolapsing medial scallop of the posterior mitral leaflet was resected, and the edge of leaflet was sewn onto a mitral annulus. A Duran flexible ring was sutured and fixed along the mitral Circulation Journal Vol.67, September 2003 annulus. A water injection test confirmed no regurgitation. Transthoracic echocardiography 10 days after the mitral valve repair showed mild mitral regurgitation, reaching the deep left atrium from the posterior mitral commissure. The dimension of the left atrium in systole and the left ventricle in diastole was 34 mm and 45 mm, respectively. Three weeks after the mitral valve repair, the patient was discharged with no complaints. After 2 months, he was readmitted complaining of fatigue and shortness of breath. His palpebral conjunctivae were anemic and bulbar conjunctivae icteric, but splenomegaly was not apparent. Laboratory data were as follows: red blood cell (RBC): 206×10 4 / l; hemoglobin: 6.2 g/dl; haptoglobin: <10 mg/dl; reticulocytes: 15.6×10 4 / l; lactate dehydrogenase (LDH): 3,235 IU/L; total bilirubin: 1.6 mg/dl. All these values had been within the normal range 5 months earlier. The Donath-Landsteiner test, Coombs test, Ham test and sugar water test were all negative. Drug-induced hemolytic anemia was not apparent, because there was no reduction of hemolysis after stopping the administration of any drug without furosemide, which was administered before the mitral valve repair. The