Rheumatic heart disease (RHD) is the leading cause of mitral valve disease in the developing world. In general, mitral valve repair is preferred over replacement. Although it is very successful in degenerative disease, its results in the rheumatic valve are not as successful as that for degenerative repair. Our approach has been to repair rheumatic mitral valves when the anatomic substrate appears to permit it, and we aimed by this study to present our immediate and midterm follow-ups of our cohort of rheumatic valve repair patients. From February 2011 to March 2013, 52 consecutive patients underwent mitral valve repair for rheumatic disease with different surgical techniques at the National Heart Institute of Egypt. Patients who had concomitant aortic or coronary artery bypass surgery were excluded. Also, patients needing an emergency operation or redo ones were excluded. On the contrary, patients who had concomitant tricuspid valve surgery were included. Demographic, intraoperative, and perioperative outcome data were recorded prospectively. All patients underwent TTE before hospital discharge. During follow-up, patients were contacted by telephone and invited for follow-up TTE yearly after their operations. Fifty-two patients with rheumatic disease underwent mitral repair. Their mean age was 25.92 ± 9.81 years. The study population was 78.8% female. Forty-nine patients were in New York Heart Association functional class III or IV. Repair procedures included implantation of Carpentier-Edwards Classic mitral annuloplasty ring (100% of the whole study group). Mitral commissurotomy and repair of the subvalvular apparatus were generally performed. Thirteen neochordae were implanted. Anterior leaflet extension with an autologous pericardial patch was used in 4 patients; annular decalcification, in 2 patients; tricuspid repair with De Vega technique, in 18 patients (34.5%); and repair with Carpentier-Edwards Classic tricuspid annuloplasty ring, in 9 (17.3%) patients. There was no operative mortality. The mean follow-up time was 59.9 ± 5 postoperative months (range, 49-60 months). Only 2 patients (3.8%) died. Follow-up echocardiography revealed more-than-or-equal-to-moderate (2+) grade of MR in 5 patients. During the follow-up period, the mean LV end-diastolic diameter decreased significantly from 5.57 ± 1.06 cm to 4.93 ± 0.74 cm (<0.001). The mean pulmonary artery pressure decreased from 44.94 ± 17.01 mmHg to 35.69 ± 7.92 mmHg postoperatively (P < .001). The mean mitral valve area increased from 1.2 ± 0.9 cm2 to 2.3 ± 0.2 cm2 postoperatively (P < .001). The mean mitral valve gradient decreased significantly from 12 ± 4.9 mmHg to 4.3 ± 1.9 mmHg postoperatively (P < .001). The mean MR grade decreased from 3.73 ± 0.45 to 0.96 ± 1.08 postoperatively (P < .001). We conclude that repair is possible in patients with rheumatic mitral valve dysfunction. Current techniques with some modifications can be efficient to restore both the anatomy and physiology (better function) of the mitral valve and can lead to favorable early and midterm outcomes. We, therefore, recommend that the number of rheumatic mitral repair procedures should be increased in developing countries to achieve the best results.