OBJECTIVE: Patients with hypertrophic obstructive cardiomyopathy due to diffuse hypertrophy extending to or below the papillary muscles are poor candidates for alcohol septal ablation and suboptimal candidates for transaortic septal myectomy. In addition, the outflow obstruction is often aggravated by an abnormal mitral valve and subvalvular apparatus. METHODS: We performed transatrial myectomy in 12 patients with diffuse hypertrophy, who were highly symptomatic despite maximal medical therapy. All had at least moderate mitral regurgitation and systolic anterior motion. The anterior mitral leaflet (AML) was detached from commissure to commissure, allowing an easy myectomy through this AML toward the base of the anterior papillary muscle, with mobility fully restored. The abnormal chordae from the septum to the anterior papillary muscle and AML were divided. The continuity of this AML was restored with augmentation using an autologous pericardial patch. The height of the posterior mitral leaflet was reduced and the repair completed using an oversized annuloplasty ring. RESULTS: The peak intraventricular gradients decreased spectacularly from 98.8 ± 6.29 to 19.2 ± 13.4 mm Hg (P < .001), and the systolic anterior motion and mitral regurgitation disappeared. One patient died of left ventricular diastolic dysfunction. All other patients left the hospital in New York Heart Association class I or II. CONCLUSIONS: We believe that this technique is preferable for patients with hypertrophic obstructive cardiomyopathy and diffuse hypertrophy extending to the midportion of the left ventricle or beyond. It results in disappearance of outflow tract gradients and allows correction of the mitral valve abnormality.
OBJECTIVE:Patients with hypertrophic obstructive cardiomyopathy due to diffuse hypertrophy extending to or below the papillary muscles are poor candidates for alcohol septal ablation and suboptimal candidates for transaortic septal myectomy. In addition, the outflow obstruction is often aggravated by an abnormal mitral valve and subvalvular apparatus. METHODS: We performed transatrial myectomy in 12 patients with diffuse hypertrophy, who were highly symptomatic despite maximal medical therapy. All had at least moderate mitral regurgitation and systolic anterior motion. The anterior mitral leaflet (AML) was detached from commissure to commissure, allowing an easy myectomy through this AML toward the base of the anterior papillary muscle, with mobility fully restored. The abnormal chordae from the septum to the anterior papillary muscle and AML were divided. The continuity of this AML was restored with augmentation using an autologous pericardial patch. The height of the posterior mitral leaflet was reduced and the repair completed using an oversized annuloplasty ring. RESULTS: The peak intraventricular gradients decreased spectacularly from 98.8 ± 6.29 to 19.2 ± 13.4 mm Hg (P < .001), and the systolic anterior motion and mitral regurgitation disappeared. One patient died of left ventricular diastolic dysfunction. All other patients left the hospital in New York Heart Association class I or II. CONCLUSIONS: We believe that this technique is preferable for patients with hypertrophic obstructive cardiomyopathy and diffuse hypertrophy extending to the midportion of the left ventricle or beyond. It results in disappearance of outflow tract gradients and allows correction of the mitral valve abnormality.