Lunular hypertrophy and aortic valve disease

Cuspid malcoaptation secondary to abnormal hypertrophy in combination with stiffening involving the line of apposition (lunular hypertrophy) has not been recognized as a cause of aortic valve dysfunction. This entity was found in 50 adults (mean age, 62 years). Thirty-three had pure aortic valve insufficiency (> or = 3+, n = 13; < 3+, n = 20), 13 had mixed aortic valve insufficiency and stenosis (> or = 3+, n = 2; < 3+, n = 11), and 4 had pure aortic valve stenosis. Forty-one had a history of rheumatic heart disease and advanced mitral valve disease, and 7 had coronary artery disease. All underwent shaving of the hypertrophic protuberances, which in 26 patients constituted the entire aortic valve repair. In the remaining 24 patients, aortic valve repair included one or more additional procedures; there were 15 commissurotomies, 12 debridements of calcium deposits from the base of the cusps, and 5 cusp resuspensions. Concomitant mitral valve repair was performed in 26 patients, mitral valve replacement in 15, tricuspid valve repair in 11, coronary artery bypass grafting in 7, and repair of an ascending aortic aneurysm in 2. In 2 patients, the attempt to repair the aortic valve was unsuccessful, necessitating valve replacement. There were 5 operative deaths (10%), but none were related to aortic valve repair. Forty-three patients entered follow-up (mean, 56 +/- 57 months). Three patients (7%) suffered late recurrent aortic valve insufficiency (at 6, 48, and 72 months). The remaining 40 patients (93%) had trivial or no recurrent aortic valve dysfunction. The 6-year actuarial freedom from aortic valve-related problems was 92%.(ABSTRACT TRUNCATED AT 250 WORDS)