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 p ure aortic valve insufficiency (greater than or equal to 3 +, n = 13; < 3 +, n = 20), 13 had mixed aortic valve insufficiency and stenosis ( greater than or equal to 3 +, n = 2; < 3 +, n = 11), and 4 had pure ao rtic valve stenosis. Forty-one had a history of rheumatic heart diseas e 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 proc edures; there were 15 commissurotomies, 12 debridements of calcium dep osits from the base of the cusps, and 5 cusp resuspensions. Concomitan t mitral valve repair was performed in 26 patients, mitral valve repla cement in 15, tricuspid valve repair in 11, coronary artery bypass gra fting in 7, and repair of an ascending aortic aneurysm in 2. In 2 pati ents, the attempt to repair the aortic valve was unsuccessful, necessi tating valve replacement. There were 5 operative deaths (10%), but non e were related to aortic valve repair. Forty-three patients entered fo llow-up (mean, 56 +/- 57 months). Three patients (7%) suffered late re current aortic valve insufficiency (at 6, 48, and 72 months). The rema ining 40 patients (93%) had trivial or no recurrent aortic valve dysfu nction. The 6-year actuarial freedom from aortic valve-related problem s was 92%. We conclude that lunular hypertrophy may cause aortic valve dysfunction, primarily insufficiency. Long-term correction can be ach ieved through sculpturing of the involved cusps.