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Ann Thorac Surg 1994;57:305-310
© 1994 The Society of Thoracic Surgeons


Articles

Lunular hypertrophy and aortic valve disease

Nadiv Shapira, MD*,a,b, Javier Fernandez, MDa,b, Kathryn J. Hirshfeld, RNa,b, A.Jorge Serra, MDa,b, Kathleen W. McNicholas, MDa,b, Mark Scott, MDa,b, Gerald M. Lemole, MDa,b

a Division of Cardiovascular Surgery, Medical Center of Delaware, Wilmington, Delaware, USA
b Deborah Heart and Lung Center, Browns Mills, New Jersey, USA

* Address reprint requests to Dr Shapira, Suite 205, Medical Arts Pavilion, 4745 Ogletown-Stanton Rd, Newark, DE 19713-2070.


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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 (≥3+, n = 13; <3+, n = 20), 13 had mixed aortic valve insufficiency and stenosis (≥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, arid 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 S 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%. We conclude that lunular hypertrophy may cause aortic valve dysfunction, primarily insufficiency. Long-term correction can be achieved through sculpturing of the involved cusps.


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{star} Presented at the Twenty-eighth Annual Meeting of The Society of Thoracic Surgeons, Orlando, FL, Feb 3–5, 1992.


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  1. Davies MJ, Path FRC. The aortic valveIn: Davies MJ, Path FRC, editors. Pathology of cardiac valves. London, Boston: Butterworths; 1980. pp. 1-61.
  2. Guiney TE, Davies MJ, Parker DJ, Leech GJ, Leatham A. The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study Br Heart J 1987;58:358-368.[Abstract/Free Full Text]
  3. Olson LJ, Subramanian MB, Edwards WD. Surgical pathology of pure aortic insufficiency: a study of 225 cases2nd ed. Mayo clin Proc. 59. 1984. pp. 835-841.
  4. Shapira N, Fernandez J, McNichqlas KW, et al. Hypertrophy of nodules of Arantius and aortic insufficiency: pathophysiology and repair Ann Thorac Surg 1991;51:969-972.[Abstract/Free Full Text]
  5. Shapira N, Lemole GM, Fernandez J, et al. Aortic valve repair for aortic stenosis in adults Ann Thorac Surg 1990;50:110-120.[Abstract/Free Full Text]
  6. Duran C. Invited commentary to Shapira N, et al Ann Thorac Surg 1991;51:972.[Free Full Text]
  7. Duran C, Alonso J, Gaite L, et al. Long-term results of conservative repair of rheumatic aortic valve insufficiency Eur J Cardiothorac Surg 1988;2:217-223.[Abstract/Free Full Text]
  8. Duran C, Kumar N, Gometza B, Halees ZA. Indications and limitations of aortic valve reconstruction Ann Thorac Surg 1991;52:447-454.[Abstract/Free Full Text]
  9. Bonow RO, Rosing DR, McIntosh CL, et al. The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function Circulation 1983;3:509-517.
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This Article
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