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Circulation. 2002;105:1407-1411
doi: 10.1161/01.CIR.0000012626.81324.38
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(Circulation. 2002;105:1407.)
© 2002 American Heart Association, Inc.

Prevalence of Anderson-Fabry Disease in Male Patients With Late Onset Hypertrophic Cardiomyopathy

B. Sachdev, MRCP; T. Takenaka, MD PhD; H. Teraguchi, MD; C. Tei, MD PhD; P. Lee, MRCP MD, PhD; W.J. McKenna, MBBS FRCP, FESC; P.M. Elliott, MBBS MD, MRCP

From the Department of Cardiological Sciences, St Georges Hospital Medical School, London, UK (B.S., W.J.M., P.M.E.); the First Department of Internal Medicine, Kagoshima University, Kagoshima, Japan (T.T., H.T., C.T.); and the Metabolic Unit, University College London Hospitals, London, UK (P.L.).

Correspondence to Dr P.M. Elliott, Department of Cardiological Sciences, St George’s Hospital Medical School, Cranmer Terrace, London, SW17 0RE, United Kingdom. E-mail pelliott{at}sghms.ac.uk

Background— Although studies have suggested that "late-onset" hypertrophic cardiomyopathy (HCM) may be caused by sarcomeric protein gene mutations, the cause of HCM in the majority of patients is unknown. This study determined the prevalence of a potentially treatable cause of hypertrophy, Anderson-Fabry disease, in a HCM referral population.

Methods and Results— Plasma {alpha}-galactosidase A ({alpha}-Gal) was measured in 79 men with HCM who were diagnosed at >=40 years of age (52.9±7.7 years; range, 40–71 years) and in 74 men who were diagnosed at <40 years (25.9±9.2 years; range, 8–39 years). Five patients (6.3%) with late-onset disease and 1 patient (1.4%) diagnosed at <40 years had low {alpha}-Gal activity. Of these 6 patients, 3 had angina, 4 were in New York Heart Association class 2, 5 had palpitations, and 2 had a history of syncope. Hypertrophy was concentric in 5 patients and asymmetric in 1 patient. One patient had left ventricular outflow tract obstruction. All patients with low {alpha}-Gal activity had {alpha}-Gal gene mutations.

Conclusion— Anderson-Fabry disease should be considered in all cases of unexplained hypertrophy. Its recognition is important given the advent of specific replacement enzyme therapy.


Key Words: Anderson-Fabry disease • cardiomyopathy • hypertrophy




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