© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Cardiac hypertrophy in Friedreich's ataxia
Charité/Franz-Volhard-Klinik & Virchow-Klinikum, Humboldt University of Berlin, Wiltbergstr. 50, 13125 Berlin, Germany
Dear Editor,
Recently, Lodi et al. described a deficiency of cardiac energetics in Friedreich's ataxia (FRDA) patients in the absence of cardiac dysfunction and hypertrophy [1]. The authors concluded that cardiac metabolic dysfunction proceeds the development of myocardial hypertrophy.
In this manuscript left ventricular hypertrophy (LVH) was defined as a septal (IVS) or posterior (PW) wall thickness of 
11 mm.
Most researchers, however, define hypertrophy when wall thickness is 13 mm [2–4]. This is a well-established and widely used criterion for hypertrophy.
Also, wall thickness depends on height, weight and sex. Therefore, Vasan et al. suggested determining wall thickness in relation to these variables [5]. Hypertrophy could be then determined as a wall thickness larger than the 95th percentile of normal wall thickness as suggested by examination of the Framingham Heart Study population [5].
Lodi et al. did neither use the criterion of 13 mm nor did they adjust wall thickness to height, weight, and sex. Therefore, the classification of patients only with IVS 11 mm as hypertrophy may not be correct. Because of the limitations in defining LVH by Lodi et al. we cannot follow their conclusions. In particular, the similar degree of energy depletion in patients with and without LVH as classified by Lodi et al. may be purely the result of the arbitrary definition of myocardial hypertrophy. Thus, we would suggest recalculating the data with respect to accepted definitions of myocardial hypertrophy.
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- Lodi R., Rajagopalan B., Blamire A.M., et al. Cardiac energetics are abnormal in Friedreich ataxia patients in the absence of cardiac dysfunction and hypertrophy: an in vivo 31P magnetic resonance spectroscopy study. Cardiovasc. Res. (2001) 52:111–119.
[Abstract/Free Full Text] - Charron P., Dubourg O., Desnos M., et al. Diagnostic value of electrocardiography and echocardiography for familial hypertrophic cardiomyopathy in a genotyped adult population. Circulation (1997) 96:214–219.
[Abstract/Free Full Text] - Maron B.J., Moller J.H., Seidman C.E., et al. Impact of laboratory molecular diagnosis on contemporary diagnostic criteria for genetically transmitted cardiovascular diseases: hypertrophic cardiomyopathy, long-QT syndrome, and Marfan syndrome: a statement for healthcare professionals from the councils on clinical cardiology, cardiovascular diseases in the young, and basic science, Americal Heart Association. Circulation (1998) 98:1460–1471.
[Free Full Text] - McKenna W.J., Spirito P., Desnos M., et al. Experience from clinical genetics in hypertrophic cardiomyopathy: proposal for new diagnostic criteria in adult members of affected families. Heart (1997) 77:130–132.
[Abstract/Free Full Text] - Vasan R.C., Larson M.G., Levy D., et al. Distribution and categorization of echocardiographic measurements in relation to reference limits. The Framingham Heart Study: formulation of a Height- and Sex-specific classification and its prospective Validation. Circulation (1997) 96:1863–1873.
[Abstract/Free Full Text]
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