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Article:
Mariacarolina Salerno, Valentina Esposito, Vincenzo Farina, Giorgio Radetti, Angela Umbaldo, Donatella Capalbo, Letizia Spinelli, Stefania Muzzica, Gaetano Lombardi, and Annamaria Colao
Improvement of cardiac performance and cardiovascular risk factors in children with GH deficiency after two years of GH replacement therapy: an observational, open, prospective, case-control study
J Clin Endocrinol Metab 2006; 0: jc.2005-0981v1 [Abstract]
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[Read eLetter] Is left ventricular performance effectively preserved in children with growth hormone deficiency?
Piercarlo Ballo, Arianna Bocelli and Maurizio de Martino, Department of Pediatrics, Meyer Children’s Hospital, University of Florence, Italy; and Sergio Mondillo, Department of Cardiovascular Diseases, University of Siena, Italy   (17 February 2006)

Is left ventricular performance effectively preserved in children with growth hormone deficiency? 17 February 2006
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Piercarlo Ballo,
Cardiologist
Cardiology Operative Unit, S. Andrea Hospital, La Spezia, Italy,
Arianna Bocelli and Maurizio de Martino, Department of Pediatrics, Meyer Children’s Hospital, University of Florence, Italy; and Sergio Mondillo, Department of Cardiovascular Diseases, University of Siena, Italy

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Re: Is left ventricular performance effectively preserved in children with growth hormone deficiency?

pcballo{at}tin.it Piercarlo Ballo, et al.

We read with interest the article by Salerno et al. (1) concerning cardiac performance in children with growth hormone deficiency (GHD). The authors found that children with GHD had reduced left ventricular (LV) mass index but preserved systolic and diastolic function in comparison with controls, and that 1 year of replacement therapy increased LV mass with no changes in LV function. These results are clinically relevant, as they suggest that 1) replacement treatment is effective in normalizing cardiac morphology, and 2) GHD affects LV size but not LV performance, substantially leading to small but normal functioning left ventricle.

A major issue in the interpretation of these findings derives from the methods used to assess LV systolic performance. When LV function is quantified using classical echocardiographic indices, such as ejection fraction or fractional shortening, by Salerno et al., they can overestimate effective systolic performance. A more appropriate quantification of LV systolic function can be assessed by calculation of the shortening at the midwall (2). Also, because systolic shortening is negatively related to LV afterload, adjustment for LV wall stress is required to obtain a load-independent index of systolic function (3). Consequently, determination of afterload- and rate-adjusted extent or velocity of midwall shortening is usually performed to measure effective LV myocardial contractility in children (2). In addition, M-mode determination of mitral annulus excursion and tissue Doppler analysis of myocardial velocities have recently gained ground as accurate techniques to assess long-axis LV systolic performance (4).

Similar considerations should be made regarding LV diastolic function. Although the authors correctly measured mitral inflow indices such as the E/A ratio and the isovolumic relaxation time, these measurements provide only a rough estimation of effective diastolic dysfunction, because of their dependence on confounding variables such as LV systolic function, loading conditions, heart rate, mitral regurgitation and left atrial pressure. This explains the conflicting data existing in literature regarding mitral inflow parameters in untreated children with GHD (1,5). Determination of load-independent indices by tissue Doppler imaging may allow more reliable quantification of effective LV diastolic performance (4).

Based on these considerations, the results of the interesting study by Salerno et al. indicate that children with GHD have normal LV endocardial function regardless of treatment, but whether these subjects show a depression in effective myocardial contractility, long-axis systolic function, or load-adjusted diastolic performance remains to be established. Considering the prognostic impact of such indices, this point is of clinical relevance. Further studies are needed to clarify whether GHD is associated with preserved LV performance, and to investigate the effect of replacement therapy on effective cardiac function.

REFERENCES

1. Salerno M, Esposito V, Farina V, Radetti G, Umbaldo A, Capalbo D, Spinelli L, Muzzica S, Lombardi G, Colao A. Improvement of cardiac performance and cardiovascular risk factors in children with GH deficiency after two years of GH replacement therapy: an observational, open, prospective, case-control study. J Clin Endocrinol Metab 2006 Jan 10; [Epub ahead of print]

2. Calabro R, Pisacane C, Pacileo G, Russo MG. Left ventricular midwall mechanics in healthy children and adolescents. J Am Soc Echocardiogr 1999;12:932-40.

3. Ballo P, Mondillo S, Guerrini F, Barbati R, Picchi A, Focardi M. Midwall mechanics in physiologic and hypertensive concentric hypertrophy. J Am Soc Echocardiogr 2004;17:418-27.

4. Ayabakan C, Ozkutlu S. Left ventricular myocardial velocities in healthy children: quantitative assessment by tissue Doppler echocardiography and relation to the characteristics of filling of the left ventricle. Cardiol Young 2004;14:156-63.

5. Szczepaniska Kostro J, Tolwinska J, Urban M, Gardziejczyk M, Glowinska B. Cardiac mass and function, carotid artery intima media thickness, homocysteine and lipoprotein levels in children and adolescents with growth hormone deficiency. J Pediatr Endocrinol Metab 2004;17:1405- 13.


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