European Heart Journal Advance Access originally published online on May 6, 2007
European Heart Journal 2007 28(13):1663; doi:10.1093/eurheartj/ehm134
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Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study: reply
Pediatric Cardiology Unit
Second University of Naples
Via Omodeo 45
Naples 80128
Italy
Pediatric Cardiology Unit
Second University of Naples
Via Omodeo 45
Naples 80128
Italy
Pediatric Cardiology Unit
Second University of Naples
Via Omodeo 45
Naples 80128
Italy
Tel: +39 081 193 638 51 Fax: +39 081 560 56 48 E-mail address: giodisal{at}yahoo.it
We thank Song very much for the interest in our work.1 In our study, we demonstrated a significant increase in left ventricular (LV) circumferential end-systolic stress, in agreement with previous studies,1–5 and a significant correlation between myocardial deformation properties, insulin levels, and HOMA, in agreement with previous studies.4
We agree with Song that we did not suggest any further hypotheses about putative mechanisms that link obesity, insulin levels, and myocardial disturbances. However, this was not the aim of our study, and several hypotheses on this topic, as he reported, have already been formulated in other papers.5–9
Conversely, the subclinical abnormalities in LV function, described in previous studies, although important, may exclusively reflect the role of comorbidities that contribute to LV dysfunction (e.g. hypertension, diabetes, coronary artery disease, and obstructive sleep apnoea) as well as altered loading, especially, as conventional echo-Doppler measures are load-dependent.
In our view, the uniqueness of our study is the evaluation of the effect of obesity in a clinical model potentially able to exclude the effect of other comorbidities on ventricular function using the more sensitive ultrasonic-derived strain and strain rate imaging.
Indeed, we studied myocardial deformation properties in healthy children with excess weight who have no other clinically appreciable cause of heart disease, in whom hypertension was excluded using both office and ambulatory blood pressure measurements.
About our methodology, unfortunately from the letter, it is not clear which methodological aspect of our study needs to be clarified.
Further studies, specifically designed, are needed to better describe the pathophysiological mechanism linking obesity and abnormal LV function.
References
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