Cardiac MR Center, Hygeia Hospital
4 Eythrou Stavrou Street
Maroussi 15123, Greece and
Harvard Medical School
Boston, MA, USA
Tel: +30 210 686 7000
Fax: +30 210 682 1931
E-mail address: pdanias{at}hygeia.gr;
pdanias{at}bidmc.harvard.edu
Dartmouth Medical School
5 Coliseum Ave, Suite 209
Nashua, NH 03063, USA
We read with interest the paper by Friberg et al.,1 regarding the association between left ventricular (LV) mass and obesity in adolescents. The authors reported that, compared with lean controls, the obese had higher absolute and height-indexed LV mass. This difference was statistically significant in females but not in males and there was a difference in LV mass between genders, as expected. These findings are, overall, similar to our recently published data in young (20- to 40-year-old) adults, and further our understanding of obesity-related cardiac abnormalities in a younger age group.2 In this sense, the data by Friberg and colleagues1 represent a significant contribution.
There are a few points we wish to address, which may be important for the interpretation of studies assessing cardiovascular structure and function in relation to body adiposity. Several factors affect LV mass including endocrine, renal and other chronic diseases, medications, and daily habits such as exercise, smoking, alcohol, or illicit drug use. None of these issues was directly addressed by Friberg et al.1 It is important to ascertain whether all of the above factors, particularly the daily habits that may pertain to the adolescent population studied by Friberg,1 were either equally distributed between study groups, or were controlled for in the analysis.
The authors performed sub-group analyses between obese and lean males and females with two of the four sub-groups containing <10 subjects. Such analyses should be viewed with scepticism. We believe that the most likely reason why there was no difference in LV mass among the male sub-groups was because of inadequate statistical power. The authors correctly pointed out that in order to have an 80% power to identify a difference in LV mass of 10 g/m (mass/height) between two groups (alpha=0.05 and standard deviation of 10 g/m), one would need at least 20 subjects in each group.
The authors did not report on the LV volumes in the two study groups, although these data were readily available. We have found that young, healthy, obese males have a higher LV end-diastolic volume (absolute and height indexed), but similar LV end-systolic volume.2 It would be interesting to know whether the obese adolescents also had a similar pattern of LV hypertrophy to the one we found in obese adults, characterized by primarily eccentric remodelling.
The difference in fasting insulin concentrations between obese and lean adolescents reported by the authors is striking and is indicative of insulin resistance among the obese. There was no association between LV mass and fasting hyperinsulinaemia, in agreement with similar findings in adults,3,4 in addition to data suggesting that insulin resistance is not independently associated with LV mass.5,6 As our previous findings have suggested an association between indices of cardiovascular structure and fasting serum ghrelin levels in healthy young adult males,3 it would also be of interest to investigate this association in adolescents. Such information would help improve our understanding of the interplay between endocrine factors and cardiovascular function in obesity.
References
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