European Heart Journal Advance Access originally published online on October 5, 2005
European Heart Journal 2005 26(24):2742; doi:10.1093/eurheartj/ehi572
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Impaired left ventricular function in obesity?
The Academic Unit of Molecular
Vascular Medicine
Leeds General Infirmary
Great George Street
Leeds LS1 3EX, UK
Tel: +44 113 392 5401
Fax: +44 113 392 5744
E-mail address: dianebarker{at}hotmail.com
Cardiac Transplant Unit
South Manchester University Hospital
Manchester, UK
The Academic Unit of Molecular
Vascular Medicine
Leeds General Infirmary
Great George Street
Leeds LS1 3EX, UK
The Academic Unit of Molecular
Vascular Medicine
Leeds General Infirmary
Great George Street
Leeds LS1 3EX, UK
We read with interest the findings of Sasso et al.1 regarding the effects of insulin on left ventricular function during exercise in obese subjects. The authors conclude that their results ‘suggest a metabolic pathogenesis for the impaired left ventricular function in obesity’. This may be true, but the data they divulge do not support this conclusion. Most importantly, their interpretation that lower 
LVEF (changes from rest to submaximal exercise) in obese/ overweight subjects represents reduced ventricular performance is contingent upon the assumption that LVEF would increase indefinitely. As we all know, this assumption can never be true because mathematically, LVEF can never exceed the inviolable maximum of 100%. Moreover, their data show that the LVEFs during exercise were also not statistically different between the groups (Table 4). Because of similar exercise values, the size of LVEF is dependent on the resting LVEF. Their observation of lower LVEF was therefore entirely explained by the higher resting LVEFs in the obese/ overweight subjects, as shown clearly in Table 4, and had nothing to do with ‘reduced ventricular performance’.
Previous work has shown that left ventricular end systolic volume (LVESV) is a more reliable indicator of cardiac function than LVEF.2 We have taken the liberty of further analysing the data presented by Sasso et al.1 and find that there are no apparent differences in LVESV between any of the insulin or saline and lean vs. obese or overweight groups, either at rest or during the submaximal exercise (Figure 1), consistent with previous reports.3 This further confirms the view that their conclusion is not supported by their own data.
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As LVEF is well known to be load- and rate-dependent, and these are likely to be different in the lean vs. overweight cohorts during exercise, it is surprising that no heart rate or blood pressure data were presented in the article, especially because in the Methods section, the authors describe that these variables were actually measured. No doubt, availability of such data would allow readers to gain more insight into what their data convey.
References
- Sasso FC, Carbonara O, Nasti R, Marfella R, Esposito K, Rambaldi P, Mansi L, Salvatore T, Torella R, Cozzolino D. Effects of insulin on left ventricular function during dynamic exercise in overweight and obese subjects. Eur Heart J 2005;26:1205–1212.
[Abstract/Free Full Text] - White HD, Norris RM, Brown MA, Brandt PW, Whitlock RM, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 1987;76:44–51.
[Abstract/Free Full Text] - Carabello BA, Gittens L. Cardiac mechanics and function in obese normotensive persons with normal coronary arteries. Am J Cardiol 1987;59:469–473.[CrossRef][Web of Science][Medline]
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