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J Am Coll Cardiol, 2007; 49:375, doi:10.1016/j.jacc.2006.10.031
(Published online 3 January 2007). © 2007 by the American College of Cardiology Foundation |
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* Department of Cardiovascular Diseases, Ochsner Medical Center, 1514 Jefferson Highway, New Orleans, Louisiana 70121 (Email: clavie{at}ochsner.org).
There is nothing new except what has been forgottenMarie Antoinette (1)
We read with interest the recent study by Elmariah et al. (2) as well as the intriguing editorial by Feldman (3) regarding potential genetic factors to explain gender differences in heart failure (HF) prognosis. Elmariah et al. (2) demonstrated that peak oxygen consumption (VO 2) was significantly lower in women with HF than in men and that this cardiopulmonary variable did not predict HF prognosis or the need for cardiac transplantation as well in women as it did in men. We firmly agree with this assessment and have made this point (although in a smaller number of women) in several publications during the past decade, sources not cited in their excellent study (4–9).
Although our initial observations were made nearly 10 years ago in a small sampling of women with HF (4), we subsequently sorted this issue out in more detail by noting that higher body fat is an independent predictor of better HF prognosis, which may partly explain the well-recognized "obesity paradox" (7,8,10–13). Because women typically have considerably higher levels of percent body fat and, for practical purposes, fat weight is not aerobically active, it would make sense that VO 2 corrected for total body weight would be lower in groups of patients with higher body fat (e.g., women and more obese patients) (5–9,11,13,14). However, if one adjusts peak VO 2 for lean body mass as opposed to total weight, both genders and obese versus lean patients have more similar functional capacities, and this assessment allows for more accurate determination of HF prognosis (5,6,8,9,13). We have most recently demonstrated that peak O 2 pulse (peak VO 2/peak heart rate) adjusted for lean body mass was even slightly superior to peak VO 2 corrected for lean body mass for HF prognostication (6).
Therefore, we agree with these investigators that this evidence must be considered when cardiopulmonary metabolic parameters are used for prognostic stratification of women with HF (4–6,9). Furthermore, a simple and very inexpensive determination of percent body fat by the sum of the skin-fold method (or using more sophisticated and expensive techniques such as dexa scanning or underwater weighing) and correcting VO 2 or O 2 pulse for lean as opposed to total weight should substantially improve the accuracy of cardiopulmonary testing for HF stratification, particularly in women and in other groups of patients with higher percent body fat. Finally, although in some situations complex mechanisms are involved, we believe that this is an example of where one may often reach for complex explanations for findings when in fact the simple explanation may be staring us in the face!
As Edward R. Murrow noted: "The obscure we see eventually. The completely obvious, it seems, takes longer" (15).
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