Editorial Commentary Role of Body Size on Cardiovascular Function

Physiological comparisons of cardiovascular (CV) structure/function among individuals or groups of individuals are often difficult because of differences in body dimensions. To have meaningful clinical and scientific comparisons, differences in body size must be accounted for. Although there is a plethora of data demonstrating that body size is an important determinant of CV structure/function, and although most researchers recognize the need to adjust CV parameters for differences in body size, there remains considerable confusion as to the most appropriate method to account for these differences. Chirinos et al1 in this issue of Hypertension highlight 2 important issues facing CV research: which body dimension descriptor, height, weight, body mass index (BMI), or body surface area (BSA), is optimal for scaling various CV measures; and which mathematical scaling method should be used. Chirinos et al1 examined the relationship between measures of resting CV parameters, with height, body weight, and BSA and concluded, as have numerous previous studies, that BSA was the most appropriate descriptor, because it incorporates changes in both height and weight, which were evident between their lean versus obese groups. It is important that the selection of the body size descriptor be based both on the accuracy of its measurement, and its physiological relevance to the CV parameter. In most circumstances BSA is not measured, but rather is estimated through formulae. BSA incorporates both low (adipose tissue) and high (skeletal and cardiac muscle) metabolically active tissues. A greater muscle mass necessitates a larger energetic requirement, and thus theoretically, the scaling of CV parameters to fat-free mass (FFM) may be the most appropriate body size descriptor. But what role does adipose tissue (AT) have on the changes in CV function, and should this be included when scaling these data? During exercise the extra weight from AT places extra burden on the CV system to respond to exercise, and blood flow to the AT increases to facilitate fatty acid metabolism. O’Connor et al2 have previously shown that the reserve capacity during exercise of CV parameters varied significantly with the percentage of body fat. Thus in this setting would body weight, BSA, or fat mass be a more appropriate body dimension descriptor than FFM? Perhaps more important than selecting the body dimension descriptor is the scaling technique used to adjust for differences in body size. There is a misconception that simply dividing the CV parameter to a measure of body size (ie, ratiometric scaling) removes the effects of body size on the CV parameter. Instead, a preferred approach might be the allometric scaling method, whereby the CV function is divided by the variable of interest raised to a scalar exponent, which is derived from an equation that linearly relates the two.3 The allometric method accounts for the nonlinearity of the relationship between a CV parameter and body size, providing a dimensionless variable. Indeed Chirinos et al1 reported that when the arterial variables were scaled allometrically to height, weight, or BSA, the effects of body size on CV parameters were completely removed. However, they also reported that many of the CV parameters could be scaled ratiometrically to BSA,1 producing dimensionless variables, an approach that would be more suitable for clinical research. The work of Chirinos et al1 illustrates the importance of scaling for body size to separate the normal physiological relationship between body size and CV function from the pathological effects of excess AT on CV function. Of note, in Chirinos et al,1 with the exception of characteristic impedance (Zc), the differences in arterial function between individuals without and with abdominal obesity are evident when normalized to BSA irrespective of the scaling approach used. For example, individuals with abdominal obesity had a higher arterial elastance, resistance, augmentation index, and a lower compliance compared to lean individuals when scaled ratiometrically or allometrically to BSA (Figure). Thus despite the allometric modeling process being theoretically and statistically superior to the ratiometric method, both methods had similar findings. Zc, however, did not differ when scaled allometrically to BSA but was higher when scaled ratiometrically to BSA in individuals with abdominal obesity versus no abdominal obesity (Figure). Could this lack of difference in Zc with ratiometric versus allometric scaling to define the effect of obesity be attributed to the transfer of the power function exponent, which was derived from a subset of their lean cohort to the entire population? The relationship between the body descriptor and CV parameter is likely to differ in the lean versus obese individuals, therefore, is it correct to extrapolate the b-exponent calculated from the lean to the mixed individuals? This is the conundrum that perplexes this field. But can we see the meat through the fat? Although once thought of as an inert tissue, AT is now considered a complex endocrine organ that releases a variety of factors that regulate The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. From the Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Md. Correspondence to Edward G. Lakatta, MD, Laboratory of Cardiovascular Science, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224-6825. E-mail [email protected] (Hypertension. 2009;54:459-461.) © 2009 American Heart Association, Inc.