(Circulation. 1995;92:3156-3157.)
© 1995 American Heart Association, Inc.
Articles |
From the Division of Pediatric Cardiology, Children's Medical Center, Medical College of Virginia/Virginia Commonwealth University, Richmond.
Correspondence to Richard M. Schieken, MD, Children's Medical Center, PO Box 980026, Richmond, VA 23298-0026. E-mail schieken@gems.vcu.edu.
| Introduction |
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After the identification of risk factors for the development of coronary heart disease in adults, investigators described the distribution of these risk variables in the pediatric population.5 6 They asked whether the level of these variables would predict the risk for subsequent development of coronary heart disease when these children became adults.7 Tracking, or the persistence of peer rank order over time, was one principal strategy used to detect risk.8 Those individuals who persistently tracked in the upper part of the distribution for a variable considered to be a risk factor were thought to be at higher risk as adults.
Because excess LV mass is related to coronary heart disease morbidity and mortality in adults, physicians have sought to determine the range of "normal" values of LV mass across the entire age range of children. The purpose of this quest has usually been to define the outliers from the normal distribution; these children were then categorized as having an abnormal value or "disease." Individuals above the 95th percentile were considered to have abnormal values.
LV mass in children has undergone studies similar to the traditional analysis of coronary heart disease risk factors. Initial studies were performed to establish the normal ranges over the childhood ages to allow clinical laboratories to identify children with abnormal values.9 Strategies to adjust LV mass, within an age, for body size differences quickly followed.10 Because the changes in LV mass during childhood that occurred with increasing body size did not appear to follow a simple linear curve, investigators suggested that allometric signals or exponential coefficients of body size be used to adjust for variation to develop a universal formula appropriate for the childhood years.11 12 The strong relation between body size and LV mass was confirmed by a genetic epidemiological study that described and quantified the presence of shared genetic effects influencing both LV mass and body size during the prepubertal years.13 In that study, the investigators suggested that lean body mass, rather than obesity, probably was responsible for the common genetic pathways.
But what about the effects of obesity and blood pressure levels on the size of children's hearts? Studies performed on school children participating in the Muscatine Study found that age, sex, height, weight, blood pressure, and obesity all contributed to the variance in LV mass.14 That study pointed out the difficulty to predict during active growth years the eventual LV size. Using a less sophisticated measure of obesity, namely skin-fold thickness, Goble et al15 suggested that because LV mass varied inversely with skin folds, the most important determinant of heart size was lean body mass. In their study, the determinants were somewhat different for boys than for girls. Moreover, even after adjustment for body size differences, boys had greater LV mass than girls. Other investigators found that both obesity and persistently elevated blood pressure influence LV mass.16 17 Because LV mass is a risk factor for coronary heart disease in adults, it was recommended that obese children lose weight to reduce their heart size, thus reducing their risk. Using the newer technique of dual-energy x-ray absorptiometry to determine lean body mass, Daniels et al1 suggested that lean body mass, not obesity, is the major determinant of LV mass.
Recently, genetic deletion polymorphism has been found in the angiotensin-converting enzyme gene.18 Individuals with certain forms of this gene, despite having normal blood pressures and normal body mass indexes, may have LV hypertrophy. No children were included in that study. Subsequent genetic studies may identify children with deletion polymorphism who develop LV hypertrophy. Whether this hypertrophy is expressed during childhood or whether it predicts a disease state is currently not known.
Daniels et al1 have provided us with important insights into the developmental biology of the growth of the heart. We have learned that lean body mass, not obesity or blood pressure, is the major determinant of heart size. Because LV mass is established as a predictor for coronary heart disease only in adults, until full growth of both the body and the heart is achieved, it remains very difficult to consider LV mass a risk factor for coronary heart disease in children.
| Footnotes |
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| References |
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3. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990;322:1561-1566. [Abstract]
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RM. Tracking of blood lipids and blood pressures in school age
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Keil U, Lorell BH, Riegger GAJ. Association between a deletion
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