(Hypertension. 1996;27:339-345.)
© 1996 American Heart Association, Inc.
Articles |
Weights at Birth and in Early Infancy, Systolic Pressure, and Left Ventricular Structure in Subjects Aged 8 to 24 Years
From the National Institute of Health and Medical Research (INSERM), Unit 258, Hôpital Broussais, Paris (M.Z., C.B.-K., P.D.), and the Preventive Medicine Center, Vandoeuvre-lès-Nancy (E.L., G.S.), France.
Correspondence to Dr Mahmoud Zureik, Institut National de la Santé et de la Recherche Médicale, Unit 258, Hôpital Broussais, 96 rue Didot, 75014-Paris, France.
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Abstract |
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Abstract The objective of this study was to determine whether systolic pressure and left ventricular mass in children, adolescents, and young adults are related to fetal and infant growth. Blood pressure measurements and M-mode echocardiography were performed in 210 subjects aged 8 to 24 years whose information on weights at birth and in early infancy, written by physicians, was obtained from the children's health record booklets. Systolic pressure, adjusted for sex and current height or for sex, current age, weight, and height, was the highest in subjects with low birth weight. No association was observed between systolic pressure and weight at either 9 months or 2 years. Left ventricular mass, adjusted for sex and current height or for sex, current age, weight, and height, increased with decreasing weight at 9 months or 2 years, independent of systolic pressure. Increased ventricular mass associated with reduced infant growth was concentric, resulting from a proportionate thickening of the posterior wall and interventricular septum. Left ventricular mass was not related to birth weight. These findings were observed in both sexes and in all age subgroups and were independent of gestational age, birth order, and parental risk factors. This study supports the hypothesis that systolic pressure and left ventricular mass might be partly determined during fetal life and early infancy. The mechanisms that underlie the associations of blood pressure and left ventricular structure with weights at birth and in early infancy should be studied thoroughly.
Key Words: blood pressure • echocardiography • epidemiology • growth • hypertrophy, left ventricular
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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It has been hypothesized that cardiovascular disease has some of its origins during fetal life and infancy. Poor growth in fetal life and infancy has been associated with a higher rate of coronary heart disease in adult life in both men and women.1 2 3 4 Hypertension and LV hypertrophy may be possible links between reduced growth and later cardiovascular risk. On the one hand, hypertension is a well-accepted risk factor for ischemic heart disease and stroke, and increased echocardiographically measured LVM has been shown to be a strong predictor of cardiovascular morbidity and mortality and all causes of death.5 6 7 8
On the other hand, low birth weight, a proxy for intrauterine influences, has been associated with high BP in adult life9 10 11 as well as in childhood.9 12 13 14 Low weight at 1 year, a proxy for growth influences in early infancy, was related to increased LVM in adult life in the only study that assessed the relation between early growth and LV structure.15 However, this study, conducted on a small proportion of the birth cohort from which they arose,2 comprised men born in the early century, when healthcare systems and environmental conditions were different. Findings need to be confirmed in other populations and should be investigated in women. Furthermore, differences in LV structure according to fetal and infant growth among subjects at an earlier age, if demonstrated, would lead to a better understanding of the early developmental stages of LV hypertrophy.
Thus, we examined the relationships of weight at birth and weights at 4 months, 9 months, 2 years, and 6 years with SBP and LV structure in a sample of 210 males and females aged 8 to 24 years.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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In the framework of the Nancy Stanislas Cohort Study, which has a cohort of 1000 families and is designed to explore the role of environmental and genetic factors related to cardiovascular diseases, 100 consecutive Caucasian families were recruited for study of the relationships of weights at birth and in early infancy with BP and echocardiographic measurements. All families were of Caucasian origin, composed of both natural parents (aged <60 years) and at least two offspring (aged
8 years, n=214), and examined in
the
Preventive Medicine Center of Vandoeuvre-lès-Nancy, France,
between June and December 1994. The population screened in this center
is composed of families living in the South Lorraine area (East France)
and volunteering to have a free health checkup
examination.16 All members of one family were examined on
the same day. On the day of examination, parents and children completed
a self-administered questionnaire that provided information on
medical history, education level, and lifestyle habits. Two trained nurses measured BP with subjects in the supine position after a 10-minute rest on the right arm with a mercury sphygmomanometer and appropriately sized cuff, using the first and fifth phases of the Korotkoff sounds. The average of two BP measurements (5-minute intervals), taken before the echocardiographic examination, was used. Weight (to the nearest 100 g) and height (to the nearest 0.1 cm) were measured in subjects who did not have on shoes or clothes. Tanner stage of sexual development was recorded by a physician based on a scale ranging from 1 to 5, where stage 1 is prepubertal and stage 5 represents adult status.17
Fetal and infant growth data were provided from the child's health record booklet, which is systematically delivered at birth to the parents of each infant. This health record booklet contains information written by physicians on weight and height at birth, length of gestation, dates of further examinations and corresponding weights and heights, medical history in infancy, and vaccinations. Weights at birth, 4 months, 9 months, 2 years, and 6 years were available for 214 (100%), 181 (85%), 175 (82%), 140 (65%), and 180 (84%) subjects, respectively. Examinations at birth, 4 months, and 9 months are necessary to obtain financial benefits granted by the Health Authorities. Examination at 6 years corresponds to preschool medical checkup. There were no significant differences in birth weight between subjects who had available data on weight at different ages in early infancy and those who did not. Birth weight was recorded to the nearest 10 g for 156 subjects (75%) and up to the nearest 100 g for the others. Weights at 4 and 9 months were recorded to the nearest 100 g for 130 subjects (72%) and up to the nearest 500 g for the others. Weights at 2 and 6 years were recorded up to the nearest 500 g for all subjects.
Echocardiography
Subjects underwent standard M-mode
echocardiography with a commercially available
ultrasonograph (Ultramark 4 Ultrasound System) equipped with a 3.5-MHz
transducer and strip-chart recorder. Measurements were made
according to the recommendations of the American Society of
Echocardiography18 using a leading
edge–to–leading edge convention with the ultrasound beam at
or just below the tips of the mitral valve leaflets and were averaged
over three cycles. LVM for parents and their infants was calculated by
the correction of the American Society of
Echocardiography cube mass with the following
formula19 : LVM (g)=0.8·1.04 ([LVID
(cm)+PWT (cm)+IVST
(cm)]3-[LVID (cm)]3)+0.6,
where LVID
is LV internal dimension, PWT is posterior wall thickness, and IVST is
interventricular septal thickness.
This formula has been validated anatomically for children with normal hearts and for adults.19 20 LV wall thickness was calculated as the average of septal and posterior wall thicknesses. All echocardiography was performed by a unique experienced sonographer who was not aware of BP and fetal and infancy growth data.
The reproducibility of echocardiographic measurements was assessed by analyzing the interreader variability, which was determined by having a second experienced sonographer recalculate blindly LVM from the original trace performed by the first examiner in a series of 50 offspring. Correlations, coefficients of variation, and percent differences between LV measurements made by the two readers were used to assess interreader variability. Percent differences were calculated with the following formula: % Difference=100·(Absolute Measurement Difference)/(Average of the Two Measurements).
LV measurements obtained by the two observers were highly correlated (r=.86, P<.001, coefficient of variation [CV]=9.4%, % difference=5.5 for LVM; r=.91, P<.001, CV=3.1%, % difference=2.5 for LV internal dimension; and r=.88, P<.001, CV=6.1%, % difference=4.6 for LV wall thickness).
Statistical Analysis
Pearson's correlation, ANCOVA, and
linear regression were used
to assess the associations among BP, echocardiographic
measurements, and weights at birth and in early infancy. Prior
analyses indicated that the associations did not depend on the
sex of the subjects, so we report all results for males and females
combined. To prevent confounding effects of sex, age, and body size at
examination in this sample of children, adolescents, and young adults,
three prior adjustments were made for SBP and
echocardiographic measurements before their
associations with weights at birth and in early infancy were reported:
adjustment for sex alone; adjustment for sex and current height (as
height is an important correlate of BP and LVM during growth); and
adjustment for sex and current age, height, and weight. These
adjustment methods of SBP and LV measures have been previously used in
populations of similar age.21 22 Additional
analyses used LVM/height,23
LVM/height2.13,24 and
LVM/height2.7.25
For control of the effect of sib-sib correlations on the relations between BP, echocardiographic measurements, and weights at birth and in early infancy, analyses were repeated using the maximum likelihood methods proposed by Donner and Koval,26 which give an estimation of the regression parameters using correlated observations. Twin pairs were excluded (two pairs); analyses were performed in 210 subjects.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Subjects under study were aged 8 to 24 years (mean, 13.2; SD, 3.7). Their current mean anthropometric measurements, BP and echocardiographic data, and weights at birth and in early infancy are shown in Table 1
. SBP, LVM, and LV
internal dimension in males were significantly higher than in females.
Weights at birth and in early infancy (up to 2-year measurements) were
also significantly greater in males. One hundred ninety-nine
subjects (94.8%) were born at term (37 weeks or later).
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Birth weight was related to weights at 4 months (r=.47,
P<.01), 9 months (r=.45, P<.01), 2
years (r=.37, P<.01), and 6 years
(r=.23, P<.01). SBP and LVM were strongly
correlated with current age, weight, and height (coefficient
correlations ranged from .53 to .74, P<.01 for all). After
adjustment for sex and height, SBP was positively associated with LVM
(r=.21, P<.01). Neither age nor Tanner stage at
examination was significantly associated with any weight variable
at birth or in infancy. Current weight and height adjusted for sex,
age, and Tanner stage were weakly associated with weights at birth, 4
months, 9 months, and 2 years and more strongly with weight at 6 years
(Table 2).
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The relations between weight at birth, weight in early infancy, and SBP
are shown in Table 3. Whichever the adjustment used,
mean SBP was the highest in subjects with the lowest birth weight. In
the multiple regression model adjusted for sex and height, SBP
decreased by 3.7 mm Hg (95% confidence interval [CI], 1.1-6.3) for
every kilogram increase in birth weight. This was found in both sexes
and was not changed by adjusting birth weight for duration of gestation
or by limiting the analysis to individuals born at term. The
relationship of weight at 4 months with SBP was less consistent
and only significant when adjusting for sex, age, weight, and height.
Subjects who had a lower weight at 9 months or 2 years tended to also
have higher SBP, but the associations did not reach statistical
significance. Weight at 6 years was positively related to
sex-adjusted SBP, but this association was no longer significant
after allowing for height (Table 3). When a simultaneous
analysis of the relation of weights at birth and in early
infancy with SBP was performed, only the inverse effect of birth weight
on SBP persisted.
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The relations between weight at birth, weight in early infancy, and LVM
are shown in Table 4. Sex-adjusted LVM was not
related to weights at birth and in early infancy (up to 2 years). In
contrast, LVM adjusted for sex and height or for sex, age, weight, and
height was negatively associated with weight at 9 months or 2 years
(Table 4). For every kilogram increase in weight at 9 months
and 2
years, LVM adjusted for sex and height decreased by 3.6 g (95% CI,
0.9-6.3) and 3.4 g (95% CI, 1.1-5.7), respectively. Further adjustment
for current SBP did not alter these results. No significant
associations were observed between LVM and weights at birth and 4
months. As for SBP, the positive association of sex-adjusted LVM
with weight at 6 years disappeared after allowing for height. When a
simultaneous analysis of the relation of weights at
birth and in early infancy with LVM was performed, decreased weight at
2 years remained significantly associated with increased LVM, but
weight at 9 months was no longer statistically significant.
Sex-adjusted LVM/height2.7 was also negatively related
to weights at 9 months and 2 years (Table 4). Similar results
were
observed for LVM/height and LVM/height2.13 (data available
from authors).
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When sib-sib correlations were taken into account in the regression models adjusting for sex and height, the results were not modified. SBP increased by 3.6 mm Hg (95% CI, 0.9-6.3) for a 1-kg increase in birth weight, and LVM increased by 3.3 g (95% CI, 1.1-5.5) for every kilogram increase in weight at 2 years.
When the components of LVM were studied separately, mean left posterior
wall thickness and interventricular septal thickness
fell significantly with increasing weight at 9 months and 2 years
(Table 5). LV internal dimension was not related to any
weight variable at birth or in early infancy.
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To evaluate the possibility of confounding effects of parental factors,
their relationships with sex- and height-adjusted SBP and LVM of
the offspring were studied. SBP was positively related to mother's
current BP (r=.17, P<.05) and father's
current
BP (r=.16, P<.05). Increased LVM was not
significantly associated with increased mother's and father's
current
height-adjusted LVM (r=.12 and .12, respectively).
Neither SBP nor LVM was associated with maternal age, mother's and
father's education levels (used as indicators of socioeconomic
influences), or paternal and maternal heights. Allowing for parental
factors in a multiple regression model did not modify the relationships
of SBP and LVM with birth weight and early growth variables.
Moreover, when the relationships of SBP and LVM with weights at birth
and in early infancy were analyzed within categories of sex,
age, Tanner stage, birth order, and parental factors,
consistent results were observed. For more concision, only the
results concerning SBP are shown in Table 6.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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This study conducted in a sample of 210 subjects aged 8 to 24 years showed that SBP (adjusted for sex and height or for sex, age, weight, and height) increased with decreasing birth weight and that similarly adjusted LVM was negatively related to weight at 9 months or 2 years. These associations were independent of gestational age, birth order, and parental factors. Increased LVM associated with reduced infant growth was concentric, resulting from a proportionate thickening of posterior wall and interventricular septum.
In this study, we paid careful attention to reducing as much as possible the technical variability of LV measurements. The same sonographer performed all measures, and the interreader reproducibility was quite satisfactory. We do not think that missing data for infant growth could alter our results because subjects who had available data were not different from those who did not. Our study sample included families volunteering for a free health checkup. Although these families were probably not representative of the whole population of the region, selection bias is unlikely because mean weight and body mass index in this sample were very close to the corresponding 50th percentile values for the French population.27 Because all members of a family were screened together, systematic measurement errors might have induced a slight overestimation of familial correlations. However, the familial correlations of SBP and LVM were of a magnitude similar to those generally reported.28 29 Furthermore, analyses were repeated taking into account sib-sib correlations, and similar results were observed.
The major limitation of this study is the wide range in age of the
subjects, implying wide variations in height, weight, BP, and
echocardiographic measurements. Current height and
weight are clearly confounding factors for the relations of SBP and LVM
with weights at birth and in early infancy. On the one hand, SBP and
LVM are strongly correlated with age, weight, and height in this sample
of children, adolescents, and young adults, in accordance with previous
studies.21 22 30 On the other hand,
current body size is
associated with weights at birth and in early infancy (Table
2
),
although the correlation coefficients remained weak (up to 2 years).
Indeed, any statistically significant relationship of weights at birth
and in early infancy with BP and LV size could be partly related to
differences in body size. Conversely, a real relationship could be
masked by unadjusting for anthropometric variables. Examples of
confounding effects on both these directions were found in this study
(Tables 3 and 4). We systematically compared
adjustment on height
as the sole parameter of body size with adjustment on age,
weight, and height, which might have introduced some kind of
overadjustment.
The association of weight at birth and sex-adjusted SBP was of borderline significance, and allowing for height was sufficient to reveal a strong inverse relationship of SBP with weight at birth. Consistent with previous findings among children,9 12 13 14 young adults,31 and adults in both men9 10 32 33 34 and women,9 11 33 34 the inverse relation between birth weight and BP in this study was observed at all ages and in both sexes. However, no evidence of an association between birth weight and BP has been shown in some other studies.35 36 37 38 Higher BP was associated with low birth weight but not with low weight at 9 months or 2 years. This confirms and extends the results of previous studies that found the inverse association of BP with weight at birth but not with weight at 1 year.9 11 As expected, the positive association between SBP and weight at 6 years disappeared once the confounding effect of current body size was taken into account. All these results suggest that BP levels might be initially determined in utero rather than during postnatal growth.39 The magnitude of the association between SBP and birth weight in this report is higher than that observed in childhood studies9 12 and similar to or lower than that observed in adults,9 34 suggesting that the effect of birth weight on BP is amplified from infancy to older age.9
Concerning echocardiographic measurements, adjustment or a priori indexation for height was necessary to identify the significant association of weight at 9 months or 2 years with LVM. It was not surprising that unadjusted or sex-adjusted LVM was unrelated to weights at birth and in very early infancy. Linear growth is the major determinant of cardiac growth in children and adolescents,30 40 and height correlates strongly with LVM, even in adults.41 Therefore, methods for adjusting or indexing LVM for growth are essential,30 and their utility for comparison between individuals of different size is widely accepted. In our study, we used, as has been proposed in the literature,23 24 25 different functions of height for normalization of LVM for body size. Consistent results were observed. The similarity of our findings with those of the only study15 that has assessed, in an adult population, the relationship of LVM with weights at birth and 1 year is noteworthy. Concentric enlargement of the left ventricle in adult life was associated with low weight at 1 year in a sample of 290 men born during the period from 1920 to 1930 (mean age, 66.9 years) in East Hertfordshire, UK.15 Furthermore, low birth weight, in the East Hertfordshire Study as well as in ours, was associated with increased SBP9 but not with increased LVM.15 The association observed between increased LVM in subjects at an earlier age (8 to 24 years) and reduced infant growth is of great importance. LVM demonstrates tracking through childhood and adolescence30 and probably adult life, and concentric LV hypertrophy has been shown to predict cardiovascular disease.7
The mechanisms that link fetal and infant growth to BP and LV structure are still a matter for speculation. Disturbance activity of growth-related hormones, leading to changes in the normal development of the vasculature and vessel wall and subsequently to an increase in vascular resistance and BP, has been suggested.42 This may include growth hormone, insulin-like growth factor-1, and insulin.42 43 44 It was also hypothesized that increased fetal exposure to maternal glucocorticoids may lead to intrauterine growth retardation and high BP.45 High concentration of glucocorticoids in the fetus could affect the development of fetal vasculature and its responses to pressor agents.46 Another possible explanation is that reduced arterial compliance, which was shown to be associated with retarded fetal growth,34 hypertension, and cardiac hypertrophy,47 might be involved.
The fact that LVM was inversely associated with weight at 9 months or 2 years and was not related to birth weight may suggest that retarded fetal growth induces, if causal, changes in LV structure only if it persists during early infancy. The initial LV weight at birth and up to 1 year is strictly dependent on the number of cardiomyocytes,48 but cardiac myocyte growth, the major determinant of postnatal increase in LVM, is determined by ventricular loading and circulating hormones.49 The final weight of the left ventricle would depend, therefore, on both the initial number of cardiomyocytes and the extent of their growth.48
In conclusion, this study supports the hypothesis that SBP and LVM may be partly determined during fetal life and early infancy. The mechanisms that underlie the associations of BP and LV structure with weights at birth and in early infancy should be studied thoroughly.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We particularly thank L. Muller, MD, for performing echocardiographic measurements, M.-T. Guillaneuf, MD, for reinterpreting tracings for the reproducibility study, and A. Bingham for technical assistance with the manuscript.
Received August 1, 1995; first decision August 30, 1995; accepted November 30, 1995.
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