Published online before print November 6, 2006, doi: 10.1161/01.HYP.0000250434.73119.7a
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(Hypertension. 2007;49:225.)
© 2007 American Heart Association, Inc.
Original Articles |
Maternal and Neonatal Influences on, and Reproducibility of, Neonatal Aortic Pulse Wave Velocity
From the Clinical Epidemiology and Cardiovascular Medicine Group (A.K., J.O., M.B., V.A., J.K.C.), Division of Cardiovascular and Endocrine Sciences, University Department of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom; and Evidence for Population Health Unit (P.M.), University of Manchester, Medical School, Manchester, United Kingdom.
Correspondence to J. Kennedy Cruickshank, Division of Cardiovascular and Endocrine Sciences, Core Technology Facility (3rd Floor), University of Manchester, 46 Grafton St, Manchester M13 9NT, United Kingdom. E-mail clinep{at}manchester.ac.uk
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Abstract |
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Aortic pulse wave velocity (aPWV), a noninvasive measure of vascular stiffness, is an independent predictor of cardiovascular disease both before and in overt vascular disease. Its characteristics in early life and its relationship to maternal factors have hardly been studied. To test the hypothesis that infant aPWV was positively related to maternal anthropometry and blood pressure (BP) at 28 weeks gestation, after adjusting for neonatal anthropometry and BP, 148 babies born in Manchester were measured 1 to 3 days after birth. A high reproducibility of aPWV, assessed in 30 babies within 3 days of birth, was found with a mean difference between occasions of –0.04 m/s (95% CI: –0.08 to 0.16 m/s). Contrary to our hypothesis, a significant inverse relation was found between neonatal aPWV (mean: 4.6 m/s) and maternal systolic BP (mean: 108.9 mm Hg; r=–0.57; 95% CI: –0.67 to –0.45) but not maternal height nor weight. Neonatal aPWV was positively correlated with birth length, birth weight, and systolic BP. In multiple regression, neonatal aPWV remained significantly inversely associated with maternal systolic BP (adjusted ß coefficient: –0.032; 95% CI: –0.040 to –0.024; P<0.001), after adjustment for maternal age, birth weight, length, and neonatal BP (all independently and positively related to aPWV) and for gestational age, maternal weight, and height (unrelated). These results suggest that infant aPWV may be a useful index of infant vascular status, is less disturbing to measure than infant BP, and is sensitive to the gestational environment marked by maternal BP.
Key Words: aortic pulse wave velocity • neonatal • pregnancy • maternal blood pressure • birthweight • reproducibility
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Introduction |
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Aortic pulse wave velocity (aPWV) in adults is a powerful predictor of all-cause and cardiovascular disease mortality and, as found in
4 outcome studies,1–4 displaces systolic blood pressure (SBP) or pulse pressure as a predictive factor, perhaps because it is a direct index of vascular structure and function, further along the casual pathway of vascular pathology.1 Primary prevention or early intervention in high blood pressure (BP) requires its early detection. It has become well established that high BP is frequently detectable in childhood as levels above the 90th centile for age.5 However, little is known about the natural history of other arterial characteristics in childhood, such as distensibility and flow wave reflections. Maternal factors during pregnancy, not the least the mother’s own BP, have long been known to influence infant and later childhood vascular development and BP.6–10 However, the maternal-infant BP relationship has been uncertain.11–14 In part this may have been because of measurement errors, both random and systematic, from disturbance of the neonate by the observer until the recent availability of reliable semiautomatic methods. It is clear that children of women with more extreme forms of hypertension in pregnancy, such as pre-eclampsia, have higher BP and risk of later vascular events than those of "control" women,7,10 but across the range of usual BP in pregnancy, transmission of risk to the next generation is less clear.15 Another approach may be to examine arterial distensibility in infancy.
To our knowledge there have been few studies of arterial distensibility in early life, and most of them were done on small sample sizes.16–20 Some methods have not been validated in young age groups, but direct measures of flow using Doppler methods offer a useful approach. To develop this area, we measured aPWV in a cohort of infants, testing the hypothesis that maternal BP would be directly and positively related to neonatal aPWV, independent of other maternal and infant factors.
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Methods |
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Participants
The women were recruited around 20 weeks of pregnancy at the time of their second ultrasound scan. At 28 weeks gestation, a glucose tolerance test was done, and 2 measures of brachial BP were taken after the woman had been sitting for
5 minutes; the readings were taken 1 minute apart, using a validated Omron 705CP monitor with an appropriate-sized cuff. The mean of the 2 readings was used for analysis. Information on prepregnancy weight, birth weight, sociodemographic status and ethnicity, and the participants’ family history of hypertension, weight, and height were recorded. We visited the mother and neonate within a day after delivery, when babies were measured for neonatal anthropometrics, BP, and aPWV. Babies with vascular anomalies or with patent ductus arteriosus (PDA) were not included. BP was measured with a Critikon Dinamap machine, as in other neonatal studies,14 with a neonatal cuff and a rest period of 2 minutes in quiet surroundings. Infant BP was measured once before and once after aPWV, and the mean of the 2 readings was used in the analysis. All of the newborn measurements were made by 1 pediatrician (A.K.) in the postnatal wards of St Mary’s Maternity Hospital (Manchester, United Kingdom).
The protocol for measuring aPWV required the infant to lie in a supine position for 2 to 5 minutes before testing. To examine the longest, least folded part of the aorta, we measured between the left subclavian artery at its origin from the aortic arch and the abdominal aorta just above the aortic bifurcation (on the skin around the umbilicus; Figure 1A). An infrared probe was placed in the supraclavicular space or suprasternal notch aimed at the root of the left subclavian artery. A 4-MHz ultrasound transducer was placed over the abdominal aorta (Figure 1B). The flow waves from these 2 aortic sites were simultaneously recorded. Two software systems for vascular compliance were used to measure aPWV: PULSE50.EXE (data capture) and PULSE12.EXE (analyser of time delay).21,22 The latter contains an algorithm (developed by Wright et al23) for detection of the onset of the systolic upstrokes (foot-to-foot) of the flow velocity waveforms in the proximal and distal signals. High-quality waveforms were captured (an average of 23, the minimum, to 30 waveforms); the distance between the sampling sites was measured with a tape. aPWV is calculated by dividing the distance traveled by the time differential between the 2 waveforms using the following formula: aPWV=Probsep (m)/TT(s), where TT is transit time between the 2 probes, and Probsep is the distance between the sampling sites (Figure 1C).
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Reproducibility
To test the reproducibility of aPWV measurements within subject measured by the same observer, 30 neonates had 2 aPWV recording sessions, at baseline and up to 1 to 3 days later. The Bland and Altman criteria were used to assess the level of agreement24: the mean difference between the 2 measurements for each individual (assessed using the 95% CI of the mean difference) should not be significantly different from 0. Also, differences between the 2 measurements should be independent of their mean. We also estimated within subject coefficient of variation.25
Data are presented as proportions and means for the 2 groups, defined by the median of maternal SBP at 28 weeks gestation. Comparison of proportions between groups was tested using a 
2 test, t tests, and ANOVA, with 95% CIs where appropriate.
The univariate or unadjusted relationship between infant aPWV and maternal SBP was examined using simple linear regression. To adjust for potential confounding factors and to identify the independent predictors of aPWV at birth, we fitted a multiple linear model using backward stepwise regression. A forward stepwise model gave very similar results (data not shown). Other maternal factors included were sociodemographic status, ethnicity, age, 2-hour plasma glucose values after the glucose tolerance test, prepregnancy height and weight, and weight gain at 28 weeks gestation; infant factors were birth size (as either birth weight or birth length), gestational age, gender, SBP, and heart rate. Analyses were done with the statistical software packages of intercooled Stata version 8.2 and SPSS version 11.5.
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Results |
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Reproducibility Study
The mean difference in aPWV between the 2 occasions was –0.04 m/s (95% CI: –0.08 to 0.16 m/s, note including 0), indicating not only a minimal absolute difference between paired readings but also that there was no evidence of a systematic difference between the first and second measurement. The difference in aPWV between the 2 occasions was plotted against the mean of both measures and showed that the variation in differences was relatively constant with increasing values of aPWV (Figure 2). The within-subject coefficient of variation was 0.05 or 5%.
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Pulse Wave Velocity Study
A total of 148 women with a mean age of 31.9 years (95% CI: 30.9 to 32.8 years) were included. Fifty-four percent (82) classified themselves as (and were also by origin of 3 of 4 grandparents) white European, and 28% (35) were similarly classified as Pakistani. The mean gestational age of the babies was 39.1 weeks (95% CI: 38.8 to 39.5 weeks), birth weight was 3418 g (95% CI: 3342 to 3495 g), mean birth length was 50.5 cm (95% CI: 50.1 to 50.9 cm), and aPWV was 4.6 m/s (95% CI: 4.53 to 4.73 m/s).
Table 1 shows maternal and infant characteristics between groups defined by median maternal SBP at 28 weeks (108 mm Hg). The mean aPWV was higher in babies whose mothers’ SBP at 28 weeks was <108 mm Hg than babies whose mothers’ SBP at 28 weeks was 108 mm Hg (P<0.001). Reported prepregnancy weights of women in the upper half of the BP distribution were 3 kg heavier on average than those in the lower half, which meant their mean prepregnancy body mass indices were 1.3 kg/m2 higher. Weight gained at 28 weeks was similar. There were no other differences in maternal or neonatal characteristics, except as defined by maternal BP. Infant BP and anthropometry were also similar between infant groups defined by maternal BP (Table 1).
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Maternal SBP at 28 weeks gestation showed a strong inverse relationship with aPWV (r=–0.57; 95% CI: –0.67 to –0.45; Figure 3). Maternal SBP was also inversely associated with infant birth weight (r=–0.18; –0.33 to –0.02), but there was no statistically significant association between maternal and infant SBP (r=–0.11; 95% CI: –0.26 to 0.06). Maternal weight and height at 28 weeks were not associated with the infant SBP, diastolic BP, heart rate, or aPWV.
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In simple linear regression models, maternal BP and age were statistically significant predictors of the babies’ aPWV (Table 2). Birth weight, birth length, neonatal SBP and diastolic BP, and heart rate but not pulse pressure were also individually significantly associated with aPWV. There were no differences found by gender or ethnic groups, nor were sociodemographic or family history variables significant. Only maternal SBP, maternal age, infant length, and infant SBP were statistically significant predictors of aPWV in a multiple regression model selected using backward stepwise regression. Forward stepwise regression models gave the same results. The 4 predictors in the final model (Table 2, right) explained 43% of the total variation in aPWV. When associations of neonatal SBP were tested, even after excluding aPWV, none of the maternal or infant variables were significantly related, except gender (males had significantly higher SBP than females; P=0.03), with maternal SBP marginally so (P=0.064). Infant size, measured as either birth length or birth weight, was not associated with infant SBP.
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Discussion |
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To the best of our knowledge, this report is the first to identify the relationship of maternal factors with neonatal aPWV. We found a strong inverse relation between maternal SBP at 28 weeks and neonatal aPWV and good reproducibility of neonatal aPWV in the first days of postnatal life.
The reproducibility results are similar to those we obtained in adults whose mean age was 
60 years.23 That the aPWV method does give such reproducibility at 2 widely separated times of life may be because of capturing the 23 to 30 cardiac cycles that generate the mean aPWV result. This differs from most BP data, including those here, which are based on means of only 2 or 3 systolic and diastolic cycles and are inevitably less precise estimates of an average BP level. Despite the imprecise characterization of maternal BP at 28 weeks gestation, the inverse relation that we found with neonatal aPWV was strong (Figure 3) and robust, being independent of other potential and neonatal confounders, such as anthropometry (Table 2). Furthermore, this relationship was found in a sample of healthy, term neonates, none of whose mothers was on antihypertensive treatment. The distribution of maternal SBPs was also right across the usual low-medium range for pregnancy, with very few high values (see the horizontal axis of Figure 3). The average of 4.6 m/s for aPWV at birth is close to that reported in slightly older infants and young children.16 The finding of the inverse relation between BP and neonatal aPWV is the opposite of our original hypothesis. There are few reports on PWV in infancy/early childhood available with which to compare our data16–20 and none with the relatively large number of neonates that we have studied.
The mechanisms by which maternal blood flow modulates neonatal arterial growth are not known. The development of the aortic media involves the formation of alternating layers of smooth muscle cells and elastic laminae.26 The number of elastic lamellae is greatest in the proximal part of the aorta. They begin to develop early in fetal life, and rates of elastin synthesis in blood vessels increase to a maximum in the perinatal period; thereafter, these rates fall rapidly.27 There seems to be a critical period during development of the aorta, and failure to synthesize adequate amounts of elastin during this period is apparently impossible to replace later. In lambs between 120 days of gestation and 21 days after birth, thoracic aortic media cross-sectional area increased by 144%, whereas this index for abdominal aorta increased by only 69%. These differences in growth rates were greater postpartum.28 How these characteristics of thoracic and abdominal aorta are reflected by aPWV is not known. At this age, the thoracic aorta grows more quickly than the abdominal aorta; it is possible that infants of women with higher maternal BP in pregnancy have adapted with slightly greater thoracic aortic medial cross-sectional area and, therefore, lower aPWV. Conversely, in infants of mothers with lower BP (and placental blood flow) in pregnancy, there may be some degree of compensatory vasoconstriction as it happens to close the patent ductus. Animal data suggest that enhanced vasoconstriction is a feature of vascular smooth muscle during pregnancy.29 It is also of interest that Steer et al reported a "u"-shaped relationship between perinatal outcome and maternal diastolic BP.30
An intriguing issue, answerable by continued longitudinal study through early childhood and later life, is which infants go on to develop stiffer, less distensible, aorta later in childhood and adult life. Results from work >20 years ago support this idea.16 Laogun and Gosling’s work16 on schoolchildren showed that aPWV (again measured from the arch to just above the bifurcation to minimize reflection artifact) fell slowly in early childhood but then decreased markedly around the ages of 10 to 12 years in both boys and girls, perhaps related to puberty, hence, its inverse, aortic compliance or distensibility, increased to its maximum at these ages. Thereafter, from age 14 years, compliance declined inexorably over the life span (ie, aPWV increased). It is likely that several of the factors that we have measured here, and then others relating to postnatal growth, influence this rise in compliance or fall in aPWV in later childhood and then its ongoing decline. Our hypothesis would be that the children whose mothers were in the upper parts of the maternal BP distribution will begin to show by that time increasing stiffness in their aorta in part independent of their BP.
It is possible that the changes in cardiac physiology around birth and the closing of the PDA could be important influences on aPWV. We only included babies in whom clinically the PDA was no longer detectable. Other perinatal hemodynamic changes, including rising pulmonary pressures and their consequences, could not be assessed, but we aimed to minimize these effects by measuring most babies 24 hours after birth. Undetected abnormal flows seem unlikely to account for the consistent maternal BP/aPWV relationship that we found.
Our results of positive correlations between aPWV at birth and both birth weight and birth length contrast with the finding of an inverse relation between birth weight and PWV in later life31,32 attenuated after adjusting for current height.32 In young adulthood, the inverse correlation was not consistent33,34 and in children and adolescents, aortic stiffness, in particular, has shown little relationship with birth weight.35 However, the positive relationship reported by Oren et al34 was in agreement with our findings. Differences with respect to age, methods used to assess arterial stiffness, the arterial segments measured, and adjustment for confounders make the studies that investigated the relationship difficult to compare. However, note our "adaptive" hypothesis above, by which arteries may later "stiffen" inexorably after peak distensibility has been reached around adolescence. We measured aPWV using the arch-abdominal segment as the wave travels between these 2 sites in 1 direction and the effect of reflection from the peripheral arterial tree in the aorta is minimal, hence interfering in the flow waveform harmonics much less. Also, to reduce the influence of body contours on the distance measure (between the 2 sites), the tape measure was held above the surface of the body, parallel to the plane of the examination table. The length value (to the nearest 0.1 cm) was taken in duplicate straight after capturing the signals, and the mean was used for aPWV calculation. Movements of the subjects could cause problems in getting consistent high-quality waveforms; however, the high heart rate in infancy made the procedure easier by allowing rapid recapture once the neonate settled.
SBP at birth was on an average of 70.7 mm Hg for the whole group of babies, which is consistent with that reported for term infants (70 mm Hg).36 As early as 1 day of life, Miller et al37 showed a significant relation between a neonate’s BP and high maternal BP during pregnancy. Similar significant correlations have been found during the following 2 days of the child’s life.6,7,38 The maternal-infant SBP relation was of borderline significance in our study, whereas the maternal SBP-neonatal aPWV relation was stronger and inverse. Adjusting for confounding did not alter the later correlation. Thus, it seems that neonatal aPWV is a more precise indicator of maternal environment during pregnancy than neonatal SBP.
In conclusion, these results suggest that measurement of neonatal aPWV was reproducible and may be closely but inversely related to maternal BP around 28 weeks gestation and more so than neonatal BP. aPWV may also, therefore, be a useful index of arterial structure and function at this age and, by implication, in later infancy and childhood, as in adult life. Assessing the effects of differing maternal conditions during pregnancy on the infant’s vasculature may be a useful area of further work.
Perspectives
Relationships and characteristics of aPWV, a powerful index of prognosis in adults, have not been investigated in early life. We examined the reproducibility of this measure of arterial distensibility in neonates and tested its relationship with maternal factors at 28 weeks gestation. Reproducibility over the first 72 hours of life was impressive in the 30 infants examined, and in 140 infants, we found, contrary to our hypothesis, that children’s aPWV was inversely related to maternal systolic BP, independent of positive relationships with birth weight, length, and SBP. The results suggest that aPWV simply measured in resting infants may be a useful measure of the infant’s vasculature and should supplement the limited data available on the development of BP alone.
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Acknowledgments |
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We thank Prof Stephen Greenwald for his help in setting up some of the initial equipment.
Sources of Funding
A.K. was a Government of Syria PhD scholar. Other funding was from Diabetes United Kingdom and the British Heart Foundation.
Disclosures
None.
Received December 23, 2005; first decision January 11, 2006; accepted October 6, 2006.
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References |
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1. Cruickshank K, Riste L, Anderson SG, Wright JS, Dunn G, Gosling RG. Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function? Circulation. 2002; 106: 2085–2090.
2. Boutouyrie P, Tropeano AI, Asmar R, Gautier I, Benetos A, Lacolley P, Laurent S. Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study. Hypertension. 2002; 39: 10–15.
3. Laurent S, Katsahian S, Fassot C, Tropeano A, Gautier I, Laloux B, Boutouyrie P. Aortic stiffness is an independent predictor of fatal stroke in essential hypertension. Stroke. 2003; 34: 1203–1206.
4. Blacher J, Safar M, Guerin A, Pannier B, Marchais S, London G. Aortic pulse wave velocity index and mortality in end-stage renal disease. Kidney Int. 2003; 63: 1852–1860.[CrossRef][Medline] [Order article via Infotrieve]
5. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004; 114: 555–576.
6. Zinner SH, Lee YH, Rosner B, Oh W, Kass EH. Factors affecting blood pressures in newborn infants. Hypertension. 1980; 2: 99–101.[Abstract]
7. Seidman DS, Laor A, Gale R, Stevenson DK, Mashiach S, Danon YL. Preeclampsia and offspring’s blood pressure, cognitive ability and physical development at 17-years-of-age. Br J Obstet Gynaecol. 1991; 98: 1009–1014.[Medline] [Order article via Infotrieve]
8. Law CM, de Swiet M, Osmond C, Fayers PM, Barker DJ, Cruddas AM, Fall CH. Initiation of hypertension in utero and its amplification throughout life. BMJ. 1993; 306: 24–27.
9. Himmelmann A, Svensson A, Hansson L. Relation of maternal blood pressure during pregnancy to birth weight and blood pressure in children. The Hypertension in Pregnancy Offspring Study. J Intern Med. 1994; 235: 347–352.[Medline] [Order article via Infotrieve]
10. Vatten LJ, Romundstad PR, Holmen TL, Hsieh CC, Trichopoulos D, Stuver SO. Intrauterine exposure to preeclampsia and adolescent blood pressure, body size, and age at menarche in female offspring. Obstet Gynecol. 2003; 101: 529–533.[CrossRef][Medline] [Order article via Infotrieve]
11. Ibsen KK, Gronbaek M. Familial aggregation of blood-pressure in newly born infants and their mothers. Acta Paediatr Scand. 1980; 69: 109–111.[Medline] [Order article via Infotrieve]
12. Mausner JS, Hiner LB, Hediger ML, Gabrielson MO, Levison SP. Blood pressure of infants of hypertensive mothers: a 2-year follow-up. Int J Pediatr Nephrol. 1983; 4: 255–261.[Medline] [Order article via Infotrieve]
13. Hashimoto N, Kawasaki T, Kikuchi T, Takahashi H, Uchiyama M. The relationship between the intrauterine environment and blood pressure in 3-year old Japanese children. Acta Paediatr. 1996; 85: 132–138.[Medline] [Order article via Infotrieve]
14. Gillman MW, Rich-Edwards JW, Rifas-Shiman SL, Lieberman ES, Kleinman KP, Lipshultz SE. Maternal age and other predictors of newborn blood pressure. J Pediatr. 2004; 144: 240–245.[CrossRef][Medline] [Order article via Infotrieve]
15. Churchill D, Perry IJ, Beevers DG. Ambulatory blood pressure in pregnancy and fetal growth. Lancet. 1997; 349: 7–10.[CrossRef][Medline] [Order article via Infotrieve]
16. Laogun AA, Gosling RG. In vivo arterial compliance in man. Clin Phys Physiol Meas. 1982; 3: 201–212.[CrossRef][Medline] [Order article via Infotrieve]
17. Hu J, Wallensteen M, Gennser G. Increased stiffness of the aorta in children and adolescents with insulin-dependent diabetes mellitus. Ultrasound Med Biol. 1996; 22: 537–543.[CrossRef][Medline] [Order article via Infotrieve]
18. Schack-Nielsen L, Molgaard C, Larsen D, Martyn C, Michaelsen KE. Arterial stiffness in 10-year-old children: current and early determinants. Br J Nutr. 2005; 94: 1004–1011.[CrossRef][Medline] [Order article via Infotrieve]
19. Hsieh KS, Chen PL, Fu SE. A simple, noninvasive method to investigate vascular characteristics in children. Angiology. 1996; 47: 361–367.[Medline] [Order article via Infotrieve]
20. Gardiner HM, Taylor MJ, Karatza A, Vanderheyden T, Huber A, Greenwald SE, Fisk NM, Hecher K. Twin-twin transfusion syndrome: the influence of intrauterine laser photocoagulation on arterial distensibility in childhood. Circulation. 2003; 107: 1906–1911.
21. Greenwald S, Denyer H, Sobeh MS. Noninvasive measurement of vascular compliance by a photoplesythmographic technique. SPIE. 1997; 2970: 89–97.[CrossRef]
22. Loukogeorgakis S, Dawson R, Phillips N, Martyn CN, Greenwald SE. Validation of a device to measure arterial pulse wave velocity by a photoplethysmographic method. Physiol Meas. 2002; 23: 581–596.[CrossRef][Medline] [Order article via Infotrieve]
23. Wright JS, Cruickshank JK, Kontis S, Dore C, Gosling RG. Aortic compliance measured by non-invasive Doppler ultrasound: description of a method and its reproducibility. Clin Sci (Lond). 1990; 78: 463–468.[Medline] [Order article via Infotrieve]
24. Bland JM, Altman DG. Statistical methods for assessing agreement between 2 methods of clinical measurement. Lancet. 1986; 1: 307–310.[CrossRef][Medline] [Order article via Infotrieve]
25. Bland M. An Introduction to Medical Statistics. 3rd ed. Oxford, United Kingdom: Oxford University Press; 2000.
26. Davis EC. Elastic lamina growth in the developing mouse aorta. J Histochem Cytochem. 1995; 43: 1115–1123.[Abstract]
27. Martyn CN, Greenwald SE. Impaired synthesis of elastin in walls of aorta and large conduit arteries during early development as an initiating event in pathogenesis of systemic hypertension. Lancet. 1997; 350: 953–955.[CrossRef][Medline] [Order article via Infotrieve]
28. Langille BL, Brownlee RD, Adamson SL. Perinatal aortic growth in lambs: relation to blood flow changes at birth. Am J Physiol. 1990; 259: H1247–H1253.[Medline] [Order article via Infotrieve]
29. Dieye AM, Gairard A. Endothelium and aortic contraction to endothelin-1 in the pregnant rat. Can J Physiol Pharmacol. 2000; 78: 372–377.[CrossRef][Medline] [Order article via Infotrieve]
30. Steer PJ, Little MP, Kold-Jensen T, Chapple J, Elliott P. Maternal blood pressure in pregnancy, birth weight, and perinatal mortality in first births: prospective study. BMJ. 2004; 329: 1312–1316.
31. Martyn CN, Barker DJ, Jespersen S, Greenwald S, Osmond C, Berry C. Growth in utero, adult blood pressure, and arterial compliance. Br Heart J. 1995; 73: 116–121.
32. te Velde SJ, Ferreira I, Twisk JW, Stehouwer CD, van Mechelen W, Kemper HC. Birthweight and arterial stiffness and blood pressure in adulthood-results from the Amsterdam Growth and Health Longitudinal Study. Int J Epidemiol. 2004; 33: 154–161.
33. Montgomery AA, Ben Shlomo Y, McCarthy A, Davies D, Elwood P, Smith GD. Birth size and arterial compliance in young adults. Lancet. 2000; 355: 2136–2137.[CrossRef][Medline] [Order article via Infotrieve]
34. Oren A, Vos LE, Bos WJ, Safar ME, Uiterwaal CS, Gorissen WH, Grobbee DE, Bots ML. Gestational age and birth weight in relation to aortic stiffness in healthy young adults: 2 separate mechanisms? Am J Hypertens. 2003; 16: 76–79.[CrossRef][Medline] [Order article via Infotrieve]
35. Lurbe E, Torro MI, Carvajal E, Alvarez V, Redon J. Birth weight impacts on wave reflections in children and adolescents. Hypertension. 2003; 41: 646–650.
36. Bartosh SM, Aronson AJ. Childhood hypertension. An update on etiology, diagnosis, and treatment. Pediatr Clin North Am. 1999; 46: 235–252.[CrossRef][Medline] [Order article via Infotrieve]
37. Miller FC, Read JA, Cabal L, Siassi B. Heart rate and blood pressure in infants of pre-eclamptic mothers during the first hour of life. Crit Care Med. 1983; 11: 532–535.[Medline] [Order article via Infotrieve]
38. Zinner SH, Rosner B, Oh W, Kass EH. Significance of blood pressure in infancy. Familial aggregation and predictive effect on later blood pressure. Hypertension. 1985; 7: 411–416.
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