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170 D. Ley, K. MarsÏ—l<br />

mals decreases IGF-I expression in many tissues and<br />

in the circulation [76, 77]. Circulatory levels of IGF-I<br />

have been shown to be decreased in SGA fetuses and<br />

in fetuses with abnormal blood flow velocity [78, 79].<br />

In our study at 18 years of age, the central field vision,<br />

as represented by the Rarebit mean hit rate<br />

[72], ranged from 93 to 100% in subjects with birthweight<br />

AGA and from 48 to 100% in those with<br />

birth-weight SGA with the median hit rate being significantly<br />

lower in the SGA group as compared with<br />

that in the AGA group (p=0.03). Eight of the SGA<br />

subjects and none of the controls had a hit rate below<br />

the normal range (p=0.006). The deviant hit rates<br />

detected by the Rarebit microdot perimetry in some<br />

SGA subjects may reflect defects in the matrix of detectors,<br />

i.e., the neural channels, and may be caused<br />

by disturbed axonal growth or development. This<br />

finding of abnormal function lends support to the<br />

previously mentioned morphological finding of reduced<br />

neuroretinal rim area in subjects with IUGR.<br />

Fetal Aortic Blood Flow and Postnatal<br />

Cardiovascular Function<br />

Aortic Vessel Wall Characteristics<br />

and Blood Pressure at 9 Years of Age<br />

We used an electronic phase-locked echo-tracking<br />

system DIAMOVE (Teltec, Lund, Sweden) for non-invasive<br />

monitoring of pulsatile diameter changes in<br />

the descending aorta [81, 82] of a subgroup of 68<br />

children from the original Malmæ cohort. Neither abnormal<br />

fetal aortic blood flow nor birth-weight deviation<br />

were reflected in any significant changes in elastic<br />

modulus or stiffness of the abdominal aorta at 9<br />

years of age [80]. Within the examined group, the<br />

subjects with the highest body weight at the time of<br />

examination had the highest levels of systolic blood<br />

pressure. These results support the hypothesis that<br />

the link between fetal growth failure and high blood<br />

pressure in adult life may mainly be expressed among<br />

those with obesity.<br />

Children born SGA had significantly lower vessel<br />

diameters than those born AGA and these differences<br />

remained significant after adjustment for body surface<br />

area. These findings resemble in part those of<br />

Stale et al. [83] who found lower values of end-diastolic<br />

diameters in SGA fetuses than in AGA fetuses<br />

of the same gestational age using an identical technique<br />

for aortic measurements; however, when the fetal<br />

aortic diameters were adjusted for estimated fetal<br />

weight, the relationship was reversed. The larger<br />

weight-related diastolic diameter taken together with<br />

the finding of a lower relative pulse amplitude in the<br />

SGA fetuses suggested an increase in diastolic blood<br />

pressure, possibly as a response to the increased peripheral<br />

resistance, namely that of the placental circulation,<br />

found in pregnancies complicated by IUGR.<br />

The present findings obtained at 9 years of age [80]<br />

showed no evidence of an increase in diastolic blood<br />

pressure related to restricted fetal growth. On the<br />

contrary, IUGR was associated with lower diastolic<br />

blood pressure. As the influence of the increased resistance<br />

to fetal blood flow caused by the abnormal<br />

placenta in fetal growth restriction will cease to exist<br />

after birth, it would seem plausible that the postulated<br />

compensatory increase in blood pressure during<br />

the fetal period would no longer be present in childhood.<br />

Pulse pressure was significantly higher within the<br />

group of children born SGA than in those born AGA<br />

[80]. An increase in pulse pressure has previously<br />

been described in SGA infants at 6 weeks of age [84]<br />

and has been associated with signs of low arterial<br />

compliance and hypertensive disease in adults [85,<br />

86]; however, we were unable to detect any corresponding<br />

changes in aortic compliance in association<br />

with either abnormal fetal aortic blood flow or SGA<br />

birth weight. A previous study of human aortic compliance<br />

and its normal variation with age found a<br />

profound increase in compliance between 4 and 11<br />

years of age [87]. Aortic compliance thereafter exhibited<br />

a gradual decrease with values beyond 16 years<br />

being similar to those of healthy adults. This may imply<br />

that changes in aortic vessel compliance due to<br />

fetal causes may be detectable at a later age when<br />

aortic compliance decreases due to the normal ageing<br />

process. The increase in pulse pressure observed in<br />

the SGA group [80] might suggest, in the absence of<br />

changes in elastic modulus and stiffness of the<br />

abdominal aorta, the possibility of corresponding<br />

changes in more peripheral segments of the arterial<br />

tree.<br />

Size and Function of Large Arteries<br />

at 18 Years of Age<br />

At 18 years of age [88], vascular mechanical properties<br />

of the common carotid artery (CCA), abdominal<br />

aorta (AO), and popliteal artery (PA) were assessed<br />

by echo-tracking sonography in 21 adolescents with<br />

IUGR and abnormal fetal aortic blood flow, and in 23<br />

adolescents with normal fetal growth and normal<br />

fetal aortic blood flow, all belonging to the Malmæ-<br />

Lund follow-up cohort [71±73, 89]. Endothelium-dependent<br />

and endothelium-independent vasodilatation<br />

of the brachial artery was measured by high-resolution<br />

ultrasound.<br />

The IUGR group had significantly smaller mean<br />

vessel diameters compared with controls in the AO<br />

and PA in proportion to the body size, with a similar<br />

trend in the CCA. Stiffness in all three vascular re-

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