Iliac arteries in children with a single umbilical artery: Structure, calcifications, and early atherosclerotic lesions

Abstract

Iliac arteries in children with a single umbilical artery: structure, calcifications, and early atherosclerotic lesions. With a single umbilical artery a unique haemodynamic situation arises during fetal development, resulting in a different calibre and structure of the iliac arteries on the two sides of the body. On the side of the single umbilical artery, the enlarged iliac arteries have the structure of elastic arteries, whereas the smaller and thin-walled iliac arteries, which do not participate in the placental circuit, show the typical structure of muscular arteries. These differences of the arterial structure determine the morphological pattern of early calcifications which are regularly present in the iliac arteries on both sides of the body, but are usually more conspicuous in the large iliac arteries on the side of the single umbilical artery. In 2 children, aged 18 months and 4 years, atherosclerotic lesions were present in the wide common iliac artery on the side of the obliterated single umbilical artery. These lesions represent the earliest atherosclerotic changes to be found in the human. They are probably related to the remodelling of these arteries, beginning after birth as an adaptation to decreased blood flow.Aplasia of one umbilical artery occurs in 0 75-1 1% of consecutive deliveries and is frequently associated with congenital malformations

Characteristics of Arterial Stiffness in Very Low Birth Weight Premature Infants

“…These findings are consistent with the hypothesis put forth by Martyn and Greenwald (13) that an early failure to synthesize adequate amounts of elastin during a critical window in fetal life is impossible to compensate later and may trigger the later persistence of low arterial compliance. Observations in infants born with a single umbilical artery or in the donor infant in twin-twin transfusion syndrome confirm that structural adaptations in the wall of large arteries and their repercussions on elastic properties occur in response to an alteration in blood flow and that such adaptations persist for several years (14,40). This hypothesis is supported by the inverse trend of pulse wave velocity, an indicator of the aortic stiffness, with gestational age in healthy young adult (16).…”

Cardiovascular Remodeling and Dysfunction Across a Range of Growth Restriction Severity in Small for Gestational Age Infants – Implications for Fetal Programming –

“…Changes in local hemodynamic flow and pressure because of placental dysfunction in the fetal circulation may result in increased wall stress after hypertrophic changes in the arterial wall. 28 Alternatively, chronic hypoxia may lead to impaired elastin synthesis in the arterial wall during the critical fetal period, thus leading to increased arterial stiffness. 29 In this study, increased aIMT, aortic stiffness and DBP in SGA infants affected myocardial deformation; however, the SGA infants in our study showed no signs of concentric hypertrophy (increased RWT and increased LVM), which are characteristics of cardiac remodeling in hypertensive patients.…”

Impaired Endothelial Function and Increased Carotid Stiffness in 9-Year-Old Children With Low Birthweight

“…For example, subjects born with a single umbilical artery exhibit a significant difference in vessel wall compliance between the 2 iliac arteries, and in the iliac artery accommodating increased blood flow in utero, established atherosclerotic changes have been described already in childhood. 24,25 Moreover, selective atherosclerosis of the carotid arteries in elderly people has been reported to be more prevalent and severe in subjects with LBW. 26 As an interesting explanation for this association, it has been suggested that the preferential perfusion of the fetal head and the altered blood flow velocity waveforms that can be seen in intrauterine growth retardation may selectively accelerate degenerative processes in the carotid arteries.…”