YF Cheung

Abstract

Arterial stiffness, the rigidity of the arterial wall, owes its significance to a direct relationship with impedance of the arterial system, and hence the left ventricular afterload. In adults, arterial stiffness has been considered as a marker of vascular disease and is emerging as an independent cardiovascular risk factor. There is accumulating evidence that this may also be true in children. Several paediatric clinical entities may affect normal functioning of the arterial system and may have an impact on long term cardiovascular health. Both prenatal and postnatal influences affect the age-dependent evolution of arterial stiffness. The prenatal influence of reduced fetal growth is illustrated by the findings of increased arterial stiffness in individuals born small and the growth-restricted donor twins in twin-twin transfusion syndrome. Postnatal structural alteration of arteries secondary to childhood vasculitides increases peripheral conduit arterial stiffness significantly. Furthermore, the magnitude of vascular inflammation during the acute phase may have important bearings on late arterial stiffening. Functional alterations of the arteries may also increase arterial stiffness. Endothelial dysfunction, documented in children with familial hypercholesterolaemia, obesity and beta-thalassaemia major, has a direct relationship with arterial stiffening. Alternatively, enhanced sympathetic tone, as might occur in childhood sleep-related disorders, may increase arterial stiffness. With the availability of noninvasive techniques for the determination of arterial stiffness in children, longitudinal studies incorporating this measurement may unveil its prognostic value in the paediatric at-risk population.