Reversed circulation in acardiac fetuses is associated with anatomic inversions in the aortic wall.
Blood vessel anatomy is probably related to hemodynamic factors which change during development. This principle has been postulated as the basis for differences in the numbers of elastic lamellae in the tunica media of the proximal and distal human aorta. Recent studies of human fetuses at varying stages confirmed that the number of elastin lamellae in the aortic wall varied along its length (spatially) and with age (temporally). These findings suggest that hemodynamic influences during prenatal development induce structural changes in the aortic wall. Acardiac fetuses provide a model for studying the effects of hemodynamic changes on the structure of elastic arteries because blood flow through the aorta in such fetuses is reversed and greatly reduced. Also, analysis of the vascular structure of acardiac fetuses would further define the characteristic features of this congenital disorder. In the present study, we have examined the gross and histological anatomy of the aorta from seven acardiac fetuses. In each case, the microscopic architecture of the aorta was deranged and the normal proximal-distal differences in arterial caliber and number of elastin lamellae were reversed. In the proximal aorta, medial lamellar units were thin, fragmented, and irregular. In some segments, only traces of medial lamellar units existed. We believe that these anatomic abnormalities represent degenerative or dysplastic responses to reversed flow and pressure gradients in the aorta. These findings are consistent with the hypothesis that aortic wall structure is influenced by hemodynamic factors during development.
Park
H W
HW
Department of Pediatrics, University of Washington, Seattle 98195.
Kapur
R P
RP
Shepard
T H
TH
D001011:Aorta / Q000002:abnormalities* / Q000196:embryology / Q000473:pathology; D001775:Blood Circulation; D006330:Heart Defects, Congenital / Q000503:physiopathology*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000002:abnormalities / Q000196:embryology / Q000473:pathology