Intracardiac anomalies cause disturbances in fetal flow patterns which in turn influence dimensions of the great vessels. At birth the aortic isthmus, which receives 25% of the combined fetal ventricular output, is normally 25 to 30% narrower than the descending aorta. A shelf like indentation of the posterior aortic wall opposite the ductus characterizes the junction of the isthmus with descending aorta. In tetralogy of Fallot, pulmonary atresia, and tricuspid atresia, when pulmonary blood flow is reduced from birth, the main pulmonary artery is decreased and ascending aorta increased in size. Conversely in intracardiac anomalies where blood is diverted away from the aorta to the pulmonary artery, isthmal narrowing or the posterior indentation may be exaggerated. Analysis of 162 patients with coarctation of the aorta showed 83 with an intracardiac anomaly resulting in increased pulmonary blood flow and 21 with left sided lesions present from birth. In contrast no patients with coarctation were found with diminished pulmonary flow or right sided obstructive lesions. From this evidence the hypothesis is developed that coarctation is prevented when flow in the main pulmonary artery is reduced in the fetus.
CITATION STYLE
Shinebourne, E. A., & Elseed, A. M. (1974). Relation between fetal flow patterns, coarctation of the aorta, and pulmonary blood flow. British Heart Journal, 36(5), 492–498. https://doi.org/10.1136/hrt.36.5.492
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