Joseph et al. [1] have described well the techniques for opening percutaneously the completely occluded aortic isthmus. We would submit, however, that what they have crossed and dilated so well is not congenital atresia of the aortic isthmus, but acquired complete occlusion in congenital coarctation of the aortic isthmus.
Atresia or interruption of the aortic arch as an isolated congenital malformation is extremely rare [2-5]. To find four such patients among 26 undergoing balloon angioplasty of aortic coarctation would be more than extraordinary. Intimal proliferation due to turbulent flow, however, is found at the aortic coarctation site in virtually all patients, tends to progress with age, and not uncommonly completely occludes the lumen [6]. Among 70 aortic coarctations serially sectioned and examined histologically, we found 4 (6%) with complete occlusion of the lumen, and in each the mechanism of occlusion was intimal proliferation (Fig. 1).
In most patients with aortic coarctation, blood flow to the descending aorta is primarily via collaterals, and consequently severe stenosis or complete occlusion at the coarctation site presents the same clinical picture. Joseph et al. [1] comment several times that the clinical features of their four patients were similar to those of patients with aortic coarctation, and the reason is that their patients had aortic coarctation.