Paper
Does stenting of thoracic aortic coarctation induce a late exercise‐induced hypertension? stay tuned…
Published Feb 1, 2010 · DOI · Hernan A. Bazan
Catheterization and Cardiovascular Interventions
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Abstract
Aortic coarctation is a congenital condition whereby the thoracic aorta narrows at the site where the ductus arteriosus (future site of the ligamentum arteriosum) inserts. A poorly understood mechanism occurs during embryogenesis, which causes aberrant smooth muscle cell migration to various parts of the aortic wall near the ductus arteriosus, leading to fibrosis of the actual aortic wall (and not just the ductus) and subsequent coarctation development. There are three types of aortic coarctation: Preductal (whereby the narrowing is proximal to the ductus arteriosus), ductal (disease occurs at the site of the ductus arteriosus), and postductal (narrowing is distal to the insertion of the ductus arteriosus). The postductal is thought to be the most common in adults and the others are implicated in infants. Because infant and adult thoracic aortic coarctation are likely a result of different pathogenesis, their disease manifestation is likely different; this fact has implications when one tries to group infant-treated aortic coarctation patients with adults. Adult aortic coarctation is universally fatal by the fifth decade if left untreated, primarily due to accelerated arteriosclerosis. Over the years, it was speculated that treatment of the thoracic aorta surgically with a Dacron graft and, more recently, with a bare-metal stent could reduce the elastic properties of the thoracic aorta and lead to exercise-induced hypertension. Various authors speculated that perhaps the compliance mismatch between the rigid prosthesis (or endoprosthesis) and the normal, nearby distensible aortic wall would increase during exercise (high-flow conditions) and behave as a ‘‘functional stenosis.’’ De Caro et al. attempt to answer this question in a detailed comparison study of 17 surgicaland 15 stent-treated young patients with thoracic aortic coarctation. It is an elegant physiologic study of these subjects with intermediate follow-up. The surgery group was older (27.4 vs. 11.7 years of age), and the authors were able to provide markedly increased longer follow-up (11.1 vs. 4.2 years), compared with the stent group. No differences in the two groups were noted in baseline blood pressure readings or in the development of exercise-induced hypertension. Although this is a well-performed study, it is limited by the small number of patients with this rare disease. Confidence in comparisons between the two groups is difficult to ascertain and, therefore, difficult to adopt into clinical practice. Unfortunately, no one in the surgery group had an interposition graft repair, but rather treatment with a primary end-to-end anastomosis, patch angioplasty, and ‘‘subclavian flap,’’ all of which are thought to be associated with a higher recurrence and/or aneurysm formation rate [1]. To better answer this important question—whether bare-metal stent treatment of the thoracic aorta may change the elastic properties such that exercise-induced hypertension may be a sequelae of therapy—the Congenital Cardiovascular Interventional Study Consortium (CCISC) [2] may gain from adopting some these authors’ well-designed methodology. Most published studies on thoracic aortic coarctation are small (under 20 patients) with intermediate follow-up being the longest (3 to 4 years); CCISC have gathered data from more than 40 hospitals encompassing over 500 children to date; preliminary results have previously been published in CCI. It will be such research consortiums that will help answer this important question of such a rare disease entity.
Stenting for thoracic aortic coarctation does not cause exercise-induced hypertension, as previously feared.
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