Aortic Coarctations and Coronary Artery Disease: The XY Factor
Aortic coarctation (CoA) is a congenital defect involving a constriction of the aortic arch, usually occurring near the site of insertion of the ductus arteriosus. Surgical and endovascular repair techniques and success rates, measured by short term survival, elimination of the gradient across the stricture, and normalization of systemic blood pressure, improved steadily over the last half of the 20th century. Despite apparently successful correction of the obstruction, however, individuals with a history of CoA demonstrate excess morbidity and premature mortality associated with hypertension, cerebrovascular accident, coronary artery disease and aortic dissection/rupture1-3. These adverse outcomes are to some extent independent of the severity of the original obstruction, type of treatment, restenosis or presence of prosthetic grafts2,4. While blood pressure usually normalizes for a time after successful repair, almost one third of CoA patients develop hypertension by adolescence5 and nearly 90% by middle age2. The etiology of the later onset hypertension remains poorly understood6. Normotensive children and young adults that had undergone successful CoA repair were found to have persistent endothelial dysfunction7 and impaired arterial reactivity8, suggesting that intrinsic vascular abnormalities might contribute to the risk for premature coronary artery disease (CAD), independent of hypertension (HTN). (SELECT FULL TEXT TO CONTINUE)
- Received May 31, 2012.
- Accepted June 1, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited