• Nicola Maschietto, Luca Semplicini, Giulio Ceolotto, Arianna Cattelan, Helen Poser Dvm, Ilaria Iacopetti, Gabriele Gerardi, Giulia Maria De Benedictis, Tommaso Pilla, Daniele Bernardini, Luca Aresu, Stefania Rizzo, Cristina Basso, Andrea Semplicini, and Ornella Milanesi.
• Pediatric Cardiology Unit, Department of Women's and Children's Health, University of Padua, Padova, Italy.
• Congenit Heart Dis. 2017 Jan 1; 12 (1): 74-83.

BackgroundStent implantation is the treatment of choice for adolescents and adults with aortic coarctation (CoAo). Despite excellent short-term results, 20%-40% of the patients develop arterial hypertension later in life, which was attributed to inappropriate response of the aortic baroreceptors to increased stiffness of the ascending aorta (ASAO), either congenital or induced by CoAo repair. In particular, it has been hypothesized that stent itself may cause or sustain hypertension. Therefore, we aimed to study the hemodynamic and structural impact following stent implantation in the normal aorta of a growing animal.MethodsEight female sheep completed the study and a stent was implanted in four. Every 3 mo we measured blood pressure of the anterior and posterior limbs and left ventricular function by echocardiography. Twelve months later invasive pressure was measured under baseline and simulated stress conditions. Expression of genes indicating oxidative stress (OS), endothelial dysfunction (ED) and stiffness, as well as pathological examination were performed in ascending (ASAO) and descending aorta (DSAO).ResultsSOD1 and MMP9 gene expression were higher in ASAO of the stented animals, compared to DSAO and controls, while NOS3 was decreased. No differences were found in blood pressure and echocardiographic parameters. No histological differences were found in the aorta of the two groups of animals.ConclusionsStent does not affect central and peripheral hemodynamics, cardiac structure and function even in the long term. However, the finding of markers of OS and increased stiffness of ASAO, proximal to the stent, points to molecular mechanisms for increased cardiovascular risk of patients with stented CoAo.© 2016 The Authors Congenital Heart Disease published by Wiley Periodicals, Inc.

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