Vascular reactivity to vasopressin and phenylephrine is potentiated by constrictor prostanoids (CP) in normotensive female (F) but not male (M) rat aorta and CP function is estrogen-dependent. This study investigated the effects of estrogen on CP function and arterial blood pressure (MAP) during development of aortic coarctation-induced hypertension (HT). M and F rats, (15-18 wks.) in four groups: normotensive (NT), hypertensive (HT), ovariectomized (OVX), and OVX estrogen-replaced (OE), underwent abdominal aortic coarctation or sham surgery (NT). At 14 days, SQ 29,548 (SQ, Thromboxane A2 (TXA2) receptor antagonist) was given i.v. to the groups. In another experiment, rats received Ridogrel (TXA2 receptor antagonist+TXA2 synthase (TXS) inhibitor) or vehicle (methyl cellulose) daily, for 14 days. Thoracic aortae were analyzed for morphology, incubated in Kreb’s Henseleit Buffer (KHB) ± angiotensin II (ANG II), or underwent continuous pulsatile flow and pressure experiments (PFP) with KHB ± ANG II. Perfusate was analyzed for thromboxane B2 (TXB2) and prostaglandin F1α (PGF1α). RT-PCR and immunohistochemistry were performed for TXS. MAP was higher in F-HT than in M-HT after 14 days. SQ infusion reduced MAP substantially more in F-HT and OE-HT than in others. Ridogrel prevented increases in MAP in F/OE-HT rats, but not M/OVX-HT. Basal release of TXB2 and PGF1α increased to a greater extent in F-HT than in M-HT relative to their controls. ANG II-stimulated TXB2 and PGF1α release increased to a greater extent in F-HT than in M-HT. With or without ANG II, TXB2 production in HT during PFP increased with estrogen. PGF1α increased during PFP with estrogen, however not with ANG II. Pressurization resulted in less diameter change in F and OE-HT than in OVX-HT. Elastin increased with HT (inhibited by Ridogrel) in all but M. Collagen increased in HT with estrogen (inhibited by Ridogrel). Neither OVX-HT nor Ridogrel had any effect on morphology. Estrogen increased TXS with HT. Estrogen enhanced vascular CP and MAP in F-HT by increased expression of TXS and collagen density in the vasculature indicating that in aortic coarctation-induced HT, CP are upregulated by estrogen. Specific forms of HT in human beings may involve estrogen-induced vascular CP upregulation.

Vascular reactivity to vasopressin and phenylephrine is potentiated by constrictor prostanoids (CP) in normotensive female (F) but not male (M) rat aorta and CP function is estrogen-dependent. This study investigated the effects of estrogen on CP function and arterial blood pressure (MAP) during development of aortic coarctation-induced hypertension (HT). M and F rats, (15-18 wks.) in four groups: normotensive (NT), hypertensive (HT), ovariectomized (OVX), and OVX estrogen-replaced (OE), underwent abdominal aortic coarctation or sham surgery (NT). At 14 days, SQ 29,548 (SQ, Thromboxane A2 (TXA2) receptor antagonist) was given i.v. to the groups. In another experiment, rats received Ridogrel (TXA2 receptor antagonist+TXA2 synthase (TXS) inhibitor) or vehicle (methyl cellulose) daily, for 14 days. Thoracic aortae were analyzed for morphology, incubated in Kreb’s Henseleit Buffer (KHB) ± angiotensin II (ANG II), or underwent continuous pulsatile flow and pressure experiments (PFP) with KHB ± ANG II. Perfusate was analyzed for thromboxane B2 (TXB2) and prostaglandin F1α (PGF1α). RT-PCR and immunohistochemistry were performed for TXS. MAP was higher in F-HT than in M-HT after 14 days. SQ infusion reduced MAP substantially more in F-HT and OE-HT than in others. Ridogrel prevented increases in MAP in F/OE-HT rats, but not M/OVX-HT. Basal release of TXB2 and PGF1α increased to a greater extent in F-HT than in M-HT relative to their controls. ANG II-stimulated TXB2 and PGF1α release increased to a greater extent in F-HT than in M-HT. With or without ANG II, TXB2 production in HT during PFP increased with estrogen. PGF1α increased during PFP with estrogen, however not with ANG II. Pressurization resulted in less diameter change in F and OE-HT than in OVX-HT. Elastin increased with HT (inhibited by Ridogrel) in all but M. Collagen increased in HT with estrogen (inhibited by Ridogrel). Neither OVX-HT nor Ridogrel had any effect on morphology. Estrogen increased TXS with HT. Estrogen enhanced vascular CP and MAP in F-HT by increased expression of TXS and collagen density in the vasculature indicating that in aortic coarctation-induced HT, CP are upregulated by estrogen. Specific forms of HT in human beings may involve estrogen-induced vascular CP upregulation.

Thesis (Ph. D.)--Ohio State University, 2009. / Title from first page of PDF file. Includes vita. Includes bibliographical references (p. 113-121).

Hypertension is a risk factor for many cardiovascular and cerebrovascular diseases such as atherosclerosis and stroke. It is therefore important to understand the effect of hypertension on temporal growth and remodeling of arteries. In this study, experimental hypertension was induced in the mini-pig by aortic coarctation. Basilar arteries and aortas were collected for analysis over an eight week period of hypertension with specimens from normotensive animals serving as controls. Changes in mechanical properties of the basilar artery were evaluated by in vitro pressure-diameter tests on intact cylindrical segments at their in situ length. The basilar arteries from hypertensive animals became less distensible, reflecting increases in both structural and material stiffness, compared to their normotensive counterparts. The circumferential stress rapidly returned toward its homeostatic value by increasing the wall thickness within two weeks. Immunohistochemistry, which is capable of illustrating the localization and distribution of protein expression, was performed to examine changes in wall constituents in the aorta. The increased medial thickness observed in hypertensive pigs compared to normotensive pigs was due to hyperplasia of smooth muscle cells (SMCs) and accumulation of extracellular matrix proteins, which were accompanied by the phenotypic modulation of SMCs. The increased interlamellar thickness, collagen fibers, and the thickness of elastic lamina found in the inner media of hypertensive animal may be associated with the gradient of stress decreasing into the outer media. SMC proliferation, if any, was found evenly distributed across the media, however. In cases showing increased proliferation and matrix protein synthesis, the SMC contractile markers were down-regulated whereas the SMC synthetic markers were up-regulated. While the aortic intima appeared normal in the normotensive animals, neointima formation, which may predispose the vessel to atheroma formation, was found in the hypertensive animals. Immunohistochemistry of Hsp47 and procollagen revealed that the endothelial cells (ECs) may produce collagen, specifically type I collagen in response to hypertension and contribute to the thickened intima. In addition, lectin staining for ECs markers and immunostaining for eNOS suggested that endothelial cells may transdifferentiate into intimal SMCs. These findings suggested an alternative role that ECs may play in hypertension-induced atherogenesis.

A expectativa de vida após correção cirúrgica da coarctação da aorta (CoAo) permanece menor que a da população geral, sendo que a maioria das mortes tardias se deve a complicações cardiovasculares, tais como: recoarctação, hipertensão arterial sistêmica (HAS), doença coronária, insuficiência cardíaca, acidente vascular cerebral (AVC) e morte súbita. Já se demonstrou que pacientes com CoAo têm estrutura e função arterial anormais, o que pode persistir mesmo após correção cirúrgica e ser responsável pela morbi-mortalidade tardias. Há pouca informação na literatura em relação ao possível remodelamento arterial após aortoplastia. O objetivo primário desse estudo foi avaliar os efeitos imediatos e após 1 ano da aortoplastia com implante de stent na reatividade e rigidez arteriais, e na espessura do complexo médiointimal (EMI). O objetivo secundário foi correlacionar os achados evolutivos da reatividade, rigidez e espessura médiointimal arteriais entre si. Vinte e um pacientes com idade mediana de 15 anos (8-39 anos) foram estudados antes da aortoplastia e após a intervenção (1 dia, 6 meses e 1 ano). A dilatação fluxo-mediada (DFM), a dilatação induzida por nitrato na artéria braquial esquerda, a velocidade da onda de pulso (VOP) carotídea, e a EMI carotídea e na artéria subclávia direita foram estudadas por meio do ultrassom. Antes do tratamento percutâneo, os pacientes apresentaram dilatação fluxo-mediada (DFM) (3,50 ± 2,01% vs 17,50 ± 3,20%, p<0,0001) e dilatação induzida por nitrato (12,51±3,66% vs 28,44 ± 6,85%, p<0,0001) prejudicadas, VOP aumentada (5,40 ± 0,79 m/s vs 4,32 ± 0,54 m/s, p<0,0001) e EMI em carótidas (0,59 ± 0,09 mm vs 0,49 ± 0,04mm, p<0,0001) e artéria subclávia direita aumentadas (1,20 ± 0,25mm vs 0,69 ± 0,16 mm, p<0,0001). Um ano após aortoplastia, não houve melhora significativa na DFM (3,61±1,86%), dilatação induzida por nitrato (12,80±3,53%), rigidez arterial (5,25 ± 0,77 m/s), EMI carotídea (0,59 ± 0,11 mm) ou EMI da artéria subclávia direita (1,21 ± 0,28 mm). Não houve correlação linear entre rigidez arterial, EMI e DFM. Pacientes submetidos à aortoplastia com balão e implante de stent não apresentaram melhora da reatividade arterial, rigidez arterial e EMI. Não houve correlação da rigidez arterial, EMI e DFM entre si. / Life expectancy after surgical repair of aortic coarctation (CoA) remains lower than general population and the majority of late deaths are due to cardiovascular complications, such as recoarctation, systemic arterial hypertension (SAH), coronary artery disease, heart failure, stroke and sudden death. It has been shown that patients with CoA have abnormal arterial structure and function, which may persist even after surgery and may be responsible for late morbidity and mortality. There is little information regarding arterial remodeling after angioplasty. The primary objective of this study was to evaluate immediate and one year results after aortic stenting on arterial reactivity and stiffness and intima-media thickness (IMT). The secondary objective was to correlate arterial reactivity, arterial stiffness and IMT. Twenty-one patients with a median age of 15 years (8-39 years) were studied before and after aortic stenting (1 day, 6 months and 1 year). The flow-mediated dilation (FMD) and nitrate-mediated dilation in left brachial artery, pulse wave velocity (PWV), carotid IMT and right subclavian artery IMT were studied by ultrasound. Before the percutaneous treatment, the patients had impaired FMD (3.50 ± 2.01% vs. 17.50 ± 3.20%, p<0.0001) and nitrate-mediated dilation (12.51 ± 3.66% vs. 28.44 ± 6.85%, p<0.0001), increased PWV (5.40 ± 0.79m/s vs. 4.32 ± 0.54m/s, p<0.0001), increased both carotid IMT (0.59 ± 0.09mm vs. 0.49 ± 0,04mm, p<0.0001) and right subclavian artery IMT (1.20 ± 0.25mm vs. 0.69 ± 0 16mm p <0.0001). One year after angioplasty, there was no significant improvement in FMD (3.61 ± 1.86%), nitrate-mediated dilation (12.80 ± 3.53%), arterial stiffness (5.25 ± 0.77 m/s), carotid IMT (0.59 ± 0.11mm) or right subclavian artery IMT (1.21 ± 0.28 mm). There was no linear correlation between arterial stiffness, IMT and FMD. Patients undergoing balloon angioplasty and stenting showed no improvement in arterial reactivity, arterial stiffness and IMT. There was no correlation among arterial stiffness, IMT and FMD.

A expectativa de vida após correção cirúrgica da coarctação da aorta (CoAo) permanece menor que a da população geral, sendo que a maioria das mortes tardias se deve a complicações cardiovasculares, tais como: recoarctação, hipertensão arterial sistêmica (HAS), doença coronária, insuficiência cardíaca, acidente vascular cerebral (AVC) e morte súbita. Já se demonstrou que pacientes com CoAo têm estrutura e função arterial anormais, o que pode persistir mesmo após correção cirúrgica e ser responsável pela morbi-mortalidade tardias. Há pouca informação na literatura em relação ao possível remodelamento arterial após aortoplastia. O objetivo primário desse estudo foi avaliar os efeitos imediatos e após 1 ano da aortoplastia com implante de stent na reatividade e rigidez arteriais, e na espessura do complexo médiointimal (EMI). O objetivo secundário foi correlacionar os achados evolutivos da reatividade, rigidez e espessura médiointimal arteriais entre si. Vinte e um pacientes com idade mediana de 15 anos (8-39 anos) foram estudados antes da aortoplastia e após a intervenção (1 dia, 6 meses e 1 ano). A dilatação fluxo-mediada (DFM), a dilatação induzida por nitrato na artéria braquial esquerda, a velocidade da onda de pulso (VOP) carotídea, e a EMI carotídea e na artéria subclávia direita foram estudadas por meio do ultrassom. Antes do tratamento percutâneo, os pacientes apresentaram dilatação fluxo-mediada (DFM) (3,50 ± 2,01% vs 17,50 ± 3,20%, p<0,0001) e dilatação induzida por nitrato (12,51±3,66% vs 28,44 ± 6,85%, p<0,0001) prejudicadas, VOP aumentada (5,40 ± 0,79 m/s vs 4,32 ± 0,54 m/s, p<0,0001) e EMI em carótidas (0,59 ± 0,09 mm vs 0,49 ± 0,04mm, p<0,0001) e artéria subclávia direita aumentadas (1,20 ± 0,25mm vs 0,69 ± 0,16 mm, p<0,0001). Um ano após aortoplastia, não houve melhora significativa na DFM (3,61±1,86%), dilatação induzida por nitrato (12,80±3,53%), rigidez arterial (5,25 ± 0,77 m/s), EMI carotídea (0,59 ± 0,11 mm) ou EMI da artéria subclávia direita (1,21 ± 0,28 mm). Não houve correlação linear entre rigidez arterial, EMI e DFM. Pacientes submetidos à aortoplastia com balão e implante de stent não apresentaram melhora da reatividade arterial, rigidez arterial e EMI. Não houve correlação da rigidez arterial, EMI e DFM entre si. / Life expectancy after surgical repair of aortic coarctation (CoA) remains lower than general population and the majority of late deaths are due to cardiovascular complications, such as recoarctation, systemic arterial hypertension (SAH), coronary artery disease, heart failure, stroke and sudden death. It has been shown that patients with CoA have abnormal arterial structure and function, which may persist even after surgery and may be responsible for late morbidity and mortality. There is little information regarding arterial remodeling after angioplasty. The primary objective of this study was to evaluate immediate and one year results after aortic stenting on arterial reactivity and stiffness and intima-media thickness (IMT). The secondary objective was to correlate arterial reactivity, arterial stiffness and IMT. Twenty-one patients with a median age of 15 years (8-39 years) were studied before and after aortic stenting (1 day, 6 months and 1 year). The flow-mediated dilation (FMD) and nitrate-mediated dilation in left brachial artery, pulse wave velocity (PWV), carotid IMT and right subclavian artery IMT were studied by ultrasound. Before the percutaneous treatment, the patients had impaired FMD (3.50 ± 2.01% vs. 17.50 ± 3.20%, p<0.0001) and nitrate-mediated dilation (12.51 ± 3.66% vs. 28.44 ± 6.85%, p<0.0001), increased PWV (5.40 ± 0.79m/s vs. 4.32 ± 0.54m/s, p<0.0001), increased both carotid IMT (0.59 ± 0.09mm vs. 0.49 ± 0,04mm, p<0.0001) and right subclavian artery IMT (1.20 ± 0.25mm vs. 0.69 ± 0 16mm p <0.0001). One year after angioplasty, there was no significant improvement in FMD (3.61 ± 1.86%), nitrate-mediated dilation (12.80 ± 3.53%), arterial stiffness (5.25 ± 0.77 m/s), carotid IMT (0.59 ± 0.11mm) or right subclavian artery IMT (1.21 ± 0.28 mm). There was no linear correlation between arterial stiffness, IMT and FMD. Patients undergoing balloon angioplasty and stenting showed no improvement in arterial reactivity, arterial stiffness and IMT. There was no correlation among arterial stiffness, IMT and FMD.

Currarino-Silverman syndrome is a rare disorder characterized by premature fusion of manubrio-sternal joint and the sternal segments, resulting in a high carinate chest deformity; it is frequently associated with congenital heart disease. Among the various heart lesions reported in this syndrome, mitral valve disease and coarctation of the aorta have not yet been described (to our knowledge). Our report consists of five children with this syndrome, four of whom had mitral valve disease, with an associated coarctation of the aorta in one patient. The fifth patient had an innocent heart murmur.

Mais informações são necessárias para definir se o tratamento percutâneo da coartação da aorta com stents é superior à angioplastia com cateter-balão. De julho de 2000 a maio de 2003, 21 adolescentes e adultos com coartação da aorta focal e média de idade de 24 anos (DP 11 anos) foram submetidos, consecutivamente, a implante de stents (grupo 1). Os resultados foram comparados com os obtidos em um grupo histórico de 15 pacientes com média de idade de 18 anos (DP 10 anos) (p = 0,103) submetidos a angioplastia (grupo 2) nos últimos 18 anos. Após o procedimento, a redução do gradiente sistólico foi maior (99% [DP 2%] versus 87% [DP 17%]; p = 0,015), o gradiente residual foi menor (0,4 mmHg [DP 1,4 mmHg] versus 5,9 mmHg [DP 7,9 mmHg]; p = 0,019), o ganho no local da coartação foi maior (333% [DP 172%] \"versus\" 190% [DP 104%]; p = 0,007) e o diâmetro da coartação foi maior (16,9 mm [DP 2,9 mm] versus 12,9 mm [DP 3,2 mm]; p < 0,001) no grupo 1. Alterações da parede da aorta, incluindo dissecções, abaulamentos e aneurismas, foram observadas em oito pacientes do grupo 2 (53%) e em um do grupo 1 (7%) (p < 0,001). Não houve complicações maiores. Cateterismo (n = 33) ou ressonância magnética (n = 2) de controle foram realizados em seguimento mediano de um ano para o grupo 1 e um ano e meio para o grupo 2 (p = 0,005). A redução do gradiente sistólico persistiu em ambos os grupos; entretanto, gradientes tardios mais altos foram observados no grupo 2 (mediana de 0 mmHg para o grupo 1 versus 3 mmHg para o grupo 2; p = 0,014). Não houve perdas no diâmetro da coartação no grupo 1 e houve ganho tardio no grupo 2 (16,7 mm [DP 2,9 mm] versus 14,6 mm [DP 3,9 mm]; p = 0,075). No grupo 1, dois pacientes necessitaram de novo implante de stent em decorrência da formação de aneurisma ou fratura da malha do stent. No grupo 2, as anormalidades da parede aórtica não progrediram e um paciente necessitou de redilatação em decorrência da recoartação. A pressão arterial sistêmica foi semelhante em ambos os grupos durante o seguimento (sistólica: 126 mmHg [DP 12 mmHg] no grupo 1 versus 120 mmHg [DP 15 mmHg] no grupo 2; diastólica: 81 mmHg [DP 11 mmHg] no grupo 1 versus 80 mmHg [DP 10 mmHg] no grupo 2; p = 0,149 e p = 0,975, respectivamente). Apesar de os desfechos clínicos terem sido satisfatórios e similares com ambas as técnicas, o uso de stents propiciou resultados mais previsíveis e uniformes para alívio da estenose, minimizando também o risco de desenvolvimento de alterações da parede da aorta. / More information is needed to define whether stenting is superior to balloon angioplasty for coarctation of the aorta. From July/2000 to May/2003, 21 adolescents and adults with discrete coarctation underwent consecutive stent implantation at a mean age of 24 years (SD 11 years) (group 1). The results were compared to those achieved by balloon angioplasty performed in the last 18 years in a historical group of 15 patients at a mean age of 18 years (SD 10 years) (p = 0.103) (group 2). After the procedure, systolic gradient reduction was higher (99% [SD 2%] vs. 87% [SD 17%]; p = 0.015), residual gradients lower (0.4 mmHg [SD 1.4 mmHg] vs. 5.9 mmHg [SD 7.9 mmHg); p = 0.019), gain at the coarctation site higher (333% [SD 172%] vs. 190% [SD 104%]; p = 0.007) and coarctation diameter larger (16.9 mm [SD 2.9 mm] vs.12.9 mm [SD 3.2 mm]; p < 0.001) in group 1. Aortic wall abnormalities, including dissections, bulges and aneurysms, were observed in eight patients in group 2 (53%) and in one in group 1 (7%) (p < 0.001). There was no major complication. Repeat catheterization (n = 33) or magnetic resonance imaging (n = 2) was performed at a median follow-up of 1.0 year for group 1 and 1.5 year for group 2 (p = 0.005). Gradient reduction persisted in both groups, although higher late gradients were observed in group 2 (median of 0 mmHg for group 1 vs. 3 mmHg for group 2; p = 0.014). There was no late loss in the coarctation diameter in group 1 and there was a late gain in group 2 (16.7 mm [SD 2.9 mm] for group 1 vs. 14.6 mm [SD 3.9 mm] for group 2; p = 0.075). Two patients required late stenting due to aneurysm formation or stent fracture in group 1. Aortic wall abnormalities did not progress and one patient required redilation due to recoarctation in group 2. Blood pressure was similar in both groups at follow-up (systolic: 126 mmHg [SD 12 mmHg] in group 1 vs. 120 mmHg [SD 15 mmHg] in group 2; diastolic: 81 mmHg [SD 11 mmHg] in group 1 vs. 80 mmHg [SD 10 mmHg] in group 2; p = 0.149 and p = 0.975, respectively). Although satisfactory and similar clinical outcomes were observed with both techniques, the use of stents yielded more predictable and uniform results for stenosis relief, also minimizing the risk of developing aortic wall abnormalities.

Mais informações são necessárias para definir se o tratamento percutâneo da coartação da aorta com stents é superior à angioplastia com cateter-balão. De julho de 2000 a maio de 2003, 21 adolescentes e adultos com coartação da aorta focal e média de idade de 24 anos (DP 11 anos) foram submetidos, consecutivamente, a implante de stents (grupo 1). Os resultados foram comparados com os obtidos em um grupo histórico de 15 pacientes com média de idade de 18 anos (DP 10 anos) (p = 0,103) submetidos a angioplastia (grupo 2) nos últimos 18 anos. Após o procedimento, a redução do gradiente sistólico foi maior (99% [DP 2%] versus 87% [DP 17%]; p = 0,015), o gradiente residual foi menor (0,4 mmHg [DP 1,4 mmHg] versus 5,9 mmHg [DP 7,9 mmHg]; p = 0,019), o ganho no local da coartação foi maior (333% [DP 172%] \"versus\" 190% [DP 104%]; p = 0,007) e o diâmetro da coartação foi maior (16,9 mm [DP 2,9 mm] versus 12,9 mm [DP 3,2 mm]; p < 0,001) no grupo 1. Alterações da parede da aorta, incluindo dissecções, abaulamentos e aneurismas, foram observadas em oito pacientes do grupo 2 (53%) e em um do grupo 1 (7%) (p < 0,001). Não houve complicações maiores. Cateterismo (n = 33) ou ressonância magnética (n = 2) de controle foram realizados em seguimento mediano de um ano para o grupo 1 e um ano e meio para o grupo 2 (p = 0,005). A redução do gradiente sistólico persistiu em ambos os grupos; entretanto, gradientes tardios mais altos foram observados no grupo 2 (mediana de 0 mmHg para o grupo 1 versus 3 mmHg para o grupo 2; p = 0,014). Não houve perdas no diâmetro da coartação no grupo 1 e houve ganho tardio no grupo 2 (16,7 mm [DP 2,9 mm] versus 14,6 mm [DP 3,9 mm]; p = 0,075). No grupo 1, dois pacientes necessitaram de novo implante de stent em decorrência da formação de aneurisma ou fratura da malha do stent. No grupo 2, as anormalidades da parede aórtica não progrediram e um paciente necessitou de redilatação em decorrência da recoartação. A pressão arterial sistêmica foi semelhante em ambos os grupos durante o seguimento (sistólica: 126 mmHg [DP 12 mmHg] no grupo 1 versus 120 mmHg [DP 15 mmHg] no grupo 2; diastólica: 81 mmHg [DP 11 mmHg] no grupo 1 versus 80 mmHg [DP 10 mmHg] no grupo 2; p = 0,149 e p = 0,975, respectivamente). Apesar de os desfechos clínicos terem sido satisfatórios e similares com ambas as técnicas, o uso de stents propiciou resultados mais previsíveis e uniformes para alívio da estenose, minimizando também o risco de desenvolvimento de alterações da parede da aorta. / More information is needed to define whether stenting is superior to balloon angioplasty for coarctation of the aorta. From July/2000 to May/2003, 21 adolescents and adults with discrete coarctation underwent consecutive stent implantation at a mean age of 24 years (SD 11 years) (group 1). The results were compared to those achieved by balloon angioplasty performed in the last 18 years in a historical group of 15 patients at a mean age of 18 years (SD 10 years) (p = 0.103) (group 2). After the procedure, systolic gradient reduction was higher (99% [SD 2%] vs. 87% [SD 17%]; p = 0.015), residual gradients lower (0.4 mmHg [SD 1.4 mmHg] vs. 5.9 mmHg [SD 7.9 mmHg); p = 0.019), gain at the coarctation site higher (333% [SD 172%] vs. 190% [SD 104%]; p = 0.007) and coarctation diameter larger (16.9 mm [SD 2.9 mm] vs.12.9 mm [SD 3.2 mm]; p < 0.001) in group 1. Aortic wall abnormalities, including dissections, bulges and aneurysms, were observed in eight patients in group 2 (53%) and in one in group 1 (7%) (p < 0.001). There was no major complication. Repeat catheterization (n = 33) or magnetic resonance imaging (n = 2) was performed at a median follow-up of 1.0 year for group 1 and 1.5 year for group 2 (p = 0.005). Gradient reduction persisted in both groups, although higher late gradients were observed in group 2 (median of 0 mmHg for group 1 vs. 3 mmHg for group 2; p = 0.014). There was no late loss in the coarctation diameter in group 1 and there was a late gain in group 2 (16.7 mm [SD 2.9 mm] for group 1 vs. 14.6 mm [SD 3.9 mm] for group 2; p = 0.075). Two patients required late stenting due to aneurysm formation or stent fracture in group 1. Aortic wall abnormalities did not progress and one patient required redilation due to recoarctation in group 2. Blood pressure was similar in both groups at follow-up (systolic: 126 mmHg [SD 12 mmHg] in group 1 vs. 120 mmHg [SD 15 mmHg] in group 2; diastolic: 81 mmHg [SD 11 mmHg] in group 1 vs. 80 mmHg [SD 10 mmHg] in group 2; p = 0.149 and p = 0.975, respectively). Although satisfactory and similar clinical outcomes were observed with both techniques, the use of stents yielded more predictable and uniform results for stenosis relief, also minimizing the risk of developing aortic wall abnormalities.