More information is needed to clarify whether stenting is superior to balloon angioplasty (BA) for unoperated coarctation of the aorta (CoA). From September 1997, 21 consecutive adolescents and adults (24 +/- 11 years) with discrete CoA underwent stenting (G1). The results were compared to those achieved by BA performed in historical group of 15 patients (18 +/- 10 years; P = 0.103; G2). After the procedure, systolic gradient reduction was higher (99% +/- 2% vs. 87% +/- 17%; P = 0.015), residual gradients lower (0.4 +/- 1.4 vs. 5.9 +/- 7.9 mm Hg; P = 0.019), gain at the CoA site higher (333% +/- 172% vs. 190% +/- 104%; P = 0.007), and CoA diameter larger (16.9 +/- 2.9 vs. 12.9 +/- 3.2 mm; P < 0.001) in G1. Aortic wall abnormalities were found in eight patients in G2 (53%) and in one in G1 (7%; P < 0.001). There was no major complication. Repeat catheterization (n = 33) and/or MRI (n = 2) was performed at a median follow-up of 1.0 year for G1 and 1.5 for G2 (P = 0.005). Gradient reduction persisted in both groups, although higher late gradients were seen in G2 (median of 0 mm Hg for G1 vs. 3 for G2; P = 0.014). CoA diameter showed no late loss in G1 and a late gain in G2 with a trend to being larger in G1 (16.7 +/- 2.9 vs. 14.6 +/- 3.9 mm; P = 0.075). Two patients required late stenting due to aneurysm formation or stent fracture in G1. Aortic wall abnormalities did not progress and one patient required redilation in G2. Blood pressure was similar in both groups at follow-up (126 +/- 12/81 +/- 11 for G1 vs. 120 +/- 15/80 +/- 10 mm Hg for G2; P = 0.149 and 0.975, respectively). Although satisfactory and similar clinical outcomes were observed with both techniques, stenting was a better means to relieve the stenosis and minimize the risk of developing immediate aortic wall abnormalities.
No abstract
Intravascular ultrasound assessment late after the ASO revealed proximal eccentric intimal thickening in most of the studied vessels. This observation suggests the development of early atherosclerosis in the reimplanted coronary arteries, which may have a role in the genesis of late coronary events.
Fetal interventions have been performed for some congenital heart diseases. However, these procedures have not gained wide acceptance due to concerns about their efficacy and safety. The aim of this study was to report on a preliminary experience with fetal cardiac interventions in Brazil. Twenty-two cardiac interventions were performed in 21 fetuses. Thirteen fetuses had critical aortic stenosis (CAS), 4 had hypoplastic left heart syndrome (HLHS) and intact interatrial septum or small patent foramen ovale, 1 had pulmonary atresia with intact ventricular septum (IVS), and 3 had critical pulmonary stenosis (CPS). The main outcome variables evaluated were technical success and procedural complications as well as pregnancy and postnatal outcomes. Success was achieved in 20 of 22 procedures (91%) with 1 failed aortic and 1 failed pulmonary valvuloplasties. There was 1 fetal death. No maternal complications occurred. One patient with CAS, severe mitral regurgitation, and hydrops died postnatally within 5 months of age. All patients with HLHS and restrictive atrial septum died after interventional or surgical procedures and prolonged hospitalizations. All patients with CPS/IVS survived and achieved a biventricular (BV) circulation after neonatal valvuloplasty and ductal stenting. A BV circulation was achieved in 4 of 8 patients with CAS and evolving HLHS (one still in utero), including 2 with initial borderline left ventricles (LV) in whom surgical LV overhaul was performed at 9 months of age. In this preliminary experience, the feasibility of fetal cardiac interventions and their outcomes were similar to those previously reported.
Background-Although the prenatal diagnosis of most fetal structural heart defects and dysrhythmias has been described, there is a paucity of information about cardiomyopathies (CMs) in prenatal life. Methods and Results--To determine the pathogenic mechanisms, hemodynamic findings, and outcome of fetal CM, we reviewed the fetal echocardiograms and perinatal histories of 55 affected fetuses. Dilated CM was diagnosed in 22 cases, including 2 with congenital infections, 5 familial cases, 6 with endocardial fibroelastosis related to maternal anti-Ro/La antibodies, and 9 idiopathic cases. Thirty-three had hypertrophic CM, 7 associated with maternal diabetes, 2 with Noonan's syndrome, 2 with ␣-thalassemia, 18 with twin-twin transfusion syndrome, 1 with familial hypertrophy, and 3 with idiopathic hypertrophy. Systolic dysfunction was present in all cases of dilated CM and 15 cases of hypertrophic CM. Diastolic dysfunction was present in 19 of 30 fetuses with assessment of diastolic function parameters. Significant mitral or tricuspid valve regurgitation was seen in 32 cases. Eight fetuses were hydropic and 23 had signs of early hydrops. Seven pregnancies were terminated. Of 46 continued pregnancies with follow-up, 29 (63%) died perinatally. The presence of systolic dysfunction, diastolic dysfunction, and significant atrioventricular valve regurgitation were identified as risk factors for mortality. By multiple logistic regression, diastolic dysfunction was associated with an 8-fold increased risk relative to the other parameters. Conclusions-Fetal CM has a broad spectrum of intrinsic and extrinsic causes. A poor outcome is observed in many affected fetuses. Diastolic dysfunction in fetal CM is associated with the highest risk of mortality. (Circulation. 2002; 106:585-591.)
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