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A 2-month-old girl with exudative pericarditis and hypertrophic obstructive cardiomyopathy is presented. The child had characteristic dysmorphic features of carbohydrate-deficient glycoprotein syndrome, which was confirmed by serum levels of carbohydrate-deficient transferrin. [ABSTRACT FROM AUTHOR]

Background: Transcatheter closure of a perimembranous ventricular septal defect (PmVSD) is usually performed with an asymmetric Amplatzer occluder, which is not an ideal device. Experience with the use of the Amplatzer muscular ventricular septal defect occluder (MVSO) to close selected PmVSDs is presented. Setting: Two tertiary referral centres for paediatric cardiology in two countries. Objective: To look at the safety and efficacy of the application of the MVSO in patients with appropriate PmVSD anatomy. Patients and intervention: The procedure was performed in 10 patients aged 3.2-40 (mean 12.5) years. All had a PmVSD with a mean diameter of 5.4 (range 4-11) mm, with an extension towards the muscular septum. The mean distance of the defect from the aortic valve was 5.4 (range 4-6) mm. In all but one patient, the MVSO was introduced in routine antegrade transvenous fashion (4-mm device in one patient, 6-mm device in five, 8 mm in two, 10 mm in one, and 12 mm in one). In one patient, the device was deployed by retrograde implantation. Results: All procedures except one were performed without complications, and complete closure of the VSD was achieved. One patient with a residual shunt developed haemolysis, which resolved over 10 days. In three patients, trivial, non-progressive tricuspid regurgitation appeared after the procedure. No other complications were observed over 1.7 (range 0.2-3.5) years of follow-up. Conclusion: Application of the MVSO for closure of selected PmVSDs seems to be a safe and effective treatment option. [ABSTRACT FROM AUTHOR]

Objective: Postinfarction ventricular septal defect (PIVSD) is a rare and life-threatening complication with high risk of both surgical and medical treatment. Another option available now is transcatheter closure. The purpose of this paper is to report the results of such treatment with Amplatzer occluders. Method: Seven patients aged from 51 to 71 years were included. The procedure was performed between 2 and 10 weeks after myocardial infarction. One patient had double residual VSD (2 months after previous surgery) and another, coexisting critical stenosis of right coronary artery (RCA). All patients were in III/IV NYHA class, on intropes, one patient on aortic balloon counterpulsation. Venous jugular approach was used to close the VSD in six patients, venous transfemoral in one patient. Implantation of six Ampaltzer atrial septal occluders (ASO) and one muscular Amplatzer VSD occluder (VSO) were performed. Results: All procedures but two were finished successfully. In one patient, the defect could not be entered neither from the venous nor the arterial side due to unusual oblique course (which was confirmed during subsequent operation). In the second patient (2 weeks after MI), the reason was unstable position of 24 mm ASO (probably due to necrotic borders of VSD). Immediate significant clinical improvement was achieved in all patients, in whom PIVSD was closed with Amplatzer occluders. In one postsurgical patient, two ASO were used; in another patient, prior to VSD closure, PTCA and stent implantation to RCA was performed. The stretched diameter of PIVSD ranged from 8 to 22 mm, the size of implanted Amplatzer occluders from 12 to 24 mm. Fluoroscopy time was 60 min (18–120). During the procedure, ventricular fibrillation requiring defibrillation was observed in three patients. One patient died 1 week after the procedure because of multiorgan failure and increasing mitral incompetence (MI). Conclusions: Despite some technical problems, implantation of Amplatzer occluders, is an attractive option of treatment of patients with subacute PIVSD. [Copyright &y& Elsevier]