Cardiac tamponade in a child with ascariasis.

Ascaris infection, when severe, may manifest with constitutional symptoms. The parasites penetrate the intestinal walls, reach the venules and lymphatics and, through the portal circulation, may affect the heart. To the best of our knowledge, involvement of the pericardium has yet to be reported. We describe here a case of severe pericardial effusion and cardiac tamponade in a child with ascariasis.

Transcatheter closure of perimembranous ventricular septal defects with the Amplatzer asymmetric ventricular septal defect occluder: preliminary experience in children.

OBJECTIVE: To close perimembranous ventricular septal defects (PMVSDs) in children with the new Amplatzer asymmetric ventricular septal defect occluder (AAVSDO). PATIENTS AND DESIGN: 10 children, aged 1.5-12 years, with PMVSDs underwent transcatheter closure with the AAVSDO. The device consists of two low profile disks made of Nitinol wire mesh with a 1.5 mm connecting waist. The left disk is 5 mm towards the apex and only 0.5 mm towards the aortic valve. The right disk is 4 mm larger than the waist. The prosthesis diameter was chosen to be 1-2 mm larger than the largest diameter of the defect (determined by transoesophageal echocardiography and angled angiocardiography). A 7-8 French gauge sheath was used to deliver the AAVSDO. RESULTS: The PMVSD diameter ranged from 2-8 mm. The device diameter ranged from 4-8 mm. After deployment of the prosthesis there was no residual shunt in 9 of 10 patients (90%). In one patient there was a trivial residual shunt that disappeared at the three month follow up. Three patients developed transient complete left bundle branch block. No other complications were observed. CONCLUSIONS: The AAVSDO appears to be a promising device for transcatheter closure of PMVSDs in children. Further studies are required to document its efficacy, safety, and long term results in a larger patient population.

Transcatheter closure of high pulmonary artery pressure persistent ductus arteriosus with the Amplatzer muscular ventricular septal defect occluder.

BACKGROUND: The design of devices currently used for closure of persistent ductus arteriosus (PDA) with high pulmonary artery pressure is not ideal and there is a risk of embolisation into the aorta. OBJECTIVE: To investigate the use of the Amplatzer muscular ventricular septal defect occluder (AMVSDO) for treatment of PDA with high pulmonary artery pressure. PATIENTS AND DESIGN: Seven patients, aged 5-12 years, with large PDAs and systemic or near systemic pulmonary artery pressure underwent attempted transcatheter closure using the AMVSDO. The device consists of two low profile disks made of a nitinol wire mesh with a 7 mm connecting waist. Balloon occlusion of the duct was performed before closure from the venous side, and prosthesis size was chosen according to the measured diameter of the occluding balloon. A 7 French sheath was used to deliver the device. All patients underwent a complete haemodynamic and angiographic study one year after occlusion. RESULTS: The mean (SD) angiographic PDA diameter was 9.8 (1.7) mm (range 7-13 mm) and the mean AMVSDO diameter was 11.4 (1.8) mm (range 9-16 mm). Q(p)/Q(s) ranged from 1.9-2.2 (mean 2.0 (0.1)). Successful device delivery and complete closure occurred in all patients (100% occlusion rate, 95% confidence interval 59.04% to 100.00%). Mean systolic pulmonary artery pressures were as follows: before balloon occlusion, 106 (13) mm Hg; during occlusion, 61 (6) mm Hg; immediately after the procedure, 57 (5) mm Hg; and at the one year follow up catheterisation, 37 (10) mm Hg. Fluoroscopy time was 10.4 (4.3) min (range 7-18 min). No complications occurred. CONCLUSIONS: AMVSDO is an important adjunct for closure of large PDAs associated with high pulmonary artery pressure. Further studies are required to document its efficacy, safety, and long term results in a larger number of patients.

Study of late potentials and ventricular arrhythmias in hypertensive patients with normal electrocardiograms.

INTRODUCTION: Although an increase in the occurrence of ventricular arrhythmias has been observed in hypertensive patients, some basic questions remain unresolved regarding the prevalence and the pathophysiology of these arrhythmias. The basic aims of this study were as follows: (1) to examine the incidence and severity of ventricular arrhythmias in a substantial number of hypertensive patients without electrocardiographic indications of hypertrophy; and (2) to examine the correlation between late potentials, hypertrophy, and ventricular arrhythmias in these patients. MATERIALS AND METHODS: We studied 78 consecutive patients (31 men, 47 women), aged 60.5 +/- 7.8 years, with a history of hypertension but a normal electrocardiogram. All patients had an echocardiographic study, 24-hour ambulatory monitoring, exercise test, and signal-averaged electrocardiogram. The latter was analyzed using a 40- to 250-Hz filter and with a noise level < or = 0.3 microV. RESULTS: Of the 78 patients studied, 21 (26.9%) had severe ventricular arrhythmias, while 57 (73.1%) had either no ventricular ectopics or sporadic isolated ventricular extrasystoles. Left ventricular hypertrophy, defined by echocardiography, was found in 58 patients (74.3%), of which 16 (27.58%) had severe ventricular arrhythmias. Five (25%) of the 20 patients without hypertrophy also had severe ventricular arrhythmias (P = NS). Ventricular late potentials were recorded in 19 (24.5%) of the 78 patients. Of these, 11 (57.89%) had severe arrhythmias, while of the 59 patients without late potentials 10 (16.94%) had severe ventricular ectopic activity. CONCLUSIONS: In hypertensive patients without electrocardiographic signs of hypertrophy, the higher prevalence of ventricular arrhythmias does not appear to be related to left ventricular hypertrophy but is correlated with the existence of ventricular late potentials.