Ceraflex versus Amplatzer occluder for secundum atrial septal defect closure. Multicenter clinical experience.

AIM: The Ceraflex atrial septal defect occluder is an alternative device to the Amplatzer septal occluder with some structural innovations including flexible connection, increased flexibility, and minimized amount of implant material. We evaluated the efficiency and safety of the Ceraflex septal occluder device in percutaneous closure of secundum atrial septal defects. PATIENTS AND METHODS: This was a prospective, nonrandomized, multicenter study of patients undergoing transcatheter closure for an atrial septal defect with the Ceraflex and the Amplatzer septal occluder devices. A clinical evaluation and follow-up transthoracic echocardiography were performed at 1, 6, and 12 months. RESULTS: Between 2010 and 2014, 125 patients underwent atrial septal defect closure with the Ceraflex septal occluder (n = 58) and the Amplatzer septal occluder (n = 67) under transesophageal echocardiography guidance. Patient characteristics, the stretched size of the defect, device size, and fluoroscopy time were similar between the groups. The immediate and follow-up complete occlusion rates for both groups were 100%. There was no device embolization, procedure-related stroke, or pericardial effusion. CONCLUSIONS: The Ceraflex septal occluder is a safe and efficient device for closure of secundum atrial septal defects with no procedural complications. The Ceraflex has similar outcomes when compared with the Amplatzer septal occluder device. The advantage of the Ceraflex septal occluder device is that it can be deployed without the tension of the delivery catheter.

Brugada-like electrocardiographic changes induced by fever.

As "time is myocardium" in the settings of acute myocardial infarction, it is important to make the diagnosis as quickly as possible, and a high clinical suspicion is needed to avoid missing the diagnosis, resulting in unwarranted interventions. The electrocardiogram is a crucial tool in the identification of acute chest pain, enabling a detailed analysis of patterns of ST-segment elevation. We describe the case of a 22-year-old man who presented with fever, with dynamic electrocardiographic changes similar to the Brugada syndrome. These electrocardiographic anomalies disappeared when the temperature returned to normal.

Spironolactone does not prevent restenosis after coronary stenting in humans.

INTRODUCTION: In animal studies, aldosterone enhanced neointimal proliferation by increasing extracellular accumulation of collagen and potentiating the effects of angiotensin II. Spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal proliferation. We conducted a placebo-controlled, double-blind, randomised study to assess the effect of spironolactone on angiographic 6-month in-stent restenosis. MATERIALS AND METHODS: Of the 310 randomised patients with significant coronary artery disease, 258 patients were available for analysis: 128 constituted the placebo group and 130 were assigned to receive spironolactone. Eligible patients were randomly assigned to receive a dose of 50 mg spironolactone or placebo orally twice a day for 6 months. The primary endpoint was the angiographic restenosis (>50% stenosis) rate at follow-up angiography. RESULTS: At 6-month follow-up angiography after stenting, there was no difference between the 2 groups in minimal lumen diameter, percent diameter stenosis, late loss, and net gain. Angiographic restenosis occurred in 46 (35.4%) of 130 patients receiving spironolactone and 50 (39.0%) of 128 in the placebo group with an odds ratio (OR) of 0.85 with a 95% confidence interval (CI) of 0.49 to 1.46 (P = 0.62). Restenosis rate was found in 60 (32.9%) of 182 lesions in the spironolactone group, and 61 (35.5%) of 172 lesions in the placebo group with an OR of 0.89 with a 95% CI of 0.56 to 1.42 (P = 0.89). CONCLUSIONS: Spironolactone did not reduce the incidence of in-stent restenosis as compared with placebo in human, contrary to the fact that reduction of neointimal formation in animal models has been observed upon administration of spironolactone.

Malignant convulsive vasovagal syncope.

A patient was referred for evaluation of repeated episodes of syncope with loss of consciousness and convulsions. A dual-chamber pacemaker with rate-drop feature was implanted.