Atrial Septal Closure Device Research Articles

Embolization of an Amplatzer Atrial Septal Closure Device to the Pulmonary Artery

A 44-year-old woman with a history of transient ischemic attack underwent closure of atrial septal defect with a 26 mm Amplatzer device. The device was released without residual shunt or impingement on intracardiac structures. Within seconds, the transesophageal echocardiography showed the initial dislodgement of the device from the atrial septum and its consequent slipping back into the right atrium close to the tricuspid valve. Soon after the device disappeared from the right atrium and it could be founded into the right ventricle under the tricuspid valve. The patient was transferred in the operating room for an emergency operation. The device could not be found in the right ventricle because its downstream migration. The Amplatzer septal occluder was identified by palpation into the pulmonary artery trunk: it was retrieved from the right ventricle through the pulmonary valve and the atrial septal defect was closed by running suture.

Interventional cardiology and the medical devices industry: is there a conflict of interest?

Interventional cardiology and the medical devices industry: is there a conflict of interest?

WORSENING SYMPTOMS OF PULMONARY HYPERTENSION AFTER CLOSURE OF AN INTERATRIAL SHUNT

PURPOSE: Systemic to pulmonary shunts such as patent foramen ovales (PFO) and atrial septal defects (ASD) are associated with cryptogenic stroke, migraine headaches, and arrhythmias. Increasingly percutaneous closure of these lesions with an atrial septal closure device (ASCD) is being performed. We present two cases where closure of an interatrial defect was performed in patients with pulmonary arterial hypertension (PAH), resulting in increased morbidity.

Is Magnetic Resonance Image Guidance the Key to Opening Chronic Total Occlusions?

Through progressive plaque growth or fibrotic organization of occlusive thrombus, atherosclerosis may result in chronic total occlusion (CTO) of a major arterial conduit. If CTO develops slowly, collateral pathways may supply sufficient perfusion to retain tissue viability despite occlusion of the major inflow conduit. However, such collateral-mediated perfusion rarely matches that provided by an open main conduit, particularly during the peak demand of regional muscular activity. Although strategies to limit regional oxygen demand (eg, β-blockers for the treatment of angina pectoris) or to enhance collateral function (eg, a walking program for superficial femoral occlusion, experimental angiogenesis) may be of some benefit, these approaches generally offer less complete return of normal physiology and relief of ischemic symptoms than does direct revascularization of the occluded vessel. With surgical bypass, the nature of the occlusion (its length, duration, tortuosity, calcification) is less important than the presence of a suitable distal anastomotic target. On the other hand, with catheter-based techniques, success depends heavily on these lesion characteristics. In fact, crossing such occluded segments with a guidewire remains the dominant barrier to catheter-based treatments of occluded arterial segments. Once the guidewire has been passed successfully into the distal true lumen, the process of dilating and stenting the segment is usually straightforward and durable, at least with the use of drug-eluting stents in coronary CTOs.1,2 Article p 1101 Devices designed to cross CTOs should have 3 key features: an ability to distinguish a true luminal path from one created within (dissection) or through (perforation) the vessel wall of the occluded segment, an ability to change direction (steer) to correct deviations from the desired path through the occlusion, and an ability to penetrate the frequently fibrotic and focally calcific substance of the occlusion through the use of either mechanical stiffness or an alternative energy modality (laser, …