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Background: Percutaneous left atrial appendage (LAA) closure can be an alternative to coumadin treatment in patients with atrial fibrillation (AF) at high risk for thromboembolic events and/or bleeding complications. We report the initial experience with this new technique., Methods: Patients were eligible if they had AF with a high stroke risk (CHADS(2) score >1), and/or contraindication for coumadin therapy. The procedure was performed under general anaesthesia, using biplane fluoroscopy and (3D) transoesophageal echocardiography (TEE) guidance. Patients were discharged on coumadin until a TEE was repeated at 45 days after closure to evaluate LAA occlusion. If LAA occlusion was achieved, oral anticoagulation was discontinued and aspirin started., Results: Percutaneous LAA closure was performed in 10 patients (50% male, age 61.6 ± 9.6 years). The median CHADS(2) score was 3 (range 2-4), median CHA(2)DS(2)-VASc score 3.5 (range 2-6) and HAS-BLED score 1.5 (range 1-4). Nine patients had a history of stroke and 2 patients had a history of major bleeding while on coumadin. Concomitant pulmonary vein isolation was performed in 9 patients. The device was successfully placed in all patients within a median of 56 min (38-137 min). Asymptomatic catheter thrombus occurred in one patient. At 45-day follow-up, no thromboembolic events occurred, TEE showed minimal residual flow in the LAA in three patients. In one patient the LAA device was dislocated, requiring successful percutaneous retrieval., Conclusion: Device closure of the LAA may provide an alternative strategy to chronic coumadin therapy in patients with AF and high risk of stroke and/or bleeding complications using coumadin.

Isolated left ventricular noncompaction is a rare cardiomyopathy that is often not recognised. So far, it is not well established how best to manage this abnormality. We describe a patient in whom the diagnosis of isolated left ventricular noncompaction was made after presentation with a subacute myocardial infarction. Because of nonsustained ventricular tachycardias during hospitalisation, which were inducible and deteriorated into ventricular fibrillation on electrophysiological examination after coronary artery bypass grafting, he received an implantable defibrillator. Whether the ventricular tachycardias were due to the myocardial infarction or to the noncompacted myocardium remains uncertain. (Neth Heart J 2007;15:109-11.).

Over the past year, there has been a sharp increase in the number of recalls, or `field safety corrective actions' concerning implantable defibrillators. This may be due to an actual rise in device or component-related problems (for which there is some evidence), overzealous reporting of potential problems (which is apparent), or most probably a combination of the two. In this day and age of increasing numbers of ICD implantations, it is essential that all concerned realise that ICDs are no more infallible than other man-made devices and that the incidence of complications is therefore likely to increase commensurately. It is also important to weigh the procedural risk of replacing the device against the risk not only of device failure, but more importantly related harm to the patient. Odds actually favour replacement in very few cases. Above all this demands critical attention to communication between stakeholders, medical, industry, patients and press. This article attempts to place a number of these issues in some perspective, and offer future directions for management of ICD recalls and safety actions.