Abstract

Radiofrequency catheter ablation of symptomatic arrhythmias has enjoyed unprecedented growth during the past 2 decades. This has been attributed to its high success rate in the treatment of a variety of arrhythmias with a discrete ablation target and the low complication rate observed in these procedures.1,2 Initial investigators performing radiofrequency catheter ablation were fortunate that the lesions created with this energy source were small and discrete. It was difficult to cause excessive collateral injury. Early recognition of the problem of sudden electric impedance rise and coagulum formation3 led to a number of strategies and technologies to minimize this occurrence. In contrast to supraventricular tachycardia ablation, catheter ablation of atrial fibrillation has pushed the limits of our ablation technologies and has shifted the ratio of efficacy to risk in an unfavorable direction.4 Aggressive ablation with extensive linear ablation, ablation of complex fractionated atrial electrograms, and empirical isolation (debulking) of the posterior left atrial wall5 have improved procedural success in patients with persistent atrial fibrillation. But with a greater volume of myocardial injury and a greater surface area of disrupted left atrial endocardium from the ablation, it is not surprising that procedure-related complications, especially embolic complications, are more prevalent. Article see p 473 The initial observations of the appearance of new asymptomatic cerebral embolism (ACE) lesions on diffusion-weighted MR imaging scans after radiofrequency catheter ablation of atrial fibrillation were striking6,7 but should not have been unanticipated. The ACE lesions observed are attributed to cerebral microembolism and have been widely reported after procedures, such as cardiopulmonary bypass,8 carotid artery stenting,9 and trans aortic valve replacement.10 The fact that ACE lesions have not been reported previously with radiofrequency ablation either has been because of good fortune or simply …

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