These types of AT can occur in patients with structurally normal atria as well as those with structural heart disease. The purpose of this review is to summarise current concepts of atypical flutters and ATs which are not dependent on the CTI.įocal ATs are defined as arrhythmias that arise from a circumscribed site of early activation and propagate to the atria in a centrifugal pattern. The demonstration of bidirectional conduction block across linear lesions has been adopted as an important endpoint in ablating atypical flutters in both atria. Through the use of multielectrode catheters and electroanatomical mapping, as well as entrainment, atypical atrial flutters and atrial tachycardias (ATs) of various mechanisms have been defined. Principles learned from these studies of typical flutter have permitted better understanding of more complex atrial arrhythmias. 1 Criteria to confirm bidirectional conduction block in the cavotricuspid isthmus (CTI) became standard procedural endpoints and improved freedom from long-term recurrences. Activation and entrainment mapping demonstrated that typical flutter arises from reentry around the tricuspid annulus. Pioneering electrophysiology studies in the 1990s defined the anatomical boundaries of typical atrial flutter, identified regions for effective catheter ablation of this arrhythmia and described procedural endpoints to minimise recurrences after ablation. Advances in understanding the mechanisms of ATs and their signature electrogram characteristics have improved the efficacy and efficiency of catheter ablation. A characteristic feature of localised reentry is highly fractionated, low-amplitude electrograms that encompass most of the tachycardia cycle length over a small diameter. Localised reentry occurs in the setting of diseased atrial myocardium that supports very slow conduction. High-resolution mapping techniques have defined details of macro-reentrant circuits, including zones of conduction block, scar and slow conduction. Macro-reentrant ATs occur in the setting of atrial fibrosis, often after prior catheter ablation or post atriotomy, but also de novo in patients with atrial myopathy. These typically arise from preferential sites such as the valve annuli, crista terminalis and pulmonary veins. Focal ATs may occur in structurally normal hearts but can also occur in patients with structural heart disease. Features that distinguish these AT mechanisms include electrogram characteristics, responses to entrainment and pharmacological sensitivities. Atrial tachycardias (ATs) may be classified into three broad categories: focal ATs, macroreentry and localised reentry – also known as ‘microreentry’.
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