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INTRODUCTION

Focal atrial tachycardia (AT) can be due to abnormal automaticity, triggered automaticity, or a small reentry circuit confined to the atrium or atrial tissue extending into a pulmonary vein, the coronary sinus, or vena cava. It can be sustained, nonsustained, paroxysmal, or incessant. Focal AT accounts for ~10% of PSVTs in patients referred for catheter ablation. Nonsustained AT is commonly observed on 24-h ambulatory ECG recordings, and the prevalence increases with age. In fact, frequent atrial ectopy and nonsustained AT is often a precursor to more significant arrhythmias such as atrial fibrillation and flutter. Though unsustained, frequent atrial ectopy or short bursts of AT may be symptomatic and require therapy similar to that required for focal AT.

AT can occur in the absence of structural heart disease or may be associated with any condition that causes atrial fibrosis, including prior catheter ablation. Areas of fibrosis can be a nidus for abnormal automaticity from damaged cells or microreentry within zones of slow conduction within and on the border of fibrotic areas. Sympathetic stimulation is a promoting factor and the emergence of AT can be a sign of underlying illness. AT with AV block may occur in digitalis toxicity. Symptoms from AT are highly variable but similar to other supraventricular tachycardias (SVTs). Incessant AT can cause tachycardia-induced cardiomyopathy.

AT typically presents with 1:1 AV conduction or with AV block that can be Wenckebach type conduction or fixed (e.g., 2:1 or 3:1). Because it is not dependent on AV nodal conduction, AT will not terminate with AV block, and the atrial rate will not be affected, which distinguishes AT from most AV nodal–dependent SVTs, such as AV nodal reentry and AV reentry using an accessory pathway (see below). An accelerated warm-up phase after initiation or cool-down phase prior to termination also favors AT rather than AV nodal–dependent SVT, as this is a common observation with triggered automaticity. P waves are often discrete, with an intervening isoelectric segment, in contrast to atrial flutter and macroreentrant AT (see below) because atrial activation from a focal source occurs though a small portion of the tachycardia cycle. When 1:1 conduction to the ventricles is present, the arrhythmia can resemble sinus tachycardia typically with a P-R interval shorter than the R-P interval (Fig. 243-1), particularly when sympathetic tone produces rapid AV nodal conduction. It can be distinguished from sinus tachycardia by the P-wave morphology, which usually differs from sinus p waves depending on the location of the focus. Focal AT tends to originate in areas of complex atrial anatomy, such as the crista terminalis, valve annuli, atrial septum, and atrial muscle extending along cardiac thoracic veins (superior vena cava, coronary sinus, and pulmonary veins) (Fig. 243-2), and the location can often be estimated by the P-wave morphology. AT from the atrial septum will frequently have a narrower P-wave duration than sinus rhythm. AT from the left atrium will ...

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