Focal atrial tachycardia

INTRODUCTION — Atrial tachycardia (AT) is a regular atrial rhythm at a constant rate of >100 beats per minute originating outside of the sinus node (waveform 1) [1]. Focal ATs (also referred to as atrial ectopic tachycardias) arise from a single site within the left or right atrium, in contrast to macroreentrant atrial arrhythmias (eg, atrial flutter) and atrial fibrillation, which involve multiple sites or larger circuits.

In the past, focal ATs were considered to be due predominantly to enhanced automaticity. Thus, they were often referred to as automatic ATs. However, the more inclusive term focal AT is preferred, as this encompasses automatic, triggered, and microreentrant etiologies that cannot be distinguished easily on the surface electrocardiogram.

Focal ATs are usually paroxysmal and self-limited, although in some patients, focal AT may be present nearly continuously (ie, incessant AT). Incessant AT is important as it may be associated with left ventricular dysfunction [2]. (See "Arrhythmia-induced cardiomyopathy", section on 'Atrial tachycardia'.)

The characteristics and management of the common, repetitive forms of focal AT are discussed here. Macroreentrant atrial arrhythmias (eg, atrial flutter), atrial fibrillation, and other forms of supraventricular tachycardia are discussed in detail separately. (See "Overview of atrial flutter" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

BACKGROUND

Definition — In 2001, the Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (now called the Heart Rhythm Society) classified regular ATs according to electrophysiologic mechanisms and anatomy [1]. The Joint Expert Group defined focal AT as "being characterized by atrial activation starting rhythmically at a small area (focus) from where it spreads centrifugally." This definition indicates that the arrhythmia arises from an area that is smaller than would be required for classical macroreentry, which conventionally is considered to be a circuit greater than 2 cm in diameter.

Incidence — Focal AT is relatively uncommon, accounting for between 5 and 15 percent of arrhythmias in adults undergoing study for paroxysmal supraventricular tachycardia [3]. Males and females seem to be equally affected.

MECHANISMS AND ETIOLOGY

Electrophysiologic mechanisms — The focal activity responsible for AT can be produced by three distinct electrophysiologic mechanisms [3-6]:

●Enhanced automaticity – Enhanced automaticity refers to an acceleration of a normal automatic pacemaker by an increase in the slope of phase four depolarization (figure 1), shortening of the refractory period, a decrease in the threshold for excitation, or some combination of these mechanisms. (See "Enhanced cardiac automaticity".)

●Triggered activity – Triggered activity is the result of electrophysiologic phenomena called afterdepolarizations. Afterdepolarizations are focal electrical events that result in repeat depolarization of a single cell or small area prior to full repolarization. Early afterdepolarizations occur during the plateau phase of the action potential, while delayed afterdepolarizations occur during phase four.

●Microreentry – Microreentry requires a small circuit, defined as <2 cm to distinguish from macroreentry, in which conduction is sufficiently slow that the tissue can recover its excitability and be re-excited by the time the wave of depolarization returns. Such slow conduction classically occurs at discrete regions of fibrosis such as following ablation or surgery or anatomic sites of change in fiber orientation.

The hypothesis that cellular uncoupling is required for the development of focal atrial tachycardias is supported by the following observations:

●Low-amplitude fractionated electrograms are commonly found in the focal areas in which these atrial arrhythmias arise [7,8].

●Focal arrhythmogenesis often occurs in regions of discontinuity in atrial architecture [8].

Sites of origin — Focal ATs do not occur randomly throughout the atria, but rather cluster at predefined anatomic locations [9]. These locations are characterized by alterations in myocardial fiber orientation or sites of automatic tissue. In a series of 186 patients with clinically documented paroxysmal or incessant AT, 63 percent of ATs arose in the right atrium (RA) and 37 percent in the left atrium (LA) (figure 2) [10]. The distribution of sites of origin among the right atrial tachycardias was:

●Tricuspid annulus (35 percent) (waveform 1)

●Crista terminalis (34 percent) (waveform 2)

●Coronary sinus ostium (17 percent)

●Perinodal tissues (9 percent)

●RA appendage (4 percent)

Left atrial tachycardias were predominantly located around the pulmonary veins (67 percent) (waveform 3). Less common sites of origin include the mitral annulus (17 percent), coronary sinus body (6 percent), left intraatrial septum (6 percent), and the LA appendage (4 percent) [10,11]. The non-coronary cusp is an unusual site for atrial tachycardia, which should be considered for apparent paraseptal tachycardias [12].

Associated conditions — Focal AT may occur in patients with organic heart disease in response to atrial stretch due to elevated atrial pressure in conditions such as hypertension and cardiomyopathy. In addition to chronic heart disease, AT can also be associated with acute events such as a myocardial infarction, pulmonary decompensation, infection, excessive alcohol ingestion, hypokalemia, hypoxia, stimulants, cocaine ingestion, and theophylline [13]. More commonly AT occurs in the absence of heart disease and generally has a benign prognosis [14].

Incessant AT resulting in cardiomyopathy — The term "incessant" is applied to an AT when the AT is present for at least 90 percent of the time a patient is monitored [15]. Incessant AT is often found in otherwise normal young individuals, including children, although it may occur in patients with organic heart disease [16-19]. The rate tends to be faster during the day than at night, and the rate may increase with exercise or pregnancy [20].

Incessant focal AT may be responsible for tachycardia-mediated cardiomyopathy, which refers to left ventricular (LV) chamber dilatation and systolic dysfunction in a patient with persistent tachyarrhythmias [18,21,22]. Focal ATs originating in the atrial appendages and pulmonary veins are more frequently associated with cardiomyopathy [23]. (See "Arrhythmia-induced cardiomyopathy".)

Post-atrial fibrillation ablation — The incidence of atrial tachycardia appears to be higher among patients who have undergone catheter ablation for atrial fibrillation (AF) [24]. Catheter ablation of persistent AF may involve an extensive biatrial ablation strategy that combines linear ablation and the targeting of complex fractionated activity beyond pulmonary vein isolation. In a multicenter international randomized study, catheter ablation for persistent AF that involved targeting complex fractionated activity or linear ablation was not associated with an increase in freedom from AF compared with pulmonary vein isolation alone [25]. This study may translate to a more conservative approach to atrial substrate modification with a consequent reduction in post ablation atrial tachycardia. ATs post-AF ablation are often incessant, associated with rapid ventricular rates, and respond poorly to pharmacologic measures. Although they may be seen as a positive sign in the longer-term restoration of sinus rhythm, post-AF ablation AT poses specific challenges often requiring repeat catheter ablation procedures. (See "Atrial fibrillation: Catheter ablation", section on 'Efficacy'.)

Medications — A 2020 scientific statement from the American Heart Association details drugs associated with AT [26].

Digitalis toxicity — In patients taking digitalis, toxicity should be suspected if a new AT develops, particularly if 2:1 or higher grade atrioventricular block is present. Digitalis should be discontinued in this case, and anti-digitalis antibodies should be considered if hemodynamic compromise is present or other dangerous arrhythmias accompany the tachycardia. (See "Digitalis (cardiac glycoside) poisoning".)

CLINICAL FEATURES — Most patients with focal AT report palpitations. Palpitations can manifest in different ways. The abrupt onset of a rapid fluttering sensation in the chest or neck is most consistent with a tachyarrhythmia such as focal AT. The symptom burden is typically higher in focal compared with reentrant supraventricular tachycardia. (See "Evaluation of palpitations in adults".)

Patients with focal AT can rarely present with syncope, predominantly if the ventricular heart rate exceeds 200 beats/minute. Syncope, however, is more frequently seen with a ventricular tachyarrhythmia such as ventricular tachycardia than with focal AT. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies", section on 'Cardiac arrhythmias'.)

Patients with other underlying cardiac comorbidities (eg, heart failure, angina) can present with symptoms associated with worsening of their underlying disease (eg, dyspnea, chest pain).

DIAGNOSIS — The diagnosis of focal AT is based primarily on electrocardiographic (ECG) findings demonstrating an atrial arrhythmia of >100 beats per minute originating from outside the sinus node [6]. The tachycardia is generally sudden in onset and offset and frequently demonstrates a change in P-wave morphology. Focal AT is suggested by bursts of atrial activity with an isoelectric interval between P waves with confirmation of “focal” as opposed to macroreentry dependent on the findings at EP study. (See 'Electrophysiologic study and catheter ablation' below.)

Electrocardiographic features

P waves — The atrial rate during focal AT is generally between 110 and 250 beats per minute. Infants, children and young adults often have faster rates.

The P-wave morphology can appear normal or abnormal, depending upon the site of origin of the tachycardia. If the focus is from the superior portion of the crista terminalis, the P wave may be similar in appearance to the sinus P wave. Usually, there is a subtle difference in P waves from sinus rhythm to AT, so comparison with an ECG with known sinus P waves is recommended whenever possible. ECG leads V1 and lead II are the most useful in assessing P-wave morphology.

Observation over several minutes with multiple ECGs is invaluable in distinguishing focal AT from sinus tachycardia. Although focal ATs are regular, the rate may accelerate or "warm up" in the first few beats of the tachycardia and decelerate in the last few beats. An abrupt onset or termination (eg, over three to four beats) favors a focal AT. Sinus tachycardia requires 30 seconds to several minutes to speed up or slow down.

In occasional patients, no P waves appear on the surface ECG, which may suggest atrioventricular nodal reentrant tachycardia (AVNRT) [27] as the responsible mechanism. However, this may occur with focal AT if the atrial and ventricular complexes are closely associated such that the P wave is buried in the QRS complex.

Atrioventricular relationship — In focal AT, AV conduction is usually 1:1. The PR interval is often in the normal range, producing a long R-P interval, which can help to distinguish focal AT from other forms of supraventricular tachycardia (SVT). AT is unlikely if a P wave is present at tachycardia termination. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'RP relationship'.)

Mobitz type 1 and 2 conduction may also be seen depending on the rate of the atrial tachycardia and the conducting properties of the AV node. The appearance of "grouped beating" as seen in Mobitz type 1 conduction (Wenckebach) favors focal atrial tachycardia as the responsible mechanism for SVT.

QRS morphology — The QRS morphology is usually the same as in sinus rhythm, although aberrant conduction may occur at higher ventricular rates.

Localization of AT focus — Algorithms which attempt to predict the origin of the atrial tachycardia focus have been proposed [6,10,28].

A P-wave algorithm was developed to predict the site of AT origin to guide mapping and ablation at the time of electrophysiology study. A study of 126 patients undergoing electrophysiology study for focal AT served as the basis for an algorithm that was able to predict the arrhythmogenic focus in 93 percent of ATs (algorithm 1) [10]. The algorithm begins with an evaluation of the P wave in lead V1 [10]:

●If the P wave in V1 is negative or biphasic with an initially positive/terminally negative deflection, the AT focus is likely in the right atrium (waveform 1 and waveform 2).

●If the P wave in V1 is biphasic with an initial negative/terminally positive deflection, the AT focus is likely paraseptal and may require transseptal puncture or mapping of the noncoronary cusp.

●If the P wave in V1 is positive, the AT focus is likely in the left atrium (waveform 3) with the exception of the crista terminalis.

With close inspection of the P wave in other leads, likely sites of origin could be predicted, including those in the coronary sinus, crista terminalis, left atrial appendage, right atrial appendage, interatrial septum, or pulmonary veins.

This algorithm was later simplified and updated with equivalent accuracy [29]. The revised algorithm included the following changes: focal AT arising from the coronary sinus os, right septum, perinodal, left septum, noncoronary cusp, and superior mitral annulus regions were grouped together as paraseptal AT. The term "paraseptal" was defined as anatomic sites in close proximity to either side of the interatrial septum with a similar-appearing P wave. Coronary sinus body was removed from the revised algorithm. The presence of an isoelectric versus negative P wave in lead I was used to discriminate between left pulmonary vein/left atrial appendage AT and right pulmonary vein AT.

Electrophysiologic study and catheter ablation — The electrophysiologic evaluation of ATs is complex and the characteristics of the arrhythmia depend upon the mechanism [3,4]. The studies are best performed initially under light sedation as automatic ATs may be more difficult to induce under deeper sedation or general anesthesia. Other ATs are inducible by premature stimulation, and less sensitive to the effects of anesthesia. The findings on electrophysiologic study vary depending upon the mechanism of AT:

●Automatic ATs cannot be initiated, entrained, or terminated by electrophysiologic stimulation (waveform 4). They may be initiated with isoproterenol or adrenaline.

●Microreentrant ATs can be initiated, terminated, and entrained by programmed stimulation.

The ability to identify the focus responsible for AT has improved with the development of invasive three-dimensional mapping systems. Once a focus has been identified, treatment with catheter ablation can be performed during the same setting. The development of high density multi-electrode mapping catheters can assist in the localization of focal AT. (See 'Chronic or maintenance therapy' below.)

DIFFERENTIAL DIAGNOSIS — Focal AT originating from the crista terminalis may be difficult to distinguish from inappropriate sinus node tachycardia, as the P wave will be similar. Focal AT more often occurs in bursts of atrial activity with rapid onset/offset compared with a more gradual acceleration and slowing seen with IAST. Additionally, IAST more often has a postural component with tachycardia on standing, an excessive heart rate response to exertion, and is responsive to ivabradine [30]. (See "Sinus tachycardia: Evaluation and management", section on 'Inappropriate sinus tachycardia'.)

TREATMENT — The management of focal AT is divided into acute treatment and chronic suppressive, or prophylactic, therapy. There are few data to guide treatment strategies. Our approach is consistent with that presented in the 2019 European Society of Cardiology guidelines for the management of supraventricular arrhythmias [31].

Acute treatment — The acute management of a patient with an AT is guided by the ventricular rate, symptoms, and the hemodynamic stability of the patient. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Assessing the patient for hemodynamic stability' and "Overview of the acute management of tachyarrhythmias", section on 'Atrial tachycardia'.)

There have been no randomized trials to assess the efficacy of the acute pharmacologic management of AT. For the acute management of patients with AT with a rapid ventricular response, we suggest the following approach, which is based upon small case series and retrospective studies, but is in general agreement with professional society guidelines [6,31]:

●Efforts should be made to identify and treat any precipitating factors (see 'Associated conditions' above). In particular, patients who present with hypokalemia should have potassium repleted.

●Efforts can be made to terminate focal AT by having the patient perform vagal maneuvers or by administering intravenous adenosine (algorithm 2) [31]. However, vagal maneuvers and adenosine are generally less effective for termination of AT than for atrioventricular (AV) nodal dependent supraventricular tachycardias (SVT). Intravenous adenosine is an important diagnostic tool in patients with SVT as generally AV nodal dependent tachycardias will terminate provided sufficient dosing and administration of adenosine. In most forms of AT, adenosine may unmask persisting rapid atrial activity in the presence of transient AV slowing. (See "Vagal maneuvers" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Intravenous adenosine'.)

●Intravenous beta blockers (eg, metoprolol or esmolol) or nondihydropyridine calcium channel blockers (eg, diltiazem or verapamil) may be given to the hemodynamically stable patient. These drugs should not be used in decompensated heart failure. They slow the ventricular response and may terminate the arrhythmia. In patients with a borderline blood pressure, cautious use of these medications (initially at low doses) may paradoxically improve blood pressure due to improved cardiac output at lower heart rates.

•Metoprolol can be given as a 2.5 to 5 mg IV bolus over two to five minutes; if there is no response, an additional bolus may be administered every 10 minutes to a total dose of 15 mg.

•Diltiazem can be given 20 mg IV bolus over two minutes; this may be repeated after 15 minutes if there is an inadequate response.

•Verapamil can be given 5 to 10 mg IV bolus over two minutes; if no response, an additional 10 mg IV bolus may be administered 15 to 30 minutes following the initial dose.

●In patients who are intolerant of, or are likely to be intolerant of, beta blockers and nondihydropyridine calcium channel blockers, we suggest intravenous amiodarone, which can provide acute rate control, may terminate the arrhythmia, and results in less hypotension than beta blockers, diltiazem, and verapamil. In appropriately selected patients, class IC (eg, flecainide) or class III (eg, sotalol) antiarrhythmic drugs can also be used. However, because of the unique risk profiles of each of these agents, decisions regarding the use of antiarrhythmic drugs, other than amiodarone, should be made with the assistance of a cardiologist experienced in arrhythmia management. In particular, class IC drugs are contraindicated in the setting of structural heart disease. In patients without structural heart disease, sotalol or flecainide is preferable to amiodarone as they are less toxic long-term therapies.

●For patients with hemodynamically unstable AT with a rapid ventricular response who do not respond to medical therapy and do not have a reversible precipitating cause, we suggest an attempt at electrical cardioversion.

However, ATs may be particularly resistant to cardioversion for two reasons. First, many ATs are caused by enhanced automaticity, and electrical cardioversion is ineffective for such arrhythmias. Secondly, ATs are often precipitated by significant underlying illnesses that both limit the efficacy of cardioversion and increase the likelihood of early arrhythmia recurrence. (See 'Electrophysiologic mechanisms' above and 'Associated conditions' above.)

Hemodynamically unstable patients with persistent AT despite treatment with rate-controlling medications and efforts at electrical cardioversion should have an attempt at chemical cardioversion using amiodarone.

Chronic or maintenance therapy — Chronic therapy of repetitive focal AT is designed to prevent arrhythmia recurrence and to control the ventricular rate if the arrhythmia recurs. Patients with relatively rare and brief arrhythmias and few or no symptoms do not require maintenance therapy. In the absence of coexisting atrial fibrillation/flutter, atrial tachycardia carries a low risk of systemic embolization and chronic oral anticoagulation is not necessary.

The published literature addressing chronic suppressive treatment of AT includes only observational studies of small numbers of patients [32]. Some of these studies included patients with atrial fibrillation and atrial flutter, which have different mechanisms and may respond differently to therapy. With these limitations in mind, we suggest the following approach for chronic treatment of patients with frequent or symptomatic AT, which is in general agreement with professional society guidelines [6,31]:

●Since focal AT may be short in duration and resolve spontaneously, we suggest initial therapy with oral beta blockers or nondihydropyridine calcium channel blockers (ie, diltiazem or verapamil). Patients who do not respond to one of these agents may have successful suppression with another.

●Patients with recurrent or refractory symptomatic AT despite therapy with beta blockers, diltiazem, or verapamil, or patients who would potentially require long-term pharmacologic therapy are candidates for catheter ablation. The threshold for considering catheter ablation is lower for younger patients, incessant tachycardia, and in patients with tachycardia-mediated cardiomyopathy. (See 'Incessant AT resulting in cardiomyopathy' above.)

●More aggressive antiarrhythmic drugs may be considered for patients who fail beta blockers, diltiazem, and verapamil who do not want or are not good candidates for ablation therapy. Class IC (eg, flecainide, propafenone) antiarrhythmic drugs can be used in appropriately selected patients in the absence of structural or ischemic heart disease. However, because of the unique risk profiles of each of these agents, decisions regarding the use of antiarrhythmic drugs should be made with the assistance of a cardiologist experienced in arrhythmia management. In patients with significant comorbidities and structural heart disease, amiodarone is frequently the preferred agent.

●Patients with recurrent symptomatic AT in whom all other therapeutic options have been unsuccessful (including catheter ablation) may also be considered for pacemaker implantation and should preferably include biventricular or his bundle pacing followed by AV nodal ablation. This typically provides symptomatic relief although generally leaves the patient pacemaker dependent.

Catheter ablation — With the advent of 3D mapping systems and high density multipolar mapping systems, radiofrequency ablation offers a potential cure in patients with recurrent atrial tachycardia [33]. In a large single-center series, mapping and ablation was performed in 303 of 345 (90 percent) patients for focal AT. Radiofrequency ablation (RFA) was not pursued in the remainder due to close proximity to the AV node, multiple changing morphologies or insufficient ectopy/tachycardia to allow the detailed mapping required to identify the responsible atrial focus. Success off medication was achieved in 272 of 303 (90 percent) patients [2].

Multiple ectopic atrial foci and the presence of structural cardiac disease are predictors of recurrence after an initially successful ablation [21].

Mapping and ablating atrial tachycardia is technically more challenging than other forms of paroxysmal SVT [34]. Atrial tachycardia can originate from any site in the right or left atrium, and even from the proximal pulmonary veins or superior vena cava. Identification of a tachycardia's origin as left versus right atrial may be difficult (figure 2) but can usually be successfully predicted using the surface ECG (algorithm 1). Localizing the origin of atrial tachycardia is discussed in detail elsewhere. (See 'Localization of AT focus' above and "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.)

Anticoagulation — Atrial tachycardia carries a low risk of systemic embolization in the absence of co-existing atrial fibrillation/flutter, and chronic oral anticoagulation is not necessary.

Treatment of incessant AT — As described above, patients with incessant AT may present with a cardiomyopathy. Even patients with normal left ventricular systolic function on initial presentation are at risk of developing a cardiomyopathy following extended periods of tachycardia. This LV systolic dysfunction typically reverses weeks to months following the restoration of sinus rhythm. As such, aggressive efforts should be made to restore normal sinus rhythm in an attempt to prevent or reverse LV systolic dysfunction. (See 'Incessant AT resulting in cardiomyopathy' above and "Arrhythmia-induced cardiomyopathy".)

While there have been occasional reports of the successful treatment of incessant AT using beta blockers and Class IC antiarrhythmic drugs (ie, flecainide), pharmacologic therapy is generally ineffective in incessant AT [6,35-37]. For this reason, if medical therapy with rate-controlling medications and antiarrhythmic drugs is unsuccessful, patients with AT and concomitant LV systolic dysfunction should undergo catheter ablation (waveform 2) [6]. Only 10 to 15 percent of patients will have recurrence of AT following catheter ablation. (See 'Catheter ablation' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Supraventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●Definition – Atrial tachycardia (AT) is a regular atrial rhythm at a constant rate of >100 beats per minute, usually paroxysmal and self-limited, which originates outside of the sinus node. Focal AT accounts for between 5 and 15 percent of paroxysmal supraventricular tachycardia in adults. (See 'Background' above.)

●Sites of origin – The majority of ATs originate in the right atrium along the crista terminalis and tricuspid annulus. Left AT predominantly originates near the pulmonary veins. (See 'Sites of origin' above.)

●Symptoms – Most patients with focal AT report palpitations. Rarely, patients may present with syncope or exacerbation of an underlying cardiac condition (eg, angina). (See 'Clinical features' above.)

●ECG features – The P-wave morphology can appear normal or abnormal, depending upon the site of origin of the tachycardia. Usually, there is a subtle difference in P waves from sinus rhythm to AT, so comparison with an ECG with known sinus P waves is advised, whenever possible. (See 'Electrocardiographic features' above.)

●Acute treatment – The acute treatment of patients with AT depends upon the presence of symptoms and the patient’s hemodynamic status:

•For symptomatic patients

-Hemodynamically unstable – Patients who are hemodynamically unstable are not candidates for medical therapy with intravenous beta blocker or nondihydropyridine calcium channel blocker because these treatments are likely to exacerbate hypotension. For such patients, we proceed with an attempt at electrical cardioversion, however this may be unsuccessful in patients with automatic AT. Hemodynamically unstable patients with persistent AT despite treatment with rate-controlling medications and efforts at electrical cardioversion should have an attempted chemical cardioversion using intravenous amiodarone. (See 'Acute treatment' above.)

-Hemodynamically stable – For a hemodynamically stable patient with symptomatic AT, we suggest acute treatment with an oral or intravenous beta blocker or nondihydropyridine calcium channel blocker (ie, diltiazem or verapamil) rather than an antiarrhythmic drug (Grade 2C). Such treatment may slow the ventricular response and/or terminate the arrhythmia. Intravenous amiodarone is an acceptable alternative that may be preferred in a patient with borderline hypotension with structural heart disease. (See 'Acute treatment' above.)

•For asymptomatic patients – For an asymptomatic hemodynamically stable patient with AT, we suggest initial observation rather than acute treatment with a beta blocker or nondihydropyridine calcium channel blocker (ie, diltiazem or verapamil) (Grade 2C). (See 'Acute treatment' above.)

●Chronic therapy – Chronic therapy of repetitive focal AT is designed to prevent arrhythmia recurrence and to control the ventricular rate if the arrhythmia recurs.

•For rare or brief episodes – Patients with relatively rare or brief AT episodes with few or no symptoms can receive treatment as needed for acute episodes of AT but do not require chronic suppressive therapy. (See 'Chronic or maintenance therapy' above.)

•For frequent symptomatic episodes

-Initial therapy – For patients with frequent, symptomatic AT, we suggest chronic management with an oral beta blocker or nondihydropyridine calcium channel blocker (ie, diltiazem or verapamil) as the initial treatment rather than an antiarrhythmic drug or catheter ablation (Grade 2C). (See 'Chronic or maintenance therapy' above.)

-For recurrent or refractory episodes – Patients with frequent, symptomatic AT who have failed initial medical therapy or require long-term medical therapy are candidates for catheter ablation. (See 'Chronic or maintenance therapy' above.)

•For incessant AT

-For few or no symptoms – For patients with incessant AT with preserved left ventricular function and few or no symptoms, an initial trial of rate-controlling medications or antiarrhythmic medications may be reasonable. The efficacy of this approach should be reassessed within two weeks and, if unsuccessful, the patient should be referred for catheter ablation. (See 'Treatment of incessant AT' above.)

-For cardiomyopathy related to incessant AT – For patients with cardiomyopathy felt to be related to incessant AT, we recommend aggressive attempts to restore a normal ventricular heart rate rather than rate control alone (Grade 1B). This can be accomplished in most patients by catheter ablation of the AT focus. In the unusual likelihood that catheter ablation is unsuccessful, pacemaker implantation, preferably including biventricular or his bundle pacing followed by atrioventricular nodal ablation, typically provides symptomatic relief. (See 'Catheter ablation' above and "Arrhythmia-induced cardiomyopathy", section on 'Treatment'.)