Intraatrial reentrant tachycardia

INTRODUCTION — Atrial tachycardias have traditionally been characterized as automatic, triggered, or reentrant. However, the European Society of Cardiology and the North American Society of Pacing and Electrophysiology in 2001 proposed a classification that takes into consideration both anatomic features and electrophysiologic mechanisms [1]. Atrial tachycardia is the overriding term that includes two major categories:

●Focal atrial tachycardia due to an automatic, triggered, or microreentrant mechanism.

●Macroreentrant atrial tachycardia, including typical atrial flutter and other well-characterized macroreentrant circuits in the right and left atrium.

Intraatrial reentrant tachycardia (IART) falls into the latter group. Furthermore, the joint American College of Cardiology/American Heart Association/Heart Rhythm Society 2015 guidelines further defined macroreentrant atrial tachycardias that do not involve the tricuspid valve isthmus as "atypical or non-cavo-tricuspid isthmus-dependent atrial flutter" [2]. These macroreentrant supraventricular tachycardias often involve the left atrium, particularly after atrial fibrillation (AF) ablation or Maze surgery for AF. They may involve any atrium where a scar, surgical or catheter-induced, may have taken place. This topic will discuss the mechanisms, clinical manifestations, and treatment of IART. Discussions of other specific atrial arrhythmias are presented separately. (See "Focal atrial tachycardia" and "Sinoatrial nodal reentrant tachycardia (SANRT)" and "Overview of atrial flutter".)

DEFINITION, PREVALENCE, AND MECHANISMS — Intraatrial reentrant tachycardia (IART) refers to any macroreentrant atrial tachycardia that does not utilize the cavotricuspid isthmus (figure 1) as a critical pathway for the reentry to perpetuate. IART generally occurs in one of three settings: post-surgical repair of congenital heart disease (incidence of 16 to 50 percent post Fontan procedure, 15 to 48 percent post Mustard or Senning procedures, 12 to 34 percent post Tetralogy of Fallot repair), post-surgical scar (incisional tachycardia), or post catheter based or surgical management of atrial fibrillation (AF) [3,4]. With the increase in AF ablation, an increase in IART is arising due to the surgical maze and catheter based procedures in the left atrium. IART has also been reported in the absence of surgical or catheter intervention [5].

Reentry refers to a circuit in which previously excited tissue is re-excited, producing an extra beat or a sustained rhythm. Sinoatrial (SA) nodal reentrant tachycardia and IART (also called reentrant atrial tachycardia) are the two major types of paroxysmal reentrant supraventricular tachycardias in which the reentrant circuit does not involve the atrioventricular (AV) node or accessory pathways (figure 2). (See "Sinoatrial nodal reentrant tachycardia (SANRT)".)

Reentry pathways are usually defined by the following characteristics:

●Two discrete but connected pathways.

●Slow conduction in one of the pathways and unidirectional block in the other pathway.

●Block in the pathway with unidirectional block following a premature beat, with conduction through the slower pathway allowing the pathway with unidirectional block to recover conduction and conduct the impulse back to the first pathway, hence initiating reentry.

Block may be anatomical (accessory bypass tract, slow or fast AVN pathway), functional (ischemia, electrolyte imbalance or anti arrhythmic agents), or both.

IART has a different activation sequence of atrial depolarization, leading to a P wave morphology that differs from that of normal sinus rhythm. In comparison, SA nodal reentrant tachycardia has an activation sequence similar to that of normal sinus rhythm so that the P waves on the surface ECG appear to be normal. Only the abrupt onset and termination of this arrhythmia distinguish it clinically from sinus tachycardia. (See 'Electrophysiological features' below and "Sinoatrial nodal reentrant tachycardia (SANRT)".)

IART was responsible for approximately 6 percent of atrial tachycardias in patients referred for electrophysiologic studies to an active electrophysiologic group [6]. Organic heart disease is common in adults with this arrhythmia. In children, intraatrial tachycardia is often associated with surgery that involves the atrium, such as the repair of an atrial septal defect or correction of transposition [7], but may occur with any repair that includes an atrial scar. IART may be quite detrimental because of the elevated heart rate and the frequent loss of normal AV synchrony. It has been suggested that there is an increased rate of right and atrial thrombosis with IART.

The other group of patients in whom IART is seen is individuals who have undergone catheter or surgical ablation for AF. The incidence varies between 2.9 percent following pulmonary vein isolation (PVI) and 31 percent following circumferential ablation associated with creation of linear lesions [8,9]. Within this group of patients, reentrant tachycardia either exists as a macro- or microreentrant tachycardia. Microreentrant tachycardias are usually seen at sites of pulmonary vein reconnection following PVI for AF. Gaps in linear lesions formed for ablation of persistent or long-standing persistent AF promote the emergence of reentrant atrial tachyarrhythmias. These arrhythmias are often less well tolerated than the AF that prompted the ablation in the first place. They are often seen around the mitral valve (peri-mitral), in the atrium roof, or, less commonly, the septum. The cavotricuspid isthmus is not uncommonly involved. Studies have shown no added advantage to the creation of these lesions [10]. Society guidelines dissuade creation of these lines, confining them only to cases where IARTs are encountered [11]. Focal IARTs are eliminated by isolating the reconnected pulmonary vein.

IART most often begins with an premature atrial complex (PAC; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) that tends to occur quite early [6,12-14]. The initiating beat may arise in either atrium, and an intraatrial conduction delay is necessary for the induction and maintenance of the arrhythmia. Ventricular premature beats very rarely initiate intraatrial reentrant tachycardia, and, if they do, it is usually due to rapid retrograde conduction through an accessory bypass tract, which results in the early prematurity usually required to initiate reentry [6].

CLINICAL MANIFESTATIONS — The clinical manifestations and significance of intraatrial reentrant tachycardia (IART) are variable, depending upon the hemodynamic effects of the increase in heart rate and the heart rate achieved. Some patients are asymptomatic, while others have symptoms that range from palpitations and lightheadedness to, in rare cases, syncope. If a patient is examined during an episode of arrhythmia, they will have a regular heart rate greater than 100 beats per minute.

Most episodes of IART do not precipitate hemodynamic compromise or limiting symptoms. However, higher ventricular rates associated with IART in a patient with underlying advanced cardiac or pulmonary disease can sometimes exacerbate their disease, leading to signs and symptoms of angina, heart failure, or worsening systemic oxygenation.

In the face of persistently elevated ventricular rates (eg, for weeks to months), particularly if baseline ventricular dysfunction exists, heart failure (tachycardia-mediated cardiomyopathy) may ensue. The atrial rates tend to be slower than the atrial rates in isthmus dependent atrial flutter, allowing 1:1 conduction from the atria to the ventricles and, subsequently, more potentially detrimental hemodynamic effects [15]. (See "Arrhythmia-induced cardiomyopathy".)

DIAGNOSIS — The diagnosis of intraatrial reentrant tachycardia (IART) should be considered in the presence of a regular but rapid pulse and heartbeat on physical examination. The diagnosis cannot be confirmed, however, without an electrocardiogram or, in most cases, invasive electrophysiologic studies.

The suspicion for IART rests on the patient's history combined with the electrocardiogram. A patient with a cardiac surgical history, particularly for correction of a congenital heart defect, presenting with what looks like atrial flutter should be considered to suffer from IART. Like other reentrant tachycardias, the onset is sudden, and vagal maneuvers may help slow the ventricular rate but will not change the atrial rate.

Electrocardiographic findings — During an arrhythmic episode, the electrocardiographic (ECG) findings in IART are similar to those of most other regular supraventricular tachycardias (SVT), with evidence of atrial activity (P waves) associated with ventricular activity (QRS complexes) in a 1:1 fashion. In the appropriate clinical setting (eg, prior cardiac surgery, prior ablation, etc), the surface ECG can be highly suggestive of IART. However, the surface ECG alone cannot reliably distinguish between IART and other types of SVT, most notably focal atrial tachycardia. (See 'Electrophysiological features' below and 'Differential diagnosis' below.)

As noted above, P wave morphology in IART is different from that in normal subjects due to a difference in the activation sequence of atrial depolarization. The sequence depends upon the reentrant circuit (figure 1) which, in turn, may involve an anatomical obstacle or result from functional changes in refractoriness. (See 'Definition, prevalence, and mechanisms' above.)

Clinically, the P wave morphology in aVL and V1 are useful clues in identifying the site of origin of the arrhythmia. A positive P wave in V1 and a negative P wave in aVL suggest a left atrial origin (waveform 1), while a negative P wave in V1 and a positive P wave in aVL suggests a right atrial origin. These changes reflect the vectorial sequence. The left atrium is posterior and to the left, so the sequence of the activation for an impulse arising in the left atrium usually is anterior towards V1 (leading to a positive P wave) and rightward away from aVL (leading to a negative P wave); the sequence is reversed with a right atrial origin. Both reentrant and automatic atrial tachycardias will show these morphologies.

However, the electrocardiogram can be misleading in non-isthmus dependent macro reentrant tachycardias, particularly after catheter ablation for atrial fibrillation where the index of suspicion is always high that the atrial tachyarrhythmia is left sided [16]. Counterclockwise isthmus dependent atrial flutter characteristically displays upright flutter waves in V1 and negative flutter waves in leads II, III, and aVF. If the isthmus dependent flutter is clockwise, leads II, III, and aVF will display upright flutter waves. V1 will remain upright as well. Any departure from this pattern, particularly in the appropriate setting (postsurgical procedure, catheter, or surgical ablation) should lead one to suspect a nonisthmus dependent IART. Left sided IART can display similar electrocardiographic findings. (See "Electrocardiographic and electrophysiologic features of atrial flutter".)

Electrophysiological features — Clinically, it is important to distinguish intraatrial reentrant tachycardia (IART) from other supraventricular tachycardias (SVT), particularly focal atrial tachycardia. Since the surface electrocardiogram alone is not reliable in distinguishing IART from other types of SVT, invasive electrophysiologic studies (EPS) are employed to help make this distinction. Since macroreentrant atrial arrhythmias, including IART, are reentrant, they can be entrained during EPS with manifest and concealed fusion, and upon cessation of atrial pacing, the post pacing interval should be within 30 milliseconds of the tachycardia cycle length. The use of newer mapping techniques such as electroanatomic mapping further helps to make this distinction where focal mechanisms display centrifugal activation patterns, reentry displays an "early meets late", and the entire cycle length of the tachycardia can be mapped to the chamber containing the tachycardia. (See "Invasive diagnostic cardiac electrophysiology studies".)

The behavior of reentrant and triggered activity atrial rhythms may be quite similar (table 1), and intracardiac recordings are usually necessary to make the diagnosis with certainty. The following criteria have been used to help identify the type of arrhythmia:

●Atrial tachycardia has conventionally been called reentry when the arrhythmia is abrupt in onset and termination and can be started or stopped by spontaneous or programmed premature beats. However, triggered activity can show the same features [17].

●A response to adenosine has been thought to be quite specific for atrial tachycardias due to cyclic AMP-mediated triggered activity and to enhanced automaticity. In several small cohort studies, adenosine was ineffective in terminating IART [18-20]. Although some studies have provided conflicting data [17,21,22], the criteria used to define macroreentry did not exclude triggered activity as the cause of the arrhythmia [19].

In comparison to the atrial abnormalities, conduction through the AV node, the specialized infranodal conduction system (His bundle, fascicles and bundle branches, terminal Purkinje fibers), and the ventricles is not directly impaired in intraatrial reentrant tachycardia. Thus, the QRS pattern and duration should not be abnormal unless the rapid rate causes some type of functional conduction disturbance.

Dual-loop figure-8 intraatrial reentry has been described that electrocardiographically mimics atrial flutter [23]. All such patients had undergone surgery for ostium secundum atrial septal defect (ASD) closure. The arrhythmias were quite resistant to antiarrhythmic therapy, and ablation of both loops may be required. This mechanism should be kept in mind in patients with corrected secundum ASD surgery.

Differential diagnosis — The differential diagnosis for intraatrial reentrant tachycardia (IART) is similar to that for other narrow QRS complex tachycardias (assuming there is normal AV conduction without bundle branch block) and includes:

●Atrial flutter

●Atrioventricular reciprocating tachycardia

●Focal atrial tachycardia

●Sinoatrial nodal reentrant tachycardia

●Sinus tachycardia, including inappropriate sinus tachycardia

●Atrioventricular nodal reentrant tachycardia

A more in-depth discussion of the differential diagnosis of narrow QRS complex tachycardias is presented separately.

TREATMENT — While intraatrial reentrant tachycardia (IART) can be transient and asymptomatic, persistent and/or symptomatic IART requires treatment to relieve symptoms and to prevent long-term sequelae such as tachycardia-mediated cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".)

Efforts to acutely terminate IART should begin with vagal maneuvers. If vagal maneuvers are unsuccessful, intravenous adenosine or verapamil can be administered. Catheter ablation of IART is generally the treatment of choice for chronic management of this arrhythmia, given its efficacy combined with the relatively poor efficacy of pharmacologic therapy.

Acute termination

Autonomic maneuvers — The autonomic innervation of the atria is less than that of the specialized myocardial areas which comprise the sinoatrial and atrioventricular nodes. Thus, vagal stimulation has a variable and often negligible effect on reentrant intraatrial rhythms. However, it has been estimated that this arrhythmia can be terminated by carotid sinus massage in approximately one-fourth of cases, particularly those arising in the right atrium [6].

As such, for the acute termination of symptomatic IART, we suggest carotid sinus massage or another vagal maneuver as the initial therapy. (See "Vagal maneuvers".)

IV adenosine and verapamil — Although there is controversy as to the specificity and efficacy of calcium channel blockers, both verapamil and adenosine have been reported to be effective in 30 to 50 percent or more of cases [17,18,21,24]. For symptomatic IART that is persistent in spite of vagal maneuvers, we suggest using adenosine via intravenous push for acute termination of the arrhythmia. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Intravenous adenosine'.)

If adenosine is unsuccessful and symptomatic IART persists, we then use intravenous verapamil. We typically give a 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.

Chronic therapy — Few studies have been published regarding chronic pharmacologic therapy in IART, which appears limited in many cases by lack of efficacy and drug toxicity [15]. Catheter ablation, however, has relatively high success rates for the acute termination of IART and for the long-term prevention of recurrences.

Catheter ablation — For IART that is symptomatic or persistent, thereby requiring long-term preventive therapy, we suggest catheter ablation as initial therapy rather than treatment with an antiarrhythmic agent. This is particularly true in younger patients who might be subject to the long-term side effect of years or decades of antiarrhythmic therapy.

Catheter ablation of macroreentrant atrial arrhythmias, including IART, has become the preferred treatment modality, with rates of acute success in terminating IART exceeding 80 percent in several cohort studies [25-28]. However, ablation does require specialized expertise and background knowledge of the predisposing factors. Electroanatomic mapping (EAD) and irrigated tipped catheters have further improved the outcomes after these ablations [28-31].

Excitable gaps are critical for all reentrant arrhythmias. An excitable gap allows a reentrant arrhythmia to be entrained, and if entrainment is achieved with concealed conduction, the critical pathway is identified. This feature is used therapeutically when overdrive atrial pacing is employed to terminate these arrhythmias. This was employed in the management of IART complicating surgically corrected transposition of the great arteries. The problem was that if it fails or if overdrive pacing accelerates the heart rate, it may lead to hemodynamic compromise and, in turn, death [32].

Since an excitable gap is usually present in IART, a PAC or atrial pacing can usually cause a beat to be inserted in the reentrant pathway, thereby terminating the arrhythmia [25,26]. Radiofrequency catheter ablation is extremely effective in patients with recurrent arrhythmias and has largely replaced chronic pacemaker therapy or surgery (waveform 2A-C) [6,25-27].

Intraatrial reentrant tachycardia is common after surgery for congenital heart disease. Radiofrequency ablation is successful, but the recurrence rate is high [33-37]. The reentrant circuit for intraatrial reentrant tachycardia often involves the tricuspid valve isthmus following the Mustard/Senning procedure and in other types of repaired congenital heart disease [37]. The circuits in patients after the Fontan procedures differ, with the lateral right atrial wall being the more common area for successful radiofrequency ablation [37].

Ablation or pacing for typical atrial flutter may give rise to macroreentrant tachycardias arising in the right atrium, with such arrhythmias occurring more frequently as the use of ablation and devices becomes more common. The term "lower loop reentry" has been used to describe counterclockwise reentry around the inferior vena cava where the anterior portion of the reentrant circuit is the IVC-tricuspid valve isthmus and the posterior arm is the low posterior right atrial wall across the crista terminalis, making it a variant of typical atrial flutter in which the superior pivot point is lower [38]. At other times, circuits may involve the free wall of the right atrium. The ECG usually shows negative atrial deflections in the inferior leads [39].

EAD has proven useful in ablating right macro-reentrant tachycardias including IART, particularly when the mid-diastolically activated isthmus can be identified [40]. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.)

Pharmacologic therapy — Available pharmacologic options for the prevention of IART include calcium channel blockers, sodium channel blockers, beta blockers, and amiodarone, all of which have been tried with some success at preventing IART recurrences. However, many patients with IART have structural heart disease, which limits the choice of available antiarrhythmic agents. If IART cannot be prevented, rate control can be attempted with non-dihydropyridine calcium channel blockers or beta adrenergic blockers.

For chronic therapy of IART when ablation is not an option or has been unsuccessful in preventing recurrent IART, we suggest verapamil as first-line therapy rather than a beta blocker or antiarrhythmic agent. This suggestion is based on the efficacy of verapamil in the acute termination of IART in addition to it generally being well-tolerated [24]. Beta blockers are also effective in some cases but have a larger spectrum of side effects. The use of calcium channel modulators, particularly class IC antiarrhythmic drugs (table 2) such as flecainide and propafenone, is limited by major toxicities and proarrhythmic actions, especially in patients with coronary artery disease.

Permanent pacemaker insertion — In rare circumstances, such as when IART persists following an unsuccessful ablation and standard pharmacologic therapy, insertion of a permanent pacemaker may be considered. Pacemaker insertion allows for the more aggressive use of rate controlling medications, especially in patients with sinus node dysfunction. (See "Sinus node dysfunction: Treatment".)

Pacemakers with anti-tachycardia features have been used to successfully terminate IART but have been associated with sudden death [41].

Our approach to treatment — Based on the available evidence, we take the following approach to treatment:

●For the acute termination of symptomatic IART, we suggest carotid sinus massage or another vagal maneuver as the initial therapy.

●For symptomatic IART that is persistent in spite of vagal maneuvers, we suggest using adenosine via intravenous push rather than verapamil for acute termination of the arrhythmia. If adenosine is unsuccessful and symptomatic IART persists, we then use intravenous verapamil.

●For IART that is symptomatic or persistent, thereby requiring long-term preventive therapy, we suggest catheter ablation as initial therapy rather than treatment with an antiarrhythmic agent.

●For chronic therapy of IART when ablation is not an option or has been unsuccessful in preventing recurrent IART, we suggest verapamil as first-line therapy rather than a beta blocker or antiarrhythmic agent. If verapamil is unsuccessful or not tolerated, beta blockers or antiarrhythmic agents can be used.

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 and clinical setting – Intraatrial reentrant tachycardia (IART) refers to any macroreentrant atrial tachycardia that does not utilize the cavotricuspid isthmus (figure 1) as a critical pathway for the reentry to perpetuate. IART generally occurs in one of three settings: post-surgical repair of congenital heart disease, post-surgical scar (incisional tachycardia), or post-catheter-based or surgical management of atrial fibrillation, although it has also been reported in the absence of surgical or catheter intervention. (See 'Definition, prevalence, and mechanisms' above.)

●Mechanism – IART, which is responsible for approximately 6 percent of atrial tachycardias in patients referred for electrophysiologic studies, has a different activation sequence of atrial depolarization, leading to a P wave morphology that differs from that of normal sinus rhythm. IART most often begins with a PAC and is perpetuated via a reentry circuit (figure 2). (See 'Definition, prevalence, and mechanisms' above.)

●Clinical manifestations – The clinical manifestations and significance of IART are variable, depending upon the hemodynamic effects of the increase in heart rate and the heart rate achieved. Some patients are asymptomatic, while others have symptoms that range from palpitations and lightheadedness to, in rare cases, syncope. (See 'Clinical manifestations' above.)

●Electrocardiographic findings – During an arrhythmic episode, the electrocardiographic (ECG) findings in IART are similar to those of most other regular supraventricular tachycardias (SVT), with evidence of atrial activity (P waves) associated with ventricular activity (QRS complexes) in a 1:1 fashion. In the appropriate clinical setting (eg, prior cardiac surgery, prior ablation, etc), the surface ECG can be highly suggestive of IART. However, the surface ECG alone cannot reliably distinguish between IART and other types of SVT, most notably focal atrial tachycardia. Because the surface electrocardiogram alone is not reliable in distinguishing IART from other types of SVT, invasive electrophysiological studies (EPS) are employed to help make this distinction. (See 'Electrocardiographic findings' above and 'Electrophysiological features' above.)

●Differential diagnosis – The differential diagnosis for intraatrial reentrant tachycardia (IART) is similar to that for other narrow QRS complex tachycardias (assuming there is normal AV conduction without bundle branch block). (See 'Differential diagnosis' above.)

●Management – While intraatrial reentrant tachycardia (IART) can be transient and asymptomatic, persistent and/or symptomatic IART requires treatment to relieve symptoms and to prevent long-term sequelae such as tachycardia-mediated cardiomyopathy.

•Acute termination

-Autonomic maneuvers – For the acute termination of symptomatic IART, we suggest carotid sinus massage or another vagal maneuver as the initial therapy (Grade 2C). (See 'Autonomic maneuvers' above and "Vagal maneuvers".)

-Pharmacologic therapy – For symptomatic IART that is persistent in spite of vagal maneuvers, we suggest using adenosine via intravenous push rather than verapamil for acute termination of the arrhythmia (Grade 2C). If adenosine is unsuccessful and symptomatic IART persists, we then use intravenous verapamil. (See 'IV adenosine and verapamil' above.)

•Chronic therapy

-Catheter ablation as initial therapy – For IART that is symptomatic or persistent, thereby requiring long-term preventive therapy, we suggest catheter ablation as initial therapy rather than treatment with an antiarrhythmic agent (Grade 2C). (See 'Catheter ablation' above.)

-Pharmacologic therapy – For chronic therapy of IART when ablation is not an option or has been unsuccessful in preventing recurrent IART, we suggest verapamil as first-line therapy rather than a beta blocker or antiarrhythmic agent (Grade 2C). If verapamil is unsuccessful or not tolerated, beta blockers or antiarrhythmic agents can be used. (See 'Pharmacologic therapy' above.)