Sinoatrial nodal reentrant tachycardia (SANRT)

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]. In 2015, the joint American College of Cardiology, American Heart Association, and Heart Rhythm Society guidelines further defined sinus node reentrant tachycardia as "a specific type of focal atrial tachycardia that is due to microreentry arising from the sinus node complex, characterized by abrupt onset and termination, resulting in a P-wave morphology that is indistinguishable from sinus rhythm" [2]. 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

Sinoatrial nodal reentrant tachycardia (SANRT), also called sinus node reentry or sinus node reentrant tachycardia, falls into the latter group of reentrant arrhythmias. This topic will discuss the mechanisms, clinical manifestations, and treatment of SANRT. Discussions of other specific atrial arrhythmias are presented separately. (See "Focal atrial tachycardia" and "Intraatrial reentrant tachycardia" and "Overview of atrial flutter".)

DEFINITION AND MECHANISMS — Initially described in the 1940s [3], SANRT has often been considered a form of atrial tachycardia. However, SANRT has an activation sequence similar to that of normal sinus rhythm so that the P waves on the surface ECG appear to be normal. In comparison, intraatrial reentry has a different activation sequence of atrial depolarization, leading to a P wave morphology that differs from that of normal sinus rhythm. (See "Intraatrial reentrant tachycardia".)

Some of the electrophysiologic features that distinguish SA nodal reentrant tachycardia and other reentrant atrial rhythms (figure 1) from automatic and triggered atrial tachycardias are summarized (table 1). The exact mechanism of SA nodal reentry is not known; however, three possibilities have been suggested [4] (see "Reentry and the development of cardiac arrhythmias"):

●Reentry occurring entirely within the SA node, based primarily on one animal study in which the reentrant pathway was localized within the SA node [5].

●Reentry involving the SA node and perinodal tissue, based on a number of studies that have suggested the reentrant loop involves more than the SA node [4,6-8]. What we call the SA node is actually the integrated activity of pacemaker cells in the compact region of the SA node [9]. These several thousand cells depolarize and produce action potentials almost synchronously and seem to influence each other through cell-to-cell coupling, a process that has been called "mutual entrainment" [10,11].

●Reentry using the SA node as the refractory center around which reentry occurs, although there is limited evidence for this potential mechanism [4].

●Using high resolution optical mapping, both micro- and macro- reentry have been demonstrated as mechanisms of SANRT in a post-myocardial infarction model. Additionally, SANRT was not seen in structurally normal hearts, as it required functional and/or structural abnormalities to support reentry [12].

Reentry with the SA node only or the SA node and perinodal tissue is the most likely mechanism of SANRT [13,14].

INCIDENCE — SANRT, an uncommon arrhythmia that rarely causes symptoms, occurs most commonly in adults and children who have structural heart disease [15-18]. In patients with supraventricular tachycardia referred for electrophysiologic study, estimates of the frequency of SANRT have ranged from 2 to 17 percent [16,19]. However, approximately 10 to 15 percent of patients who undergo electrophysiologic studies for symptomatic atrial tachycardia have sinus nodal echoes (single or multiple reentrant beats that utilize the SA node), indicating the presence of a substrate for SA nodal tachycardia [16,19]. In addition, the actual incidence of this arrhythmia may be higher than appreciated since many patients are asymptomatic and do not come to electrophysiologic study.

CLINICAL MANIFESTATIONS — In most cases, the clinical manifestations and significance of SANRT are minimal. Most patients are asymptomatic, while others have symptoms that range from palpitations and lightheadedness to, in rare cases, syncope. Symptoms, when present, tend to start and stop abruptly. During an episode of arrhythmia, the patient will have a regular heart rate greater than 100 beats per minute.

Most episodes of SANRT do not precipitate hemodynamic compromise or limiting symptoms. However, on rare occasions, SANRT can be sufficiently recurrent, rapid, and/or sustained to be symptomatic. Higher ventricular rates associated with SANRT 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 [20,21]. (See "Arrhythmia-induced cardiomyopathy".)

DIAGNOSIS — The diagnosis of SANRT should be considered in the presence of a regular but rapid pulse and heartbeat on physical examination. The electrocardiogram (ECG) will show P waves with a rate between 100 and 150 beats per minute. Given that the P waves are virtually identical to those observed in sinus rhythm, patients may often be thought to have inappropriate sinus tachycardia. In most cases, the diagnosis of SANRT cannot be confirmed without invasive electrophysiologic studies. Vagal maneuvers and adenosine can sometimes help as either will slow the tachycardia before the arrhythmia is abruptly terminated. (See "Sinus tachycardia: Evaluation and management", section on 'Inappropriate sinus tachycardia'.)

While pursuing invasive testing to make the diagnosis is not generally necessary, when symptoms are present clinically or the arrhythmia appears incessant, it is important to distinguish SANRT from other supraventricular tachycardias (SVT). In a patient with sustained tachycardia and reduced left ventricular function in whom tachycardia-mediated cardiomyopathy is a consideration, we would suggest more aggressive efforts at confirming or excluding SANRT as the diagnosis. (See "Arrhythmia-induced cardiomyopathy".)

Electrocardiographic findings — As mentioned above, SANRT has an activation sequence similar to that of normal sinus rhythm (see 'Definition and mechanisms' above). Thus, the surface ECG has P waves that are virtually identical to those observed in sinus rhythm and often will be interpreted as a sinus tachycardia. The abrupt onset and termination of the arrhythmias can aid clinically in differentiating SANRT from sinus tachycardia.

Conduction through the AV node, the specialized infranodal conduction system (His bundle, fascicles and bundle branches, terminal Purkinje fibers), and the ventricles also should be similar to normal AV conduction unless the rapid rate causes some type of functional conduction disturbance (ie, rate-related bundle branch block). The rate in SANRT is usually between 100 and 150 beats per minute. Episodes vary in length, lasting anywhere from seconds to hours.

The response to vagal maneuvers can aid in differentiating sinus tachycardia (gradual slowing in response to vagal stimulus) from SANRT (abrupt termination of the arrhythmia). Patients should undergo continuous ECG monitoring during the vagal maneuvers. (See 'Autonomic maneuvers' below.)

Electrophysiologic features — Clinically, when symptoms are present or the arrhythmia appears incessant, it is important to distinguish SANRT from other supraventricular tachycardias (SVT), particularly focal atrial tachycardia. Since the surface electrocardiogram alone is not reliable in distinguishing SANRT from other types of SVT, invasive electrophysiological studies (EPS) can be employed to help make this distinction. Since macroreentrant atrial arrhythmias, including SANRT, 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 if pacing is performed within the reentrant pathway. The use of newer mapping techniques such as electroanatomical 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. The initiation with premature atrial complexes (PACs; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) independent of intraatrial or AV nodal conduction delays or, better yet, in the presence of AV block, helps confirm the diagnosis. The P wave morphology is identical to sinus node P wave morphology. (See "Invasive diagnostic cardiac electrophysiology studies".)

SA nodal reentrant tachycardia can be initiated by PACs, atrial pacing, and, unlike intraatrial reentry, by premature ventricular complex/contraction (PVC; also referred to a premature ventricular beats or premature ventricular depolarizations) and ventricular pacing with retrograde VA conduction. The rarity of induction of intraatrial reentry by a PVC is due to the delay in retrograde VA conduction which limits the prematurity with which the premature beat can depolarize the atrium. Neither the AV node nor a bypass tract is a necessary part of the circuit. The reentrant circuit can be penetrated and reentry aborted by premature atrial depolarizations or atrial pacing.

Differential diagnosis — The differential diagnosis for sinoatrial nodal reentrant tachycardia (SANRT) 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

●Intraatrial reentrant tachycardia

●Sinus tachycardia, including inappropriate sinus tachycardia

●Atrioventricular nodal reentrant tachycardia

Only the abrupt onset and termination of the arrhythmia aids clinically in differentiating SANRT from sinus tachycardia, which is not a paroxysmal condition but manifests a gradual increase and decrease in rate (waveform 1). Other arrhythmias included in the differential diagnosis, however, typically have a P wave morphology that is different from normal, although the difference may be subtle. In addition, other reentrant tachycardias are usually, but not always, more rapid than SANRT (rate up to 240 beats per minute versus 100 to 150 beats per minute).

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

TREATMENT — Most episodes of SA nodal reentrant tachycardia require no specific therapy since the usual rates (100 to 150 beats/min) rarely produce symptoms or hemodynamic compromise. However, persistent and/or symptomatic SANRT requires treatment to relieve symptoms and to prevent long-term sequelae such as tachycardia-mediated cardiomyopathy [22]. (See "Arrhythmia-induced cardiomyopathy".)

Efforts to acutely terminate SANRT should begin with vagal maneuvers. If vagal maneuvers are unsuccessful, intravenous adenosine can be administered for the acute termination of SANRT. Chronic suppressive therapy, when necessary, is usually with verapamil, although digoxin and amiodarone have been tried with some success. Catheter ablation of SANRT is generally the treatment of choice for chronic management of this arrhythmia given its efficacy.

Autonomic maneuvers — For the acute termination of symptomatic SANRT, we suggest carotid sinus massage or another vagal maneuver as the initial therapy. (See "Vagal maneuvers".)

The SA node has extensive autonomic innervation. As a result, carotid sinus massage and other vagal maneuvers (such as the Valsalva maneuver) generally terminate SA nodal reentrant arrhythmias abruptly [13,19,21]. This is in contrast to the effect of vagal maneuvers on sinus tachycardia and reentrant intraatrial rhythms.

●The response to sinus tachycardia is characterized by gradual slowing and then gradual acceleration upon cessation of the maneuver.

●The atria are less well innervated than the sinus node. As a result, vagal stimulation has a variable and often negligible effect on reentrant intraatrial rhythms. Enhancement of vagal tone may, however, result in AV nodal blockade, which will result in a reduction in the ventricular rate without altering the atrial rate.

Pharmacologic therapy — There are no large studies of pharmacologic therapy in SA nodal reentrant tachycardia because of the rarity of the arrhythmia and its general lack of clinical consequence. Several drugs have been evaluated for both acute termination and chronic suppression of SANRT in small nonrandomized studies:

●Adenosine acutely terminated SANRT in six of six patients in a single-center cohort [23].

●Verapamil (two of two) and amiodarone (four of four) effectively prevented induction of SANRT during electrophysiologic testing in a single-center cohort [21].

●Beta blockers have not been extensively studied but failed to prevent induction of SANRT in two of two patients during electrophysiologic testing in a single-center cohort [21].

●Ouabain, an analog of digoxin, successfully prevented induction of SANRT during electrophysiologic testing in a single-center cohort. In addition, digoxin has been reported to successfully suppress recurrent SANRT for 18 months in an infant [21,24].

Radiofrequency catheter ablation — SANRT is on occasion sufficiently symptomatic or persistent to warrant specific intervention. Increasing experience is being gained with radiofrequency ablation of a portion of the reentrant circuit [16,20,25-28]. Of approximately 45 patients in these reports, the arrhythmia recurred in only one patient who then underwent a second successful ablation. Evaluation in a larger number of patients with longer follow-up is required to more accurately determine the role of ablation in this disorder. However, we feel that catheter ablation should be considered as first-line therapy for symptomatic patients or in patients with persistent tachycardia who are at risk for or who have developed tachycardia-mediated cardiomyopathy. (See "Arrhythmia-induced cardiomyopathy".)

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

●For acute termination of symptomatic SANRT that persists despite the use of vagal maneuvers, we suggest intravenous adenosine. Synchronized cardioversion can be used in an unstable patient.

●For chronic suppression of recurrent SANRT, we suggest catheter ablation rather than pharmacologic therapy. This choice is based upon the high success rates of catheter ablation in conjunction with fewer potential long-term medication side effects.

●For chronic therapy of SANRT when ablation is not an option or has been unsuccessful in preventing recurrent SANRT, we suggest verapamil or beta adrenergic receptor blockers as the first choice, followed by the combination of both if SANRT recurs. If SANRT recurs despite the combination of verapamil and beta adrenergic receptor blockers, amiodarone can be considered.

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 – Sinoatrial nodal reentrant tachycardia (SANRT), also called "sinus node reentry" or "sinus node reentrant tachycardia," is a reentrant tachyarrhythmias involving the SA node and/or perinodal tissue (figure 1). (See 'Definition and mechanisms' above.)

●Incidence – SANRT occurs most commonly in adults and children who have structural heart disease and is estimated to be responsible for anywhere from 2 to 17 percent of supraventricular tachycardias. (See 'Incidence' above.)

●Clinical manifestations – In most cases, the clinical manifestations and significance of SANRT are minimal. Most patients are asymptomatic, while others have symptoms that range from palpitations and lightheadedness to, in rare cases, syncope. (See 'Clinical manifestations' above.)

●Diagnosis – The diagnosis of SANRT should be considered in the presence of a regular but rapid pulse and heartbeat on physical examination. The electrocardiogram (ECG) will show P waves with a rate between 100 and 150 beats per minute. Given that the P waves are virtually identical to those observed in sinus rhythm, in most cases the diagnosis cannot be confirmed without invasive electrophysiologic studies. (See 'Diagnosis' above.)

●Differential diagnosis – The differential diagnosis for SANRT is similar to that for other narrow QRS complex tachycardias (assuming there is normal AV conduction without bundle branch block). Only the abrupt onset and termination of the arrhythmia aids clinically in differentiating SANRT from sinus tachycardia, which is not a paroxysmal condition but manifests a gradual increase and decrease in rate. (See 'Differential diagnosis' above.)

●Treatment – While SANRT is most often transient and asymptomatic, persistent and/or symptomatic SANRT requires treatment to relieve symptoms and to prevent long-term sequelae such as tachycardia-mediated cardiomyopathy. We take the following approach to treatment (see 'Our approach to treatment' above):

•Acute – For acute termination of symptomatic SANRT that persists despite the use of vagal maneuvers, we suggest intravenous adenosine (Grade 2C).

•Chronic

-For chronic suppression of recurrent SANRT, we suggest catheter ablation rather than pharmacologic therapy (Grade 2C). This choice is based upon the high success rates of catheter ablation in conjunction with fewer potential long-term medication side effects.

-For chronic therapy of SANRT when ablation is not an option or has been unsuccessful in preventing recurrent SANRT, we suggest verapamil or beta adrenergic receptor blockers as the first choice (Grade 2C), followed by the combination of both if SANRT recurs. If SANRT recurs despite the combination of verapamil and beta adrenergic receptor blockers, amiodarone is another option.