Sinoatrial nodal reentrant tachycardia: a case report and literature review

Abstract

Background

Sinoatrial nodal reentrant tachycardia (SANRT) is a rare form of focal atrial tachycardia, often linked with structural or congenital heart disease. Due to its electrocardiographic similarities with other supraventricular tachyarrhythmias, it is frequently misdiagnosed. Understanding its clinical presentation and effective management strategies is crucial for appropriate patient care.

Case Description

We present a case of a 45-year-old female with severe pulmonary hypertension and obstructive sleep apnea who was admitted with progressive palpitations, chest pain, and dyspnea. Initial electrocardiographic evaluation suggested atrial fibrillation with rapid ventricular response (RVR), leading to treatment with metoprolol and amiodarone. However, the tachyarrhythmia persisted, and further investigation revealed features suggestive of SANRT. The diagnosis was confirmed by telemetry findings demonstrating atrial tachycardia with a prolonged PR interval, terminating abruptly after carotid sinus massage (CSM). This immediate response to vagal stimulation solidified the diagnosis of SANRT. The patient was managed conservatively with vagal maneuver training and discharged on oral bisoprolol.

Conclusions

This case highlights the diagnostic challenges associated with SANRT and emphasizes the role of CSM as both a diagnostic and therapeutic intervention. Early recognition of SANRT is crucial, as it can mimic other supraventricular arrhythmias, leading to mismanagement. While electrophysiological studies remain the gold standard for diagnosis, non-invasive measures such as vagal maneuvers can be highly effective in terminating the arrhythmia and providing symptomatic relief.

Highlight box.

Key findings

• Sinoatrial nodal reentrant tachycardia (SANRT) is a rare atrial tachycardia often misdiagnosed as sinus tachycardia or atrial fibrillation.

• In this case, a 45-year-old female with pulmonary hypertension initially diagnosed with atrial fibrillation with rapid ventricular response (RVR) was later confirmed to have SANRT.

• Carotid sinus massage (CSM) successfully terminated the tachyarrhythmia, confirming SANRT diagnosis and demonstrating the effectiveness of vagal maneuvers.

What is known and what is new?

• SANRT originates from a micro-reentrant circuit in the sinoatrial node and is underrecognized in clinical practice.

• This manuscript highlights the importance of differentiating SANRT from other supraventricular tachycardias. It reinforces the role of CSM as both a diagnostic and therapeutic tool for SANRT.

What is the implication, and what should change now?

• Clinicians should consider SANRT in patients with recurrent tachycardia and evaluate the response to vagal maneuvers.

• Early recognition and differentiation from other arrhythmias can prevent mismanagement and unnecessary treatments.

• Increased awareness of SANRT can improve diagnostic accuracy and patient outcomes.

Introduction

Sinoatrial nodal reentrant tachycardia (SANRT), considered a type of focal atrial tachycardia, is a relatively uncommon arrhythmia, often linked with structural and congenital heart disease (1). The frequency of SANRT has been estimated to be 2 to 17 percent in patients with supraventricular tachycardia (SVT) who are referred for electrophysiological studies (2). While symptoms such as palpitations, syncope, and lightheadedness are similar to other SVTs, the majority of SANRTs are asymptomatic (3). SANRT is characterized on an electrocardiogram (ECG) by narrow QRS complexes with heart rates ranging between 100 and 150 bpm with normal P wave morphology. Premature atrial contractions may be seen preceding the onset or termination of the SANRT episode. This phenomenon is somewhat similar to other reentrant SVTs contributing to further underdiagnosis of the condition. The tachyarrhythmia is not attributed to external factors; rather, it appears to originate within the intrinsic components of the sinoatrial (SA) node. However, the specific mechanism of the reentrant circuit is debated, with theories suggesting it occurs within the SA node and/or involves perinodal tissue along with the SA node (4). The primary focus of acute management relies on maintaining hemodynamic stability. In hemodynamically unstable patients, the initial approach involves employing electrical cardioversion to abort the rhythm. For hemodynamically stable patients, non-medical interventions such as carotid sinus massage (CSM) and vagal maneuvers are attempted initially. If these prove unsuccessful, intravenous adenosine is reserved as the next step. For chronic suppression, radiofrequency ablation stands as the primary method, as it has a high success rate (5). In this report, we describe a case of SANRT presenting with intermittent palpitations that were initially thought to be due to atrial fibrillation with rapid ventricular response (RVR), however, further investigation confirmed a diagnosis of SANRT. A brief, contemporary review of the literature on SANRT is provided along with some practical suggestions for diagnosis and management. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-262/rc).

Case presentation

A 45-year-old woman presented to the hospital with progressively worsening palpitations, chest pain, and shortness of breath over the past 3 days. Her medical history included severe refractory pulmonary hypertension, and obstructive sleep apnea. Examination revealed +1 pitting edema and accentuated P2 on auscultation. Laboratory tests showed elevated brain natriuretic peptide (BNP) (532 pg/mL) and normal troponin (14 ng/L). Echocardiography indicated an estimated ejection fraction of 70%, along with severe right ventricular dilation and hypokinesis, dilated right atrium, elevated peak right ventricle pressure (90 mmHg), and severe tricuspid regurgitation. She was admitted to the medical intensive care unit for heart failure exacerbation and pulmonary hypertension management.

During admission, her heart rate remained at 140 bpm. Initially diagnosed as atrial fibrillation with RVR, she was treated with metoprolol and amiodarone, but the tachyarrhythmia persisted. Cardiology consultation later confirmed sinus node reentrant tachycardia, not atrial fibrillation. Telemetry strips revealed atrial tachycardia with prolonged PR interval terminating with a blocked premature atrial contraction. Subsequent ECGs confirmed SVT with prolonged PR interval, which abruptly terminated after CSM. This confirmed the diagnosis of SANRT, as shown in Figure 1. Figure 2 illustrates ECG with normal sinus rhythm post-CSM. The patient received instructions on vagal maneuvers and was discharged in stable condition with oral bisoprolol. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s), and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Figure 1.

ECG displaying SANRT rhythm at 140 bpm with a prolonged PR interval. ECG, electrocardiogram; SANRT, sinoatrial node reentrant tachycardia.

Figure 2.

ECG demonstrating normal sinus rhythm at 77 bpm. CSM resulted in rate normalization and PR interval adjustment. CSM, carotid sinus massage; ECG, electrocardiogram.

Discussion

We presented a case of SANRT in a patient with right heart enlargement and pulmonary hypertension, initially mistaken for sinus tachycardia and atrial fibrillation but later established as a reentrant arrhythmia that terminated abruptly with CSM. SANRT, a rare form of paroxysmal SVT, typically occurs in patients with structural heart disease (1). A substrate for SANRT is present in approximately 10–15 percent of patients undergoing electrophysiological studies for symptomatic atrial tachycardia (6). The American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society have defined SANRT as a focal atrial tachycardia from micro-reentry arising from the sinus node (7). The exact mechanism of SA nodal reentry is still somewhat unclear. Some postulated hypotheses include: reentry occurring entirely within the SA node (4), reentry involving the SA node and perinodal tissue based on several studies that have suggested the reentrant loop involves more than the SA node (6). Identification of the entry site of the tachycardia circuit in SANRT guides effective ablation treatment. In the context of SVTs, the efficacy of CSM can vary depending on the specific type of arrhythmia. For instance, focal atrial tachycardias, which can include crista atrial tachycardia, are generally less responsive to vagal maneuvers like CSM. It has been shown that vagal maneuvers such as carotid massage and direct current cardioversion are seldom effective in terminating focal atrial tachycardia (8). In contrast, SANRT often responds more favorably to CSM. A case study reported that in patients with SANRT, tachycardia could be terminated by CSM, atrial pacing and premature atrial stimulation (9).

SANRT resembles appropriate or inappropriate sinus tachycardia in regularity and sinus morphology P waves but is distinguished by abrupt initiation and termination compared to the gradual acceleration and deceleration in sinus tachycardia variants (10). Differences between SANRT and inappropriate sinus tachycardia are shown in Table 1. In our case, CSM was performed, which resulted in the abrupt termination of the tachyarrhythmia and restoration of normal sinus rhythm. The abrupt termination of the tachyarrhythmia by carotid massage, along with a resolution of the prolonged PR interval, solidified our diagnosis of SANRT in the patient. The diagnosis of SANRT should be considered in the presence of paroxysms of regular but rapid pulse and heartbeat on physical examination. Adenosine triphosphate (ATP) and its metabolite, adenosine, are valuable tools in differentiating types of atrial tachycardia. In cases of SANRT, adenosine can terminate arrhythmia by hyperpolarizing the membrane potential, thereby reducing pacemaker currents and interrupting the reentrant circuit. Conversely, focal atrial tachycardias, which often arise from automatic or triggered activity, may respond differently to adenosine. Adenosine can transiently suppress these arrhythmias, but they may not terminate as promptly or definitively as reentrant tachycardias like SANRT. Therefore, the response to adenosine administration can aid in distinguishing SANRT from focal atrial tachycardia. An immediate termination following adenosine suggests a reentrant mechanism such as SANRT, whereas a transient suppression without termination may indicate a focal atrial tachycardia (11,12).

Table 1. Characteristics of SANRT and inappropriate sinus tachycardia.

Characteristics	Sinoatrial node reentrant tachycardia	Inappropriate sinus tachycardia
Epidemiology	Adults and children with structural heart disease	Young and female patients without apparent heart disease
Rate	100–150 bpm	≥100 bpm
Rhythm	Regular	Regular
Origin/mechanism	Reentry within the SA node	SA node hyperactivity along with autonomic imbalance
Onset and offset	Starts and terminates abruptly	Accelerates and decelerates gradually
Baseline HR	Paroxysmal in nature	Most patients have elevated resting HR
Presentation	Rarely symptomatic	Highly symptomatic palpitations
ECG	Rapid HR, normal sinus P wave, can be initiated by PACs	Rapid HR, normal sinus P wave morphology
Response to vagal maneuvers	Abrupt termination of the arrhythmia	Gradual slowing of the arrhythmia

ECG, electrocardiogram; HR, heart rate; PACs, premature atrial complexes; SA, sinoatrial; SANRT, sinoatrial node reentrant tachycardia.

Most episodes of SANRT are asymptomatic and do not precipitate hemodynamic compromise; however, sustained SANRT is not as benign as previously believed and demonstrates wide variations in cycle length and could masquerade as other forms of tachycardia on the surface ECG (13). When symptomatic, patients may present with paroxysmal palpitations, dyspnea, dizziness, chest discomfort, and rarely syncope. Persistently elevated ventricular rates in the setting of baseline ventricular dysfunction could lead to heart failure due to tachycardia-mediated cardiomyopathy (7).

The majority of patients with SANRT do not need medical treatment, as heart rates ranging from 100 to 150 bpm typically do not cause significant symptoms (1). In rare cases, patients with incessant SANRT experiencing clinical symptoms may require medical intervention. Treatment may also be beneficial in preventing long-term complications, such as tachycardia-induced cardiomyopathy. For hemodynamically stable patients, initial management should include vagal maneuvers, such as carotid massage, to terminate the arrhythmia. If these maneuvers are ineffective or contraindicated, intravenous adenosine is the preferred next step, provided there are no contraindications to its use (5,14). Patients who are hemodynamically unstable, including those with tachycardia-induced hypotension, ischemic chest pain, altered mental status, respiratory failure, or shock, require immediate intervention with electrical cardioversion to promptly terminate SANRT (1). For long-term management of recurrent SANRT, radiofrequency catheter ablation is preferred over suppressive medical therapy, as it offers higher success rates while avoiding the short- and long-term side effects associated with medications (1).

In this case, an electrophysiological (EP) study was not pursued due to the patient’s clinical stability and the successful termination of tachyarrhythmia with CSM. While noninvasive diagnostic criteria, including ECG morphology and response to vagal maneuvers, strongly suggested SANRT, we acknowledge that EP study remains the gold standard for definitive confirmation. EP mapping provides direct evidence of reentrant circuits and allows differentiation from other forms of focal atrial tachycardia, including crista atrial tachycardia, which can present with similar ECG characteristics. The absence of EP study in this case limits absolute diagnostic certainty; however, the abrupt termination of tachycardia with vagal stimulation and normalization of the PR interval strongly supports the diagnosis of SANRT. Future cases, particularly those with diagnostic ambiguity, may benefit from EP evaluation to provide further confirmation and guide potential therapeutic interventions. Furthermore, in our case, ATP was not administered, and no ECG recording during ATP administration was available. Given ATP’s ability to transiently suppress SA node activity, its use could have provided additional diagnostic clarity by differentiating SANRT from focal atrial tachycardia. While the immediate termination of tachyarrhythmia with CSM strongly supports a reentrant mechanism, the lack of ATP testing remains a limitation in definitively ruling out other forms of atrial tachycardia.

Conclusions

This case highlights the diagnostic and therapeutic challenges of SANRT, a rare arrhythmia often misdiagnosed as sinus tachycardia or atrial fibrillation. The immediate termination of the tachycardia with CSM provided strong evidence for a reentrant mechanism, reinforcing the utility of vagal maneuvers in both diagnosis and acute management. While SANRT is typically benign, recognizing its clinical features is critical to preventing misdiagnosis and unnecessary treatments. EP studies remain the gold standard for definitive diagnosis, particularly in ambiguous cases. Management should be tailored to symptom severity, with vagal maneuvers and adenosine serving as first-line treatments and catheter ablation reserved for refractory or recurrent cases. Increased awareness of SANRT among clinicians can improve early identification and optimize patient outcomes.

Supplementary

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Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s), and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.