An unusual presentation of atrioventricular nodal reentrant tachycardia

1Department of Cardiology, Institute for Cardiovascular Diseases, Iasi, Romania 2Department of Cardiology, Clinical Rehabilitation Hospital, Iasi, Romania 3Department of Radiology and Medical Imaging, Institute for Cardiovascular Diseases, Iasi, Romania 4Grigore T Popa University of Medicine and Pharmacy, Iasi, Romania 5Department of Cardiovascular Surgery, Institute for Cardiovascular Diseases, Iasi, Romania More Information


Case presentation
We present the case of a 70-year-old male patient, who came to our Arrhythmia outpatient clinic in June 2020 for rest dyspnea, incessant luttering sensation in the neck and palpitations. His past medical history included a coronary artery bypass surgery (CABG) in 2012, irst degree atrioventricular block (1 st degree AVB) and slow-fast AVNRT since 2016. Due to the frequent episodes of palpitations despite the beta-blocker treatment, he underwent a radiofrequency catheter ablation (RFCA) of the slow intranodal pathway in March 2019. He had no recurrence of the arrythmia at his regular 6 months follow-ups. He remained asymptomatic until April 2020, when the current symptomatology emerged, and he presented in another clinic. His electrocardiogram (ECG) was interpreted by the general cardiologist as accelerated junctional rhythm. He had a 24 hours Holter ECG monitoring, which documented sinus rhythm with an average heart rate of 70 bpm, but also 3 episodes of supraventricular tachycardia -128 bpm, 7.5 seconds the longest, with sudden onset and termination ( Figure 1) for which the cardiologist prescribed oral Amiodarone 400 mg.
On presentation in our clinic, the physical examination showed intermittent neck pulsations, weak distal arterial pulse, postoperative scars and abdominal obesity (BMI = 30.9 kg/m 2 ). The irst ECG recorded showed sinus rhythm, 75 bpm, right axis deviation and a normal P wave and QRS morphology ( Figure 2).
On a second ECG, we observed a supraventricular rhythm with narrow QRS complex, with retrograde P wave deforming the end of the QRS complex, 95 bpm. The arrhythmia was responsive to carotid sinus massage, but rapidly recurrent ( Figure 3).
Taking into consideration the clinical and electrophysiological features of the arrhythmia, we suspected the recurrence of the AVNR rather than an accelerated junctional rhythm. We withheld the Amiodarone treatment and the patient was scheduled for an electrophysiological study (EPS) in November 2020.
On admission, he declared the persistence of the symptomatology with neck pulsation and dyspnea. The ECG recorded showed the same supraventricular arrhythmia, 75/ min ( Figure 4). The blood tests did not reveal any electrolyte imbalance.
After acknowledging the potential risks and bene its, a written informed consent was obtained from the patient prior to the EPS. We used a right femoral approach. The basal measurements documented supra-and infrahisian conduction abnormalities, with atrial-His interval (AH) =123 ms and    His-ventricle interval (HV) = 58 ms. Initially, we converted the arrhythmia to sinus rhythm by overdrive stimulation. The arrhythmia was induced again both spontaneously and with a single atrial extrastimuli -hence suggesting a reentry mechanism, with sudden prolongation of the AH interval with 90 ms and a VA interval of 0ms in the area adjacent to the coronary sinus ostium ( Figure 5). We performed an apical right ventricular stimulation during the arrhythmia and we obtained a V-A-V response which excluded the diagnosis of atrial tachycardia. Concentrical and decremental

A.
B. VA conduction excluded the presence of an occult accesory pathway. Therefore, we made the diagnosis of slow-fast AVNR with the cycle length of 800 ms (75 bpm).
After identifying the Koch triangle elements, we localized the slow intranodal pathway anatomically -in a posterior-anterior radiological position ( Figure 6A) and electrophysiologically -where the atrial de lection was small, with an atrium to ventricle ratio of 1 to 10. At this site, we performed 0:55 minutes (min) of radiofrequency applications ( Figure 6B). For safety reasons, we did not reach maximal parameters of power and temperature and we frequently checked the ablation catheter position luoroscopically, considering his AV conduction abnormalities. Post-ablation, the atrioventricular conducting parameters remained unchanged. We verify the non-inducibility of the arrhythmia using the atrial stimulation protocol by introducing up to 6 atrial extrastimuli until the nodal atrioventricular refractoriness was achieved, in basal conditions and after 1 mg of Atropine. The exposure time was 6:16 min with a radiation dose of 4995 μGy/m 2 and the total procedure time was 80 min.
The post-procedural evolution was uneventful, without recurrence of the arrhythmia clinically or on ECG. We discharged the patient the next day, maintaining the betablocker for its anti-ischemic properties. One month postablation, the patient remained asymptomatic.

Discussion
Our case presents a series of particularities which we would like to highlight: 12 months. The recurrence was probably a consequence of the submaximal parameters (power, temperature) of the radiofrequency applications imposed by the AV conduction disturbance, in order to avoid an AV block [10,23].

Conclusion
Although AVNRT is more prevalent in young healthy women and it has established ECG diagnostic criteria, it may also occur in elder male patients, with structural heart disease. Furthermore, a heart rate less than 100 bpm does not exclude the diagnosis. In these particular situations, ECG recordings during vagal maneuvers and Holter ECG monitoring can help with the differential diagnosis, which can be further con irmed and treated invasively trough EPS and RFCA.
1. The presentation of the patient was atypical. AVNRT is more common in young adults, without structural heart disease, and women are more likely to be affected than men (ratio 70:30) [6][7][8]. In addition, patients more commonly report paroxysmal episodes of regular tachycardia with sudden onset, palpitations being the most frequent symptom declared (98% of patients), alongside dizziness, dyspnea and neck pulsation 1 . Although our patient presented some of these characteristics, he was male, old, with ischemic heart disease, he did not report palpitations and the character of his arrhythmia was incessant. A possible explanation for the last two features is his relatively slow ventricular rate of 75 bpm, which can promote the re-entry mechanism, making it almost permanent and is within the normal sinus range, hence not causing palpitations. A ventricular rate less than 100 bpm is very rare in AVNRT [7,9]. Previous studies associated a slow rate AVNRT with advanced age, higher Wenckebach cycle length, AV node antegrade effective refractory period values and higher atrial vulnerability [10][11][12][13]. In our patient this could be associated with his AV conduction abnormalities, the previous RFCA procedure and the beta-blocking and Amiodarone treatment [14].
2. The event ECG was not characteristic for typical (or atypical) AVNRT and a differential diagnosis with accelerated junctional rhythm/junctional ectopic tachycardia was necessary. The rate was in the range of 60 to 130 bpm, with the P waves deforming the end of the QRS complex [15] and the patient had ischemic heart disease with CABG surgery. Nevertheless, these medical antecedents were remote from the presentation moment, there was no sick sinus syndrome which would have justi ied an escape junctional rhythm and we identi ied a series of electrophysiological features that helped us suspecting the diagnosis of slow ventricular rate typical AVNRT: • The arrhythmia was responsive to vagal maneuvers, carotid sinus massage suddenly terminating the tachycardia [16][17][18][19].
• On Holter ECG monitoring there were episodes of supraventricular tachycardia (> 120 bpm), with sudden onset and termination; also, we could identify single premature atrial beats with PR prolongation, thus suggesting a dual nodal physiology [20].
All these indings were in favor of a reentry mechanism rather than a focal automaticity and we con irmed the diagnosis during the EPS, by inducing and terminating the arrhythmia with single atrial extrastimulation [20,21].
3. In both ESC and ACC/AHA supraventricular tachycardias guidelines, the RFCA of the slow intranodal pathway is a irst-line therapy (class IB recommendation) in symptomatic patients due to its high rate of success (> 95%) and low risk pro ile [9,22]. In our case, we consider successful the irst procedure because the patient remained asymptomatic for