[CASE] The sluggish course of sluggish node disease.

A 74-year old woman presented to the ED because of the syncope after defecation which resulted in minor head injury. Head CT showed no pathology and lab tests were normal. ECG did not suggest any cardiac pathology.

Patient stated that she had been experiencing presyncopies and vertigo for about 3 months. She was admitted to our cardiology ward for observation and 24-hour holter monitoring was ordered. This is one of the events registered.

It shows an atrial flutter termination followed by long 5 sec pause and junctional escape beat. The second beat after the pause is preceeded by P wave from ectopic atrial pacemaker. The last one results from sinus node activity and efficient a-v conduction.

SNRT (sinus node recovery time) is parameter measured during atrial pacing used to diagnose SN dysfunction. It is interval between the last paced P wave and the first sinus P wave. In this case tachycardia plays a role of rapid atrial stimulation and as you can see sinus node struggles to recover after cessation of arrhythmia. SNRT is considered abnormal when it is longer than 1,6 or 2 seconds. In this case it is around 6 sec. 

This is a variant of sick sinus syndrome (SSS, SND also known by historic names lazy or sluggish sinus node) called bradycardia-tachycardia syndrome (BTS, brady-tachy for short). BTS presents itself as alternating slow (<60/min) and fast heart rates (>100/min). It occurs predominantly in elder people. 

This patient's heartbeat is either too slow or too fast, there is no heart rate in between (60-100/min). This is very typical for BTS. 

The patient has been hospitalized four times between 2014 and the of 2018 (twice because of presyncopies) but no evident pauses were registered although recurrent, paroxysmal atrial fibrillation (AF) runs were present in almost every 24-hour holter monitoring. It took some time, right?

This time she had a dual-chamber pacemaker implanted (ESC class I recommendation). 

The causal relationship between bradycardia and tachycardia is not well established but it is thought to be bidirectional. SND might be in some cases prodrome of atrial fibrillation. On the other hand chronic AF causes SND by electrically remodeling sinoatrial node. This was surely the case in our patient as she was not diagnosed with CAD nor structural heart disease was present. 

Pharmacological management of BTS is challenging beacuse antiarrhythmic and rate-control drugs can worsen SN function.

AF ablation may be a good therapeutic option for SND with concomitant atrial fibrillation as it showed reduction in sinus pauses and symptoms but more trials are still needed. 

Further reading: 

1) Choudhury M, Boyett MR, Morris GM. Biology of the Sinus Node and its Disease. Arrhythm Electrophysiol Rev. 2015;4(1):28–34. doi:10.15420/aer.2015.4.1.28

2) Tse G, Liu T, Li KH, et al. Tachycardia-bradycardia syndrome: Electrophysiological mechanisms and future therapeutic approaches (Review). Int J Mol Med. 2017;39(3):519–526. doi:10.3892/ijmm.2017.2877

3) JACKSON, L. R., RATHAKRISHNAN, B. , CAMPBELL, K. , THOMAS, K. L., PICCINI, J. P., BAHNSON, T. , STIBER, J. A. and DAUBERT, J. P. (2017), Sinus Node Dysfunction and Atrial Fibrillation: A Reversible Phenomenon?. Pacing and Clinical Electrophysiology, 40: 442-450. doi:10.1111/pace.13030

4) European Heart Journal (2013) 34, 2281–2329 doi:10.1093/eurheartj/eht150