We present a case of a 62 year-old woman admitted for further evaluation because of frequent palpitations and effort intolerance accompanied by precordial oppressions. She has been treated for arterial hypertension and hyperlipidemia since earlier, and takes propafenone 2x150 mg, and verapamil 180 mg in her therapy for palpitations.

A potential cause of problems was recognized already on a routine 12-lead electrocardiogram at the time of admission. In fact, there are numerous ventricular complexes that according to their morphology correspond to supraventricular extrasystoles (SVES), with no visible atrial activity, and are closely related to the previously duly conducted sinus complex (Figure 1). More than 10,000 such SVES were recorded in the 24-hour continuous ECG recording. Echocardiography showed that it is a structurally normal heart with preserved systolic function, and coronary angiography excluded coronary artery disease.

Electrophysiology study (EPS) was performed. Basic intracardiac elektrograms confirmed the suspicion that this is the so-called “double fire” phenomenon, or dual atrioventricular (AV) conduction. Two ventricular complexes come to one atrial complex, of which the first is conducted by the fast and the second by the slow pathway (Figure 2a and 2b). Standard EPS protocol proved dual AV node pathway physiology, excluded retrograde conduction, and induced no tachycardia or “echo” beats. After a few short energy applications in the region of the slow pathway, dual AV node physiology was completely eliminated, only with conduction via the fast pathway (Figure 3a and 3b). Arrhythmia was not inducible even after the application of isoproterenol. She was discharged home without antiarrhythmics.

Dual AV node pathway physiology or the presence of socalled slow conduction pathway is according to various studies present in up to 35% of people during EPS (1, 2).

The phenomenon of dual ventricular response to a single atrial complex was first described by Csapo in 1979 and called it a “double fire” or “non-reentrant” tachycardia (3). It is rare because it requires special characteristics of the both pathways — anterograde conduction and retrograde block, while the slow pathway must be slow enough to allow the His- Purkinje tissue to recover excitability after previous stimulation (4-6). For this reason, the conductivity phenomenon 1:2 is not constant, the AV node is inconsistently depolarized, so different forms of functional AV block (PR prolongation or Wenckebach) are often present. It is manifested by irregular ventricular rhythm on the external electrocardiogram, and the relation with the P wave is sometimes hard to follow. So it was not surprising that this arrhythmia is hard to recognize, and at faster frequency and low voltage of the P wave it can be easily confused for e.g. atrial fibrillation. The dominant symptom are palpitations, and literature has described the cases of tachycardiomyopathy caused by this arrhythmia, successfully treated with radiofrequency (RF) ablation of the slow pathway (7-9). These patients typically have no reentrant tachycardia typical for active slow pathway, such as atrioventricular nodal reentrant tachycardia (AVNRT).

A poor response to medical therapy (due to resistance of the slow pathway to most classic antiarrhythmics) and the possibility of the treatment with RF ablation, forces us to think about this type of arrhythmia that can be recognized already from the standard 12-lead electrocardiogram. Of course, electrophysiology study is required to prove it.