How to ablate typical ‘slow/fast’ AV nodal reentry tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT) accounts for about 60% of the patients presenting with paroxysmal supraventricular tachycardia (PSVT). It is the result of functional dissociation of AV nodal conduction into a so-called ‘fast pathway’ (FP) and ‘slow pathway’ (SP). The fast pathway forms the normal physiological conduction axis. It connects to the atrium in the anterior (superior) septum, close to the recording of the most proximal His bundle potential (Fig. 1). The atrio-His (AH) interval during conduction over the fast pathway generally is not longer than 220 ms. Conduction over the slow pathway, connecting to the atrium in the posterior (inferior) septum, can be revealed when an atrial impulse is blocked in the fast pathway (which generally has a longer antegrade effective refractory period than the slow pathway) leading to a sudden prolongation of the AH interval. Often the wavefront migrates back to the atrium over the fast pathway resulting in an AV nodal echo beat. Slow pathway conduction can be demonstrated in the majority of people. However, one-to-one antegrade conduction over the slow pathway, i.e. a situation where every consecutive atrial impulse is conducted over the slow pathway to the His bundle, is unusual. Therefore, perpetuation of reentry leading to AVNRT is often not possible. Even in the presence of one-to-one antegrade slow pathway conduction, a necessary prerequisite for sustained AVNRT, tachycardia may be non-inducible because of absent or weak retrograde fast pathway conduction. If reentry evolves, causing AVNRT, it uses the slow pathway as an antegrade link and the fast pathway as a retrograde link in 90% of patients: therefore, this ‘slow/