Effects of adenosine on retrograde refractoriness of accessory atrioventricular connections

A slows conduction and decreases automaticity of the sinoatrial and atrioventricular (AV) nodes and is used therapeutically to terminate reentrant supraventricular tachycardia (SVT).1,2 Although effects on accessory AV connections have been less extensively studied, adenosine has been shown to slow or block conduction in certain atypical accessory pathways exhibiting decremental conduction properties.3,4 In contrast, conduction in most typical accessory pathways is not blocked by adenosine and the effects of adenosine on AV conduction have been used to confirm surgical or catheter ablation.5,6 The effects of adenosine on accessory pathway antegrade refractoriness have been difficult to evaluate due to the short half-life of adenosine and the frequent induction of atrial fibrillation by premature atrial stimuli.7 However, adenosine does decrease antegrade refractoriness of accessory AV connections as demonstrated by transient conversion of 2:1 conduction to 1:1 conduction during atrial pacing.8 No studies to date have evaluated the effects of adenosine on retrograde conduction properties. Therefore, the present study was designed in which ventricular premature stimuli with fixed coupling intervals were introduced to determine the effects of adenosine on retrograde refractoriness of accessory AV connections. • • • The effects of intravenous adenosine on retrograde refractoriness of accessory AV connections were evaluated in 17 patients (mean age 32 6 14 years) without structural heart disease undergoing electrophysiologic study and radiofrequency catheter ablation for SVT. Twelve patients had manifest preexcitation and 5 had concealed accessory pathways demonstrating only retrograde conduction. Twelve accessory pathways were located in the left lateral region, 1 was left posterior and 4 were right posteroseptal. No patient had multiple accessory pathways and none had been taking class I or III antiarrhythmic drugs. After sedation with intravenous midazolam or propofol, or both, multipolar electrode catheters were introduced percutaneously and positioned in the high right atrium, right ventricular apex, coronary sinus, and across the tricuspid valve in a position that allowed a His potential to be recorded. Intracardiac electrograms and surface electrocardiograms were displayed and recorded with a computerized data acquisition system (Bard EP LabSystem, Tewksbury, Massachusetts). Electrograms were filtered at 30 to 250 Hz and onset of activation was defined as the first rapid deflection to cross the isoelectric line. In 6 patients, direct-current recordings of right atrial monophasic action potentials were obtained using a special catheter (EP Technologies, Sunnyvale, California). A programmable stimulator was used to pace the From the Department of Medicine, Division of Cardiology, Baystate Medical Center, Springfield, Massachusetts. Dr. Kabell’s address is: Division of Cardiology, Baystate Medical Center, 759 Chestnut Street, Springfield, Massachusetts 01199. Manuscript received October 1, 1997; revised manuscript received and accepted April 6, 1998. FIGURE 1. Refractory period determination under baseline conditions. In each panel, tracings are surface electrocardiogram leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), distal, mid-, and proximal coronary sinus (DCS, MCS, and PCS), His bundle region (His), and right ventricular apex (RVA). In panel A, a ventricular premature stimulus at a coupling interval of 340 ms (S1-S2) results in retrograde conduction to the atrium via the accessory pathway (V2 followed by A2). In panel B, a ventricular premature stimulus at a coupling interval of 330 ms captures the ventricle, but there is no retrograde conduction to the atrium (V2 without A2).