Adenosine-induced atrial fibrillation: insights into mechanism.

A trial fibrillation (AF) is a potential adverse effect of intravenous administration of adenosine. Although the mechanism is not known, this phenomenon is thought to be mediated by adenosine's effects on shortening atrial action potential duration and refractoriness. Because ade-nosine has little effect on atrial conduction velocity, the net effect of adenosine, therefore, is to shorten the wavelength of activation, thereby potentiating AF. On a cellular level, these effects are caused by activation of the inward rectifying K + current I KAdo. However, adenosine has other effects that may promote arrhythmogenesis. For example , adenosine has sympathoexcitatory effects mediated through baroreflex activation and chemoreceptor stimulation. Adenosine can also hyperpolarize dormant pulmonary vein myocytes and increase excitability, 3 as well as trigger pulmonary vein ectopy. 4 We report on a possible alternative mechanism of adenosine-induced AF, on the basis of findings during a pulmonary vein isolation procedure. These findings may have broader implications for understanding vagally mediated AF. A 67-year-old woman with a history of hypertension, hyperlipidemia, transient ischemic attack, and symptomatic persistent AF, which was medically refractory, underwent radiofrequency catheter ablation to electrically isolate the pulmonary veins. She developed multiple episodes of par-oxysmal AF after the initial procedure and 3 months later presented for a second catheter ablation procedure. An electroanatomic map of the left atrium and all 4 pulmonary veins were constructed. Interrogation of the left superior pulmonary vein with a circular mapping catheter (CMC) showed persistent entrance block with far-field signals from the left atrial appendage (confirmed by pacing the left atrial appendage with the ablation catheter). Exit block was confirmed with circumferential pacing with the CMC. Intravenous adenosine (12 mg) was administered, which resulted in AF coincident with adenosine-induced transient atrioventricular nodal block (Figure 1A). The left superior pulmonary vein remained electrically quiescent during AF. Sinus rhythm was restored with direct current (DC) cardio-version. The CMC was then positioned within the left inferior pulmonary vein where persistent bidirectional block was demonstrated. Again, 12 mg of intravenous adenosine resulted in initiation of AF, whereas the left inferior pulmonary vein remained quiescent (Figure 1B). Sinus rhythm was restored with DC cardioversion. The right inferior pulmonary vein was then interrogated and bidirectional block was confirmed. In addition to the CMC located in the right inferior pulmonary vein, a spiral catheter (St. Jude Medical Inquiry AFocus II HD 20 Pole High-Density Mapping Catheter) was positioned just proximal and posterior to the …