Adenosine is widely used in the termination of supraventricular tachycardia. One of the initial reports of atrial fibrillation induced by adenosine was by Silverman AJ et al . They described 5 patients who developed atrial fibrillation (AF) after adenosine administration. None of these patients had structural heart disease and only one had prior history of AF. Adenosine was given during electrophysiological study in these patients with supraventricular tachycardia to block atrioventricular (AV) conduction in order to unmask any potential accessory pathway. Hence the administration was during sinus rhythm and not during supraventricular tachycardia. Four of them developed AV block prior to AF while the remaining patient had accessory pathway conduction. They proposed that the shortening of atrial action potential by the action of adenosine on its receptors in atrial myocytes is the mechanism for induction of AF. They also highlighted the potential risk of AF with fast ventricular rate in case it is precipitated while treating supraventricular tachycardia mediated by an accessory pathway. Prior to this report, Belhassen B et al had reported induction of AF by adenosine triphosphate .
Strickberger SA and colleagues noted 12% incidence of AF when 12 mg adenosine was given through the femoral vein for supraventricular tachycardia during an electrophysiological study . The mean ventricular response in AF was similar in this study for those with atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia and was modest. The maximum preexcited RR rate was 214/min. They proposed that shortening of atrial action potential duration is a possible mechanism for induction of AF. In addition they noted frequent atrial ectopics, which could have contributed to precipitation of AF by the long-short sequence mechanism.
Adenosine induced AF has been reported by Israel C et al  as well. Li N et al  used optical mapping and immunoblot mapping of atria to evaluate the mechanism of adenosine induced AF in explanted human hearts. They noted higher A1 receptor expression in right atria. GIRK4 (G protein-coupled inwardly rectifying potassium channels) activated by A1 receptors were considered to be involved in maintaining reentrant drivers in lateral part of right atrium.
Li N et al. Adenosine-Induced Atrial Fibrillation: Localized Reentrant Drivers in Lateral Right Atria due to Heterogeneous Expression of Adenosine A1 Receptors and GIRK4 Subunits in the Human Heart. Circulation. 2016;134:486-498.