Use of Adenosine as an Antiarrhythmic Agent

Abstract

Since the classical observation of Drury and Szent-Gyorgyi (1929), it has been known that adenosine and adenosine triphosphate (ATP) exert pronounced electrophysiological effects on the mammalian heart. Subsequently, the properties of both compounds were widely investigated in vitro or in animals (Bellardinelli et al. 1982; Cardenas 1964; James 1965; Johnson and McKinnon 1956; Munoz et al. 1984a; Pelleg 1984, 1985a; Rubio et al. 1979; Schrader et al. 1975). The pronounced and transient depressant effects on atrioventricular conduction have attracted growing attention due to its clinical implication. In fact, these properties explain the high efficacy of purinergic compounds in terminating paroxysmal supraventricular tachycardia with a re-entrant mechanism involving the AV node (Belhassen and Pelleg 1984; Greco et al. 1982; Komor and Garas 1955; Latour et al. 1968; Somlo 1955). ATP is routinely used in Europe for acute treatment of paroxysmal supraventricular tachycardia (injectable preparation: Striadyne, Laboratories Auclair, ATP-hormonotherapia, Richter). Adenosine has been investigated more recently in man, both in the United States and in Europe (Di Marco et al. 1983,1985; Munoz et al. 1984b; Puech et al. 1985); differences in the mechanism of action demonstrated in preclinical work explain the interest of cardiologists for its clinical evaluation. In fact, while pharmacological properties and effectiveness of adenosine appear to be very similar to those of ATP, the possible differences in the mechanism of action could lead to fewer side effects and it can be thought that adenosine would probably be an alternative to other available compounds as a drug of first choice for acute management of supraventricular tachycardia.