Electrophysiologic effects of intravenous adenosine triphosphate disodium on the paroxysmal supraventricular tachycardias.

Abstract

SUMMARYWe studied the electrophysiologic effects of intravenous adenosine triphosphate disodium (ATP-2Na) on 15 patients with paroxysmal supraventricular tachycardias (PSVTs). One patient had sinus node (SN) reentry and 2 patients had intraatrial (IA) reentry. Five patients had AV nodal reentry and 7 patients had atrioventricular reentrant tachycardias (AVRTs) with accessory pathways (APs). ATP-2Na was injected during ventricular pacing (VP) in patients with AVRTs with APs. A bolus injection of ATP-2Na terminated all the PSVTs within 40 sec except in one case of IA reentry. The sites of block at the termination were the atrium in SN reentry and IA reentry, between A and H (AH) block or between H and A (HA) block in AV nodal reentry and AH block in all the AVRTs with APs. ATP-2Na during VP in patients with AVRTs with APs produced the changes of atrial activation sequences in 3 patients, induction of PSVT in 2 patients and a Mobitz type II VA block in 2 patients. The former two phenomena suggested a retrograde AV nodal block and raised the possibility of a simple test for retrograde atrial fusion during VP in patients with WPW syndrome. Chest discomfort of short duration was most commonly noted after ATP-2Na. Inosine pretreatment potentiated the effects of ATP-2Na. This combination may further alleviate the side effects of ATP-2Na, while preserving the effective action of ATP-2Na for rapid termination of PSVTs. Additional Indexing Words: Electrophysiologic effectsParoxysmal supraventricular tachycardias Ventricular pacing ATP-2Na potentiation by inosine

Effects of Intravenous ATP on Tracheal Ciliary Activity, Airway Resistance and Haemodynamics in Rats

“…In previous studies, the blocking effect of ATP on the atrioventricular nodus has been demonstrated in man (Favale et al 1985;Rinne et al 1988;, and this action has been used to treat paroxysmal supraventricular tachycardia (Tajima et al 1985;Saito et al 1986). ATP has also been shown to cause more serious cardiac arrhythmias than bradycardia (ventricular extrasystolies, bigeminy) in dog (Boarini et al 1984) and in rat (Dedrick et al 1982), possibly due to metabolic acidocis (Newberg et al 1985) and chelation of magnesium and calcium by phosphate produced by the degradation of ATP (Dedrick et al 1982).…”