PHARMACOLOGICAL ALTERATIONS IN HUMAN TYPE-I ATRIAL-FLUTTER CYCLE LENGTH AND MONOPHASIC ACTION-POTENTIAL DURATION - EVIDENCE OF A FULLY EXCITABLE GAP IN THE REENTRANT CIRCUIT

Objectives. This study compared the effect of changes in action potent ial duration versus conduction velocity on atrial butter cycle length to determine whether there is a fully or partially excitable gap in at rial flutter. Background. In an excitable gap reentrant circuit, cycle length is proportional to conduction velocity, Action potential durat ion is not a direct determinant of cycle length when the gap is fully excitable. Methods. Right atrial monophasic action potentials were rec orded from 41 patients during type I atrial flutter before and during pharmacologic interventions. Results. Adenosine (17 +/- 3 mg [mean +/- SD]) shortened (p < 0.001) action potential duration but did not chan ge cycle length. Edrophonium (10 mg) had no significant effect on acti on potential duration or cycle length. Isoproterenol (0.03 mu g/kg bod y weight per min) shortened (p < 0.05) and procainamide (15 mg/kg, the n 2 mg/min) prolonged (p < 0.001) action potential duration and cycle length. Alterations in cycle length were not correlated with changes i n action potential duration. Procainamide's prolongation of action pot ential duration was reversed by adenosine without affecting cycle leng th. Procainamide's prolongation of action potential duration and cycle length was partially reversed by isoproterenol. Adenosine's and isopr oterenol's shortening of action potential duration and isoproterenol's shortening of cycle length were enhanced by procainamide. Conclusions . Atrial butter cycle length is determined primarily by conduction vel ocity and does not depend directly on action potential duration, Atria l putter has a fully excitable gap, and procainamide does not convert the gap from full to partial excitability. Adenosine and isoproterenol interact with procainamide such that their effects are enhanced and p rocainamide's effects are diminished.