Change of Atrial Refractory Period after Short Duration of Rapid Atrial Pacing: Regional Differences and Possible Mechanisms

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Abstract
It is unknown whether there are regional differences in the cimnge of atrial effective refractory period (EBP) after a short duration of rapid atriai pacing. Furthermore, the effects of calcium channel and potassium channel on this phenomenon have not been extensively investigated. In opened‐chest dogs, the endocardial monophasic action potential duration at 90% repolarization (APD90) from the right atrial appendage, and ERP from seven atrial sites were measured before and after rapid atrial pacing at 800 beats/min for 30 minutes. Both atrial ERP and APD90 significantly shortened after rapid atrial pacing. The postpacing atria EBP and APD90 shortening persisted for 1.19 ± 3 and 123 ± 4 seconds after cessation of pacing, respectively. There was no significant difference in the magnitude or recovery course of atrial ERP shortening after pacing among the seven atrial sites. Pretreatment with nicorandil and d‐sotalol had no effects on the magnitude or recovery course of atrial EBP shortening after pacing. However, the degree of ERP and APD90shortening after pacing was significantly atten uated in the verapamil and ryanodine groups; furthermore, the recovery of ERP and APD90 after cessation of pacing was faster in the two groups. In conclusion, shortening of atrial EBP induced by short‐duration rapid atrial pacing was uniform in both atria. Both the adenosine triphosphatase (ATP) dependent potassium current and rapid component of the delayed rectifier did not significantly influence this phenomenon, but both the verapamil and ryanodine could significantly attenuate the degree of atrial ERP and APD90 shortening.