| Atrial stretch or dilation predisposes to the development of atrial arrhythmia, especially atrial fibrillation (AF). In clinical studies, the morbility of AF in patients receiving VVI pacemakers was higher than those receiving AAI or DDD pacemakers. It is believed that the arrhythmogenic effects of atrial stretch or dilation may be mediated by the phenomenon of mechano-electrical feedback (MEF), in which atrial refractoriness, especially the effective refractory period of atrium (ERPA), is changed in response to mechanical stretch. Prior studies in humans observed inconsistent effects of atrial MEF. Moreover, simultaneous atrioventricular pacing (SAVP) may cause atrial electrical remodeling through MEF as well as direct atrial pacing, which decreases the reliability of the results of SAVP on atrial MEF.The goals of the present study were: 1) Evaluate the effects of an acute atrial stretch on human ERPA, ERPA dispersion and vulnerability to atrial fibrillation. 2) Find a method that can evaluate the effects of MEF on atrial electrophysiology more directly and accurately. 3) Discuss the probable reasons for patients receiveed VVI pacemakers had higher morbility of AF than those received AAI or DDD pacsmakers.Objects and methods: Ths population of this study consisted of eighteen patients without structural heart disease, who underwent catheter radiofrequency ablation due to paroxysmal supraventricular tachycardia. Right atrial pressure , ERPA, ERPA dispersion and vulnerability to atrial fibrillation at high right atrium (HRA) and distal coronary sinus (CSd) were evaluated during sinus rhythm , rapid atrial pacing (AP) at high right atrium (HRA), rapid ventricular pacing (VP) at right ventricular apex (RVA), simultaneous AV pacing at HRA+RVA (SAVPHRA+RVA) and simultaneous AVpacing at distal coronary sinus (CSd) +RVA (SAVPCSd+RVA) at a cycle length of 400 msec.Results: Compared to during sinus rhythm, mean right atria pressure during AP did not differ significantly (9.1 4.1vs7.5 3.2cmH2O, P>0.05), where mean right atria pressure increased significantly during VP, SAVPHRA+RVA> SAVPCsd+RVA (12.944.4, 12.6 4.3, 14.5 3.9cmH2O, P<0.05) , and increased to a similar degree in VP, SAVPHRA+RVA, SAVPcsd+RVA (P>0.05) . The ERPA shortened significantly during differ pacing protocol compared to during sinus rhythm. There was a further shorting of the ERPHRA during SAVPHRA+RVA(22 14vsl2 13/10 10msec, P<0.05)and a further shorting of the ERPCSd during SAVPCSd+RVA (23 13vs 11 15/7 8msec, P<0.05) as compared with those during AP and VP. The ERPA dispersion (24 36> 26 32, 30 30, 23 34vs23 30msec, P>0.05) and vulnerability to atrial fibrillation (1/16, 2/16> 2/16, 0 /16vsO /16, P>0.05) did not increased significantly during different pacing protocol.Conclusion: Both VP and SAVP can increase atrial pressure, which leads to atrial MEF through acute atrial stretch, characteristic of shortness of ERPA in different segments. Simple VP increases atrial pressure similarly as SAVP, and without direct effect on ERPA of SAVP due to atrial pacing, thus making the results of atrial MEF more reliable. So, the method of simple VP is a good alternate to SAVP in the studing of atrial MEF. In our study, the vulnerability to atrial fibrillation did not increased with the shortness of ERPA induced by MEF, It is though that the increasment of ERPA dispersion by atrial MEF, as well as the the shortness of ERPA, may be a key factor of increasment of vulnerability to atrial fibrillation. This study's results may partly explain the reasons why patients receiveed VVI pacemakers had higher morbility of AF than those received AAI or DDD pacsmakers.
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