Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation

Background-The blockade of angiotensin II (Ang II) formation has protective effects on cardiovascular tissue; however, the role of Ang II in atrial el ectrical remodeling is unknown. The purpose of this study was to investigat e the effects of candesartan and captopril on atrial electrical remodeling. Methods and Results-In 24 dogs, the atrial effective refractory period (AER P) was measured before, during, and after rapid atrial pacing. Rapid atrial pacing at 800 bpm was maintained for 180 minutes. The infusion of saline ( n=8), candesartan (n=5), captopril (n=6), or Ang II (n=5) was initiated 30 minutes before rapid pacing and continued throughout the study. In the sali ne group, AERP was significantly shortened during rapid atrial pacing (from 149+/-11 to 132+/-16 ms, P<0.01). There was no significant difference in A ERP shortening between the saline group and the Ang II group. However, in t he candesartan and captopril groups, shortening of the AERP after rapid pac ing was completely inhibited (from 142+/-9 to 147+/-12 ms with candesartan, from 153+/-15 to 153+/-14 ms with captopril, P=NS). Although rate adaptati on of the AERP was lost in the saline group, this phenomenon was preserved in the candesartan and captopril groups. Conclusions-The inhibition of endogenous Ang II prevented AERP shortening d uring rapid atrial pacing. These results indicate for the first time that A ng II may be involved in the mechanism of atrial electrical remodeling and that the blockade of Ang II may lead to the better therapeutic management o f human atrial fibrillation.