VENTRICULAR BEATS INDUCE VARIATIONS IN CYCLE LENGTH OF RAPID (TYPE-II) ATRIAL-FLUTTER IN HUMANS - EVIDENCE OF LEADING CIRCLE REENTRY

Background Slight variation in cycle lengths of common and rapid atria l flutter in humans is an established phenomenon, but its mechanisms h ave not been completely clarified. In a previous study, we demonstrate d that in common atrial flutter the variations in atrial cycle length were due to atrial stretch affecting the revolution time of a reentran t circuit. In the present study, we investigate the nature of atrial c ycle length variations in the rapid type of human atrial flutter. Meth ods and Results Atrial interval variations of 17 episodes of rapid atr ial flutter in 14 patients were investigated by measuring the sequence of atrial intervals from intraesophageal or intra-atrial leads and th e onset of QRS complexes from a surface lead (VI). To study whether in terval variation in flutter cycle was related to ventricular activity, a phase plot was constructed in which the flutter cycle length was pl otted against the time after the previous QRS complex. This showed tha t the interval fluctuations were strictly coupled to the moment of ven tricular activation. After the onset of the QRS complex, the rapid atr ial flutter interval gradually decreased by an average of 4.1% (P<.001 ) and reached a minimum value after 300 to 600 milliseconds. Thereafte r, the intervals increased again until the next ventricular beat occur red. In 10 patients developing both common and rapid atrial flutter, t wo different phase relations were found. Whereas during common atrial flutter the atrial interval increased after the QRS complex, it decrea sed during rapid atrial flutter. In three patients, intra-atrial press ure was recorded together with the electrical activity during both com mon and rapid atrial flutter episodes. This showed that variations in atrial flutter cycle length were associated with the rise of atrial pr essure during ventricular contraction. Conclusions These findings indi cate a role of contraction-excitation feedback caused by atrial stretc h after a ventricular activation. The shortening of the atrial interva l after the onset of the QRS complex as found in patients during rapid atrial flutter can be explained by stretch-induced shortening of atri al refractoriness and consequent shortening of the revolution time of a functionally determined intra-atrial circuit.