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Figure 2 (A) Entrainment mapping from the mitral isthmus in Patient #13, whose electrocardiogram (ECG) is shown in Figure 4C. The tachycardia is accelerated to the pacing rate of 210 ms and the post-pacing interval (PPI) matches the tachycardia cycle length (TCL), confirming that the tachycardia is mitral isthmus-dependent. Note the fragmented potential (*) with diastolic activity recorded by the distal pole of the ablation catheter (Abld), consistent with a gap in the mitral isthmus line. Also shown are ECG leads I, II, V1, and V5, and bipolar electrograms recorded by the distal and proximal poles of the ablation catheter (Abld and Ablp) and a catheter placed in the coronary sinus (CSd and CSp). (B) The result of radiofrequency (RF) current application at the mitral isthmus in the same patient as in Figure 2A. After 30 s of current application at the site where the PPI matched the TCL, widely split double potentials (arrow) are now recorded. The tachycardia also slows from 240 ms to 320 ms without a change in the P-wave morphology. The electrogram recorded by the CS catheter is now in mid-diastole. (C) Another example of concealed entrainment during pacing from the distal CS in the same patient as in Figures 2A and 2B. The tachycardia is accelerated to the pacing rate, and PPI matches the TCL. The P-wave morphology during pacing (small arrow) is identical to that during tachycardia ( ). Also note the double potentials as recorded by the left atrial catheter (LAd), which was positioned at the mitral isthmus. (D) The effect of RF current application in the CS in the same patient as above. The tachycardia had slowed from 320 ms to 400 ms before termination. Also, note the double potential (arrow) recorded by the left atrial catheter (LAd) at the mitral isthmus even during sinus rhythm. The first component of the double potential occurs simultaneously with the QRS suggestive of marked delay in lateral left atrial activation. (E) An example of immediate recurrence of atrial flutter in the same patient as above. The same tachycardia reappeared repeatedly within seconds of discontinuation of RF energy with an identical cycle length. Further energy application in the distal CS at a higher power terminated the tachycardia without recurrence or inducibility. Note that the P-wave morphology of the premature atrial depolarization that triggers the tachycardia (arrow) is very similar to that during tachycardia, suggesting that the sites responsible for initiating and maintaining the tachycardia are located in the CS.
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