LETTER TO THE EDITOR
Double potentials analysis as a guide to radiofrequency ablation of atrial flutter
Pietro Turco, MDa,
Giuseppe Stabile, MDa,
Antonio De Simone, MDa and
Bilal El Jamal, MDa
a Laboratorio Elettrofisiologia, Casa di Cura Villa Maria Cecilia, Via Corriera, 1, 48010 Cotignola-RA, Italy
pietro.turco{at}tin.it
We read with interest the study by Tada et al. (1) in a recent issue of the Journal. The investigators carefully stressed the role of the double potentials (DPs) along the ablation line as a guide to radiofrequency ablation of typical atrial flutter. They analyzed DPs to the site at which an application of radiofrequency energy resulted in either a measurable slowing of conduction across the cavo-tricuspid isthmus or complete isthmus block. These sites are within or in close proximity to a gap in the ablation line. They concluded that a DP12 interval <90 ms always indicates the persistence of a gap in the ablation line, whereas a DP12 interval >110 ms always indicates the absence of a gap in the ablation line at the recording site (1).
We believe that the absolute value of the DP12 interval is limited because it depends on several factors. First: the presence of a gap in the ablation line. A longer DP12 interval means higher probability of conduction block; however, a DP12 interval <90 ms could be registered during conduction block at the recording site. Second: the site of atrial pacing. If conduction block is obtained, the DP12 interval lengthens as the distance of the pacing site from recording site shortens (2). In case of persistent slow conduction across the cavo-tricuspid isthmus, moving the pacing site along the tricuspid annulus (TA) the DP12 interval remains unchanged because the two components are linked by conduction across the isthmus (2,3). Third: conduction velocity (CV) around the TA. Published data indicated that in patients with atrial flutter the CV around the TA is 37 to 42 cm/s (4), so the possible overlapping of slowed conduction and blocked conduction values should be evaluated. Fourth: the TA perimeter. It takes a long time for stimulus to travel around an enlarged annulus. Fifth: linear ablation site. The site of linear ablation (for example lateral or septal) might have a role to determine the relative distance from the pacing site. Sixth: drug interference. Most drugs for atrial fibrillation and flutter slow atrial CV for which a lengthy time interval could be referred to very slowed conduction instead of blocked conduction.
In the study by Tada et al. (1), in Figure 2, when isthmus conduction block is obtained, the StDP1 interval is likely 56 ms (time for stimulus to cover about 2 cm distance); DP2, because conduction around TA, is at 124 ms after DP1 and so StDP2 interval is 180 ms (time for stimulus to cover about 6 cm distance along TA perimeter). It could be that the distance from coronary sinus ostium (CS) to linear ablation site is >2 cm long (because CS anatomy and/or lateral linear ablation) for which StDP1 lengthens and StDP2 shortens (for shorter distance) and thus DP12 interval is <90 ms: DP1 and DP2 get near as pacing site along TA moves away from linear ablation site.
As a reference in guiding isthmus linear ablation, it would be useful to evaluate the hypothetical conduction time interval around the TA in the single patient: TA cm (by echo) x CV cm/s (by electrophysiologic study). If isthmus conduction block is obtained, the sum of StDP1 + StDP2 interval times corresponds to complete conduction time interval around TA in that patient. The StDP1 + StDP2 interval time remains the same even if the atrial pacing site is moved along the TA: in this case, the DP12 interval lengthens as the pacing site is moved closer to the ablation line because DP1 and DP2 are not linked. In case of slowed conduction, the sum of StDP1 + StDP2 interval times is less than the hypothetical conduction time interval around TA because StDP1 and StDP2 interval times reflect a partial conduction around TA; if the atrial pacing site is moved along the TA, the DP12 interval time does not change because DP2, instead of conducting around TA, is linked to DP1 because of slowed conduction across the isthmus.
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References
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1. Tada H, Oral H, Sticherling C, et al. Double potentials along the ablation line as a guide to radiofrequency ablation of typical atrial flutter. J Am Coll Cardiol. 2001;38:750755[Abstract/Free Full Text]
2. Shah DC, Takahashi A, Jais P, et al. Local electrogram-based criteria of cavo-tricuspid isthmus block. J Cardiovasc Electrophysiol. 1999;10:662669[Medline]
3. Takahashi A, Shah DC, Jais P, et al. Partial cavotricuspid isthmus block before ablation in patients with typical atrial flutter. J Am Coll Cardiol. 1999;33:19962002[Abstract/Free Full Text]
4. Feld GK, Mollerus M, Birgerdotter-Green U, et al. Conduction velocity in the tricuspid valve-inferior vena cava isthmus is slower in patients with type I atrial flutter compared to those without a history of atrial flutter. J Cardiovasc Electrophysiol. 1997;8:13381348[Medline]
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