Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars
WG Stevenson,
PT Sager,
PD Natterson,
LA Saxon,
HR Middlekauff,
and
I Wiener
Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
OBJECTIVES. This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction. BACKGROUND. The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones. METHODS. Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current. RESULTS. Pace maps resembled tachycardia at < 30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval > 40 ms was observed at > or = 70% of reentry circuit sites. CONCLUSIONS. At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.
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