A tale of two post pacing intervals.

摘要

A 3 3-year-old man with recurrent palpitations and documented narrow QRS complex tachycardia underwent a standard transvenous electrophysiologic study including multipolar recordings from the high right atrium, His bundle region, coronary sinus, and right ventricular apex. Baseline intervals were normal and there was no evidence of ventricular preexcitation. Programmed atrial stimulation revealed a discontinuous atrioventricular node (AVN) function curve. During a drivetrain cycle length (CL) of 700 ms, the A2H2 interval was 190 ms when A2 was coupled at 540 ms, while the A2H2 interval was 290 ms when A2 was coupled at 530 ms (A2H2 "jump" = 100 ms). Ventriculoatrial (VA) conduction was central but not decremental, VA block was not observed after the intravenous administration of 18 mg of adenosine, and the VA interval and atrial activation sequence did not change during para-Hisian pacing.1 During an infusion of isoproterenol, sustained narrow QRS complex tachycardia (CL = 350 ms) was reproducibly inducible with a single premature atrial extrastimulus that did not result in an A2H2 jump. This tachycardia demonstrated a 1:1 relationship between atria and ventricles, a regular rate (spontaneous beat to beat CL variability <10 ms), an HV interval of 35 ms, and a ventriculoatrial (VA) interval of 125 ms. The earliest atrial activation was mapped to the anterior septum adjacent to the His bundle recording site where a large His potential was also recorded. Figure 1 reveals the response after the cessation of right ventricular apical pacing (CL = 330 ms) initiated during tachycardia (CL = 350 ms). Figure 2 reveals another response after the cessation of right ventricular apical pacing (CL = 320 ms) initiated during tachycardia (CL = 330 ms). What is the tachycardia mechanism? Why are the post-pacing intervals (PPI) in Figures 1 and 2 so different?