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"Paradoxical" AH shortening caused by proximal coronary sinus stimulation during orthodromic reciprocating
1First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Introduction:
During extrastimulation or entrainment of orthodromic atrioventricular (AV) reciprocating tachycardia (ORT), the atrium-His (AH) interval as measured at the His-bundle recording site is expected to lengthen due to extrastimulation-dependent or pacing rate-dependent slowing of AV nodal conduction by impulses that penetrate the tachycardia circuit. We report 6 patients in whom the AH interval "paradoxically" shortened during ORT in response to extrastimulation and rapid pacing from the proximal coronary sinus.
Methods And Results:
Accessory pathway location was right anterior (1 patient), right anteroseptal (1 patient), and left anterior (4 patients). Cycle length of ORT was stable (variation < or = 5 msec) and ranged from 325 to 410 msec. During ORT, extrastimulation and rapid pacing were performed from the proximal coronary sinus and the right atrium. Extrastimulation from the proximal coronary sinus late in diastole caused significant shortening of AH interval in all patients by a mean of 18 +/- 3 msec (range 15 to 20 msec). AH shortening was demonstrated without a change of either the timing or morphologic appearance of the low septal right atrium at the His-bundle recording site. This phenomenon was not observed during right atrial extrastimulation. Rapid pacing from the proximal coronary sinus at cycle lengths of 305 to 390 msec (i.e., 15 to 20 msec shorter than the cycle length of each ORT) again demonstrated shortening of AH interval in all patients by a mean of 15 +/- 3 msec (range 10 to 20 msec). By contrast, rapid pacing from the right atrium demonstrated classical AH prolongation at any paced cycle length.
Conclusion:
AH shortening without a change of either the timing or morphologic appearance of the low septal right atrium at the His-bundle recording site confirms the existence of a distinct posterior atrial input to the AV node. In this setting low septal right atrial activation is not requisite for AV nodal conduction. Whether activation of the low septal right atrium is essential for, or contributes to, AV nodal conduction of atrial impulses from locations other than the proximal coronary sinus needs to be determined.