A Complex Arrhythmia Defined by an Esophageal Lead

EP ROUNDS

A Complex Arrhythmia Defined hy an Esophageal Lead E. MANGIERI. CESARE GRECO, F. B A R I L L A , and GIUSEPPE GRITELLI From the Department of Cardiology and Cardiovascular Surgery, University of Rome "La Sapienza," Rome, Italy

Case Presentation A 55-year-old man with mild mitral valve stenosis presented witb sustained wide QRS tachycardia at a cycle length of 280 ms (Fig. 1). The QRS configuration showed right bundle branch block with right axis deviation, suggesting idiopathic ventricular tachycardia (VT) originating from the superior region of the left ventricle.^ Transesophageal electrogram was performed in order to analyze the temporal relation between atrial and ventricular complexes, and 1:1 atrioventricular (AV) ratio was evidenced (Fig. 1). The following hypotheses were advanced: (l) idiopathic left VT with 1:1 ventriculoatrial conduction: (2) AV nodal reentry tachycardia or ectopic atrial tachycardia with functional or preexisting right hundle branch block; (3) antidromic reciprocating tachycardia using a left-sidod AV accessory pathway (AP) as the anterograde limb of the circuit; and (4) ectopic atrial tachycardia with leftsided preexcitation. During recording (Fig. 2A), narrowing of QRS complexes with irregularity of RR intervals suddenly occurred, simultaneously with the disappearance of organized atrial activity in the transesophageal electrogram, while discrete P waves became evident in surface lead V^ Fifteen minutes later, sinus rhythm spontaneously resumed, with normal PR interval and narrow QRS complexes. Transesophageal atrial pacing was instituted during sinus rhythm, and resulted in short stimulus R interval with a QRS configuration consistent with left-sided preexcitation (Fig 2B). The anterograde refractory period of the AP, as defined

by extrastimulus technique performed via the esophagus, measured 210 ms. Commentary To proceed logically, it appears useful to start from the presence of a left-sided AP, as unmasked by transesophageal pacing (Fig. 2B). Consistent with the patient's heart disease, it is conceivable that the anomalous conduction, which was masked during sinus rhythm because of intraatrial conduction delay—as is common in mitral valve stenosis—became apparent with delivery of pacing in proximity of the left atrium via the esophagus. On this basis, wide QRS tachycardia, as shown in Figures 1 and 2A, may be reasonably interpreted as antidromic reciprocating tachycardia, or, alternatively, as ectopic atrial tachycardia with AV bypass conduction. The latter, indeed, is the correct diagnosis, as demonstrated by tracings depicted in Figure 2A. These tracings reveal the abrupt transformation of atrial tachycardia with pure left-sided preexcitation into a dissimilar atrial rhythm,

280

AAAAAAAAAAAAAAAAAAAAAAA/ 280

Address for reprints: Giii.seppe Critelli, M.D.. Via Ceresio, 11. 00199 Rome. Italy. Fax: 39-6-4463423. Received Fehruary 15,1996; revision March 22.1996; accepted May 1,1996.

1122

so Figure 1. Right bundle branch block, right axis deviation tachycardia. Transesophageal electrogram demonstrates 1:1 ventriculoatrial conduction.

July 1996

PACE, Vol. 19

A COMPLEX ARRHYTHMIA DEFINED BY AN ESOPHAGEAL LEAD

Figure 2. (Aj Spontaneous transformation of wide QHS tachycardia into a dissimilar atriai rhythm. (B) Transesophageal atrial pacing discloses the presence of a left-sided AP. See text for details.

namely, left atrial fibrillation associated with an independent right atrial tachycardia.^ The following explanations, seen as a whole, allow the exclusion of the possible occnrrence of noises or artifacts in the esophageal recording. Narrow QRS complexes with irregular RR intervals [see leads 1 and 3 in Fig. 2A) and disorganized atrial activity, as detected hy the esophageal lead that explores the left atrial activity,^ are consistent with left atrial fibrillation; distinct P waves in lead Vi [which predominantly records the right atrial activity), at the same cycle length (280 ms), as seen in the esophageal electrogram recorded during wide QRS tachycardia, are in keeping with the persistence of initial atrial tachycardia, which is now confined to the right atrium. A crucial point for full understanding of the presented arrhythmia is to establish why the occurrence of left atrial fibrillation resulted in loss of preexcitation in the presence of a left-sided AP with short refractoriness. Actually, atrial fibrillation in the left atrium near the site ofthe AP might be expected to result in preexcited, rather than narrow, QRS complexes. As shown in Figure 2A, the beginning of disorganized left atrial activity, as

evidenced by the esophageal electrogram, is coincident with the initial deflection ofthe last preexcited QRS, when the AP is refractory. At that time, defibrillating impulses coming from the left atrium, while acting as a barrier against AV node activation by right atrial impulses [with three consecutive nonconducted P waves), proceed through the normal conduction system and generate the first narrow QRS complex. Finally, it remains to be clarified why no evidence of preexcitation occurs once left atrial fihrillation has stabilized, in spite of the short AP refractoriness. This can reasonably be explained in terms of interplay between conduction over the normal and the anomalous pathways, and the electrophysiological properties ofthe receiving ventricle.^'^ Indeed, it is quite conceivable that disorganized wavefront entering both pathways could result in repetitive anterograde and/or retrograde concealed conduction through the AP, leading to the functional exclusion ofthe bypass tract. In conclusion, this report demonstrates the usefulness of transesophageal electrogram and pacing in the elucidation of complex arrhythmias.

References 1.

Ohe T, Aihara N, Kamakura S, et al. Long-term outcome of verapimil-scnsitive sustained left ventricular tachycardia in patients without structural heart disease. 1 Am Coll Cardiol 1995; 25:54-58. 2. Zipes DP, Dejoseph RL. Dissimilar atrial rhythms in man and dog. Am J Cardiol 1973; 32:618-628. 3. Pristowsky EN. Pritchett ELC, Gallagher JJ. Origin of the atrial electrogram recorded from the esophagus. Circulation 1980; 61:1017-1023.

PACE, Vol. 19

July 1996

Gastellanos A. Myerburg RJ, Graparo K, et al. Factors regulating ventricular rates during atrial flutter and fihrillation in preexcitation [WoIff-ParkinsonWhite) syndrome. Br Heart J 1973; 35:811-816. Wellens HJJ, Durrer D. Wolff-Parkinson-White syndrome and atrial fihrillation. Relation between refractory period of accessory pathway and ventricular rate during atrial fihrillation. Am j Gardiol 1984; 34:777-782.

1123