Unusual Rhythm Behind a Narrow Complex Tachycardia
A 18-year-old man presented to the emergency department with palpitations and fatigue. Twelve months earlier he had been submitted to an electrophysiological study and radiofrequency ablation for Wolff-Parkinson-White syndrome with recurrent narrow complex (orthodromic) paroxysmal supraventricular tachycardia. At admission, he presented with tachycardia at 205 beats/min and blood pressure was 105/71 mm Hg; there were no other relevant findings. The 12-lead ECG showed a regular narrow-complex tachycardia of 205 beats/min. Transthoracic echocardiography excluded structural heart disease. The tachycardia was transitorily interrupted with intravenous adenosine and resumed after 8 seconds. An intravenous bolus of verapamil was administered that interrupted the tachycardia. Figure 1 shows the ECG after conversion.
What abnormalities are present? How should we analyze the ECG combined with his medical history? What is the best management of this situation?
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Response to ECG Challenge
The ECG in Figure 1 is remarkable for showing sinus rhythm with 3 different PR intervals representing 3 distinct pathways of conduction to the ventricle. A spontaneous change in PR interval during regular sinus rhythm is noted; there are 3 different PR intervals (170, 100, and 240 ms). The shortest interval is related to a wide-complex QRS, suggesting antegrade conduction over the accessory pathway (AP). The delta wave is positive in inferior and anterolateral leads, with left bundle-branch block pattern and axis >30°, suggesting a right anteroseptal AP. The atrioventricular conduction is, therefore, performed alternately by the slow perinodal pathway (SP), the fast perinodal pathway, and an AP, forming a repeating pattern simulating ventricular trigeminy. An amplified view of the same ECG illustrating this mechanism is shown in Figure 2.
Review of 12-lead ECG during tachycardia (Figure 3) shows a narrow complex tachycardia of 205 beats/min, with an RP interval of 120 ms. It is noteworthy that the RP interval and morphology of the P wave during tachycardia are similar to the retrograde P wave observed after SP conduction during sinus rhythm, suggesting involvement of the SP as the antegrade limb of the tachycardia and the AP as the retrograde limb. In addition, retrograde P waves are narrow, positive in the inferior leads and negative in V1, suggesting anteroseptal breakout of atrial activation compatible with a bidirectionally conducting AP.
Response to intravenous adenosine bolus during tachycardia is shown in Figure 4. There is ECG evidence of interruption of tachycardia in the antegrade (atrioventricular [AV] nodal) limb. In addition, sinus beats have consistent retrograde conduction by the AP resulting in a 2:1 AV relationship. There is evidence of incomplete inhibition of the SP with persistent antegrade conduction. The fast perinodal pathway tissue has been described to be more responsive to adenosine in comparison with the SP.1
At a previous electrophysiological study, the patient presented with persistent preexcitation and AP was mapped to the anteroseptal region of the tricuspid annulus. Radiofrequency ablation of the peri-Hisian AP during orthodromic AV reentrant tachycardia (Figure 5A) was prematurely interrupted because of the appearance of a high-frequency His potential at the ablation site immediately after abolition of the AP (Figure 5B). We therefore hypothesize this may have led to incomplete ablation of the AP and inadvertent damage to the fast perinodal pathway, resulting in the current pattern of alternating AV conduction.
The literature reports the occurrence of dual AV nodal physiology in 8% to 40% of patients with AP,2 leading to a variety of possible reentrant circuits. Although this phenomenon is commonly observed in the electrophysiological electrophysiological laboratory, it is rarely evidenced in the surface ECG. A repeat EP study was performed confirming dual AV nodal physiology and documenting intermittent antegrade AV pathway conduction (Figure 6) with consistent AV echo beats during antegrade nodal conduction. An orthodromic AV reentrant tachycardia was reinduced, confirming the role of the AP in the mechanism of the clinical tachycardia. After 3-dimensional mapping with the EnSite Precision system with annotation of the His potential, successful reablation of the para-Hisian AP was performed. At the 6-month follow-up visit, the patient did not have recurrent preexcitation or tachycardia.
- © 2018 American Heart Association, Inc.
- Curtis AB,
- Belardinelli L,
- Woodard DA,
- Brown CS,
- Conti JB
- Csanadi Z,
- Klein GJ,
- Yee R,
- Thakur RK,
- Li H