Answer Rhythm Puzzle 2004 10 469

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Author(s) I.C.D. Westendorp, G.S. de Ruiter, L.V.A. Boersma, E.F.D. Wever
NHJ edition: 2007:4,157
These Rhythm Puzzles have been published in the Netherlands Heart Journal and are reproduced here under the prevailing creative commons license with permission from the publisher, Bohn Stafleu Van Loghum.
The ECG can be enlarged twice by clicking on the image and it's first enlargement
Figure 1
Figure 2

A 27-year-old female was referred to the emergency room with rapid palpitations. The ECG at presentation is shown in figure 1. The tachycardia did not respond to carotid sinus massage. A bolus of 6 mg intravenous adenosine terminated the tachycardia and restored sinus rhythm (figure 2). Cardiological evaluation including echocardiography revealed no abnormalities. Over the last few years, the patient had previous episodes of rapid palpitations lasting 15 to 20 minutes occurring once or twice a week. The paroxysms recurred despite treatment with sotalol, flecainide, and propafenone. The patient was referred for electrophysiological study (EPS) and radiofrequency catheter ablation (RFCA) if possible.

What are the likely origins of this tachycardia?


Figure 1 shows a wide-QRS tachycardia (QRS duration 120 ms, rate 150 beats/min) with complete right bundle branch block (RBBB) morphology, and a (slight) leftaxis deviation. Lead V6 shows an RS configuration. P waves are not discernible. Signs suggestive of both ventricular and supraventricular origin are present. The tachycardia was terminated by adenosine. This is (usually) suggestive of a supraventricular origin. The ECG after conversion (figure 2) shows an incomplete RBBB and

an intermediate electrical axis. If assuming a supraventricular origin, more pronounced RBBB aberrancy (due to phase-3 block) is postulated. Then,the differential diagnosis would be as follows:

  1. AV nodal re-entrant tachycardia (AVNRT),
  2. orthodromic circus movement tachycardia or less likely
  3. atrial tachycardia.

If assuming a ventricular origin, ventricular tachycardia (VT) originating in or near the Purkinje system (fascicular VT or idiopathic left ventricular VT) is likely. During EPS, clinical tachycardia was easily induced with rapid atrial pacing and programmed ventricular stimulation using extra-stimuli. Surface ECG leads and intracardiac tracings during the tachycardia are shown in figure 3. In these tracings, signs of AV dissociation are demonstrated. This limits the differential diagnosis to only two possible diagnoses: VT or AVNRT with complete retrograde block in the upper common pathway of the AV node. In the His bundle electrogram (HIS, figure 3), a His deflection is visible, which is timed at the beginning of the QRS complex (see leads I to III, and V1, figure 3). The HV interval (conduction time through the His-Purkinje system) during both sinus rhythm and supraventricular tachycardia should normally be 35 to 55 ms or more in case of bundle branch block or intraventricular conduction disturbance. This aspect rules out the possibility of an AVNRT. Thus, the tachycardia is of ventricular origin originating in or close to the left posterior fascicle (with therefore left-axisdeviation). The His deflection seen in figure 3 results from retrograde activation of the His bundle. Fascicular VT (sometimes referred to as ‘Belhassen VT’) is an idiopathic VT originating from the posterior (then with left-axis deviation) or anterior (then with right-axis deviation) fascicle of the left bundle branch. It usually presents in patients between 15 and 40 years. The arrhythmia may become incessant and if untreated may result in a tachycardia-induced cardiomyopathy. The characteristic triad in this syndrome is as follows:

  1. induction with rapid atrial pacing during EPS,
  2. RBBB morphology and commonly left-axis deviation (origin in posterior fascicular area), and
  3. absence of structural heart disease.

The VT usually occurs at rest, but catecholamine sensitivity has been described. Debate has focused on whether this arrhythmia is a triggered (adenosine-sensitive) or re-entrant (verapamil-sensitive) phenomenon.1,2 The course of the arrhythmia is usually benign, unless it causes tachycardiomyopathy. Therapy consists of calcium antagonists or RFCA. In this patient, successful RFCA in the posterior midseptal region of the left ventricle, somewhat more proximal than usual, was performed. This may explain the ‘classical’ RBBB morphology in lead V1, and why the left-axis deviation is less exaggerated than normal.