RHYTHM PUZZLE

The AV-node revisited

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A 28-year-old female was referred with complaints ofpalpitations. She had been suffering from attacks of sudden rapid heart rate since childhood, often precipitated by stress or exertion. Attacks usually lasted at least several minutes and stopped abruptly, sometimes due to squatting or Valsalva manoeuvres. Incidence varied greatly, but was no more than weekly. The patient had never experienced polyuria or syncope during an attack. Her medical history was otherwise T.A. Simmrs. A.A.M. Wida. Academic Medical Centre, Meibergdreef9, 1105 AZ Amsterdam. Address for correspondence: T.A. Simmers. E-mail: [email protected]

474

unremarkable, with the exception of Crohn's disease. Physical examination, resting 12-lead ECG, chest Xray, cardiac ultrasound and laboratory work-up were all normal. Because she was reluctant to take medication, the patient had requested catheter ablation. Her tachycardia occurred both spontaneously and was easily inducible; figure 1 is an example. The procedure and diagnosis are discussed in the answer to the puzzle - at this point we can give away that radiofrequency catheter ablation was successful, according to hard electrophysiological endpoints, and uncomplicated. Soon after, however, the patient experienced recurrent palpitations. Attacks were always related to exercise, shorter than before treatment (no more than one or two minutes) but more frequent Netberlands Heart Journal, Volume 11, Number 11, November 2003

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detail in the answer; this time cryoablation was performed successfulfly. Five months later, the patient is free of arrhythmia and off drugs. What would your diagnosis be for each of these arrhythmias?um

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200347

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475

Answer to rhythm puzzle (page 474)

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Arrhythmia I Ift aVF The patient's original history is classic: the sudden onset and cessation of attacks and effect of VI M vagal manoeuvres suggest a reA" A A" entrant tachycardia, most probably hRA,p involving the AV node. Indeed, arrhythmia number (our patient's MAP 1,2 original problem) is a narrow QRS v tachycardia with a rate of approxv v v 50ms AH 250ms RVA,d imately 120 beats/minute in this tracing. Longer duration or isoproterenol infusion caused the Stm * tachycardia to accelerate. The aw pm most obvious characteristic ofthis tracing is the lack of an identifiable P wave. Several differential diag- Figuulre4 SpOnmt sronset ofA VNRTdue to an atrialexhtruolk (Ae). A=atrial eectrogram, noses are possible: AV nodal re- H=Hisbundkek4tom,qram, HRA-signalfr)m cadmtiratthe bigh ihtatrium, RVAssignal entry tachycardia (AVNRT), frm cathete at doe rright ventrcular ape^ V=ventricular elctrogram. In this tracing, tde junctional ectopic tachycardia mappingcaeteris ,sitioned in tde His bundle region. Thefirstcomplex isstill sinus rbythm (JET), or atrial tachycardia with a -tta atacvAation isearliestatdxHRA This isfollowed byanatrialextrastok, which long PR interval (causing the P is ndu to dx ventrick with a considerable delaydue to itsprematurity (dx AH interval wave to be hidden in the pre- increawsfrom50M?si n sinus rhythm 250 nu afterAe). Retrgrade conduction to de atrium ceding QRS complex). Circus faOwso-no tatretrE gradeatrialactivation is now earlirat dx ow rnqhtatrium/Hisbundle movement tachycardia using a region (A'), and lat er at HRA (A"). Anterograde conduction is subsequently via the slow concealed bypass as the retrograde pa*way (hence a lon, w4H interval), rtrograde conduction via thefast pathway again (with limb is highly unlikely (even coresonding sortB A interval) and soforth. though it is a reentrant SVT involving the AV node), as this arrhythmia invariably has a longer RP interval with P of Koch's triangle. Following ablation, dual AV nodal physiology had been completely abolished, and no waves generally 'sandwiched' between two QRS complexes. Given the clinical presentation and incidence tachycardia was inducible. ofAVNRT relative to the other diagnoses, AVNRT is the most likely diagnosis in this case. In AVNRT, the Arrhythmia 2 P wave is usually hidden in the QRS complex or partially This is obviously quite a different arrhythmia: not only the patient's history has changed, but also the ECG. The seen after the QRS; in a minority of cases the P wave actually precedes the QRS complex. Ifthe P wave were most striking differences are the gradual rather than sudden starting and stopping of the tachycardia without to be visible, a superior P-wave axis would be expected due to the caudo-cranial activation of the atria. The the prerequisite extrasystole and critical PR (i.e. AH short RP and very long PRinterval in the common type interval) prolongation seen in AVNRT, indicating of AVNRT are due to anterograde conduction via a automaticity rather than reentry as the underlying slow pathway, and retrograde conduction via a fast mechanism, and dearAV dissoiation. In accordance, the pathway; in other words, dual AV nodal physiology is tachycardia could be neither induced nor terminated by extrastimuli at electrophysiological study. It occurred a prerequisite for this reentrant arrhythmia. At electrophysiological study, an accessory pathway could spontaneously, particularly during isoproterenol infusion. be excluded and dual AV nodal pathways demonstrated. There is only one possible diagnosis for this combination Tachycardia occurred both spontaneously and could be of automaticity and AV dissociation with normal QRS easily induced with an atrial extrastimulus, conditional width and morphology, namely junctional ectopic tachycardia (JET). Figure 5 shows spontaneous cessation to a critical delay in AH (atrium to His) interval. Figure 4 shows spontaneous onset ofthe tachycardia, which was of JET in our patient. Due to the closer relationship diagnosed as AVNRT. Radiofrequency catheter ablation between the focus of the arrhythmia and the compact AV node in JET than in AVNRT, cryoablation was was performed, aimed at the slow pathway in the base h

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Netherlands Heart Joumal, Volume I1, Number 11, Novanber 2003

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