B y p a s s Tra c t i n Pa t i e n t w ith Palpitat ions Mark E. Josephson, MD KEYWORDS
The patient is a 29-year-old man with a 15-year history of palpitations. He was the product of a normal pregnancy and was completely healthy during his adolescence. He had no family history of sudden cardiac death, atrial fibrillation, or any other atrial arrhythmia. Both parents are alive and well and three siblings have no arrhythmias. The episodes of palpitations could occur at rest or exercise. Occasionally, they would be precipitated by an earlier beat producing a thump in his chest associated with pulsation in his neck and shortness of breath. His palpitations were always regular and he never had any syncope. He was referred for evaluation. His physical examination was entirely normal and his electrocardiogram (ECG) is shown in Fig. 1. A wide QRS is present with a slurred upstroke suggesting a delta wave. The P wave is normal in morphology and is completed before the beginning of the delta wave. Where does the ECG suggest the bypass tract is located? To find the location of the bypass tract one needs to assess the first 40-millisecond vector of the delta wave.1 This is best done if there is maximum pre-excitation. Maximum pre-excitation is rather unlikely, however, in view of the completion of the P wave before any delta wave, because this should allow some component of propagation over the normal conducting system unless there is a primary abnormality in the normal conducting system. The delta wave in leads 2, 3, and F are positive, suggesting the superiorly located bypass tract. The delta wave in lead 1 also looks somewhat positive. This might lead one to suggest a right-sided pathway except when one looks at
AVL where the initial vector is isoelectric to negative, suggesting a left-sided bypass tract. Moreover, the delta waves are positive across the precordium, further suggesting a left-sided pathway is present. Nonetheless, the somewhat confusing pattern seen in sinus rhythm should raise the suspicion that more than one bypass tract might be present. Because the presence of the bypass tract does not necessarily mean that the tachycardia that caused palpitations was related to the bypass tract, an electrophysiology study was recommended. During placement of the catheters a tachycardia was initiated. The 12-lead ECG of that tachycardia is shown in Fig. 2. The tachycardia has a slightly wide QRS with the right bundle branch block pattern and no delta wave is seen. During a supraventricular tachycardia it is critical to look for P waves to make sure first that the tachycardia diagnosis is compatible with circus movement tachycardia using a bypass tract and then to determine, if possible, where the site of atrial activation is beginning. Careful analysis of the ECG suggests a P wave following each QRS with a very short RP interval.2 A short RP interval is most commonly seen with circus movement tachycardia but does not exclude atrial tachycardia with a long PR or atypical forms of atrioventricular (AV) nodal tachycardia.3 Carefully analysis of the P wave morphology, however, shows that in lead 1 and AVL it is negative and in lead 3 it is positive. This activation sequence is consistent with activation beginning in the lateral left atrium and is consistent with retrograde conduction over a left-sided bypass tract. It is inconsistent
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Bypass tract Palpitations Wolff-Parkinson-White syndrome
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Josephson
Fig. 1. Patient’s electrocardiogram on presentation.
with AV nodal tachycardia, but does not rule out an atrial tachycardia. One important clue that this is circus movement tachycardia and not atrial tachycardia is the description of the onset of tachycardia by the patient. The description of the initiating premature beat, as a thump in his chest associated with shortness of breath and a pulsation in his neck, is consistent with a ventricular premature beat. The initiation of a tachycardia by a spontaneous ventricular premature beat during sinus rhythm is nearly diagnostic of circus movement tachycardia.4 Atrial tachycardia would not be initiated by a spontaneous ventricular premature beat. A wide complex tachycardia was also induced during the electrophysiologic study (Fig. 3). This tachycardia has a QRS morphology that is different from the sinus rhythm ECG pattern of pre-excitation and is not a typical right bundle branch block pattern that was seen during the circus movement tachycardia. The QRSs across the precordium are positive and slurred, suggesting that this tachycardia is arising somewhere in
Fig. 2. A 12-lead electrocardiogram of tachycardia.
the posterior left ventricle. Positive concordance is seen. In the inferior leads the axis is superior, suggesting that this is coming from the inferior part of the left ventricle, from anarea that would be called ‘‘left inferior paraseptal.’’ This is clearly different than the QRS during pre-excitation in sinus rhythm and also does not match the P wave morphology during orthodromic circus movement tachycardia. The atrial activation sequence in the orthodromic tachycardia showed a negative P wave in leads 1 and L and positive P in the inferior leads, opposite of the QRS vectors, which were negative in the inferior leads and positive in 1 and L. This mismatch in atrial and ventricular activation confirms the presence of two left-sided bypass tracts. Multiple bypass tracts are not uncommon.5 They may be seen in 5% to 15% of patients with Wolff-Parkinson-White syndrome (WPW). To complicate matters, dual AV nodal pathways may be observed in 30% of such patients. This gives rise to the possibility of multiple types of AV and ventriculo atrial conduction and AV nodal
Bypass Tract in Patient with Palpitations reentry in patients with WPW. One should always remember the possibility of multiple bypass tracts and coexisting different arrhythmias when evaluating patients with WPW. Thorough analysis of ECG and a detailed electrophysiology study are necessary to cure the patient of the symptoms. This patient did not have AV nodal arrhythmias. Ablation of both the left inferior periseptal and left lateral bypass tracts eliminated his symptoms.
REFERENCES
Fig. 3. Wide complex tachycardia.
1. Josephson ME. Preexcitation syndromes. In: Clinical cardiac electrophysiology: techniques and interpretations. 4th edition. Philadelphia: Wolters Kluwer/Lippincott Williams and Wilkins; 2008. 2. Zimetbaum PJ, Josephson ME. Wolff-Parkinson-White syndrome and variants. In: Practical clinical electrophysiology. Philadelphia: Wolters Kluwer/Lippincott Williams and Wilkins; 2009. 3. Cardiovascular Medicine/Cardiac Arrhythmias/Preexcitation-WPW. Up-To-Date On-Line. Available at: www.uptodate.com. Accessed February 12, 2010. 4. Bar-Cohen Y, Khairy P, Morwood J, et al. Inaccuracy of Wolff-Parkinson-White accessory pathway localization algorithms in children and patients with congenital heart defects. J Cardiovasc Electrophysiol 2006; 17:712–6. 5. Wellens HJJ, Conover M. Narrow QRS tachycardia. In: The ECG in emergency decision making. 2nd edition. Philadelphia: Saunders Elsevier; 2006.
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