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A man in his late 60s with a medical history of dyslipidemia presented to the emergency department (ED) with nonprodromal syncope resulting in facial trauma. He was otherwise in good health. In the ED he was asymptomatic with normal vital signs. Physical examination findings were unremarkable except for mild facial trauma sustained during the fall. Laboratory test results were within normal limits. An initial electrocardiogram (ECG) done in the ED demonstrated normal sinus rhythm and ventricular preexcitation mediated by a left accessory pathway (Figure 1A). He was admitted to the cardiology unit under telemetry for consideration of an electrophysiology (EP) study and radiofrequency ablation. While awaiting the procedure, he presented to the nursing station stating that he felt “funny” and had a witnessed syncopal episode, striking his head on the ground. He regained consciousness in a few seconds. Telemetry obtained immediately following the syncopal event while the patient was still on the ground is shown in Figure 1B. Vital signs taken immediately after the fall were stable with a blood pressure of 92/64 mm Hg. After the patient was clinically assessed, telemetry from the moments immediately preceding the syncopal event was obtained (Figure 1C).
A, Initial ECG showing normal sinus rhythm and ventricular preexcitation mediated by a left accessory pathway. A short PR interval and Delta waves are seen in most leads. The presence of a positive Delta wave in lead V1 (right bundle branch blocklike pattern) suggests the pathway is located in the mitral ring. This ECG presents minimum preexcitation, making localization of the pathway by a surface ECG less precise. B, Telemetry rhythm strip obtained immediately postsyncopal event. C, Rhythm strip from the moments directly preceding the syncopal episode demonstrating progressive sinus bradycardia followed by a sinus arrest of 4.73 seconds, an escape beat and a secondary pause of 4.68 seconds.
Questions: What is the cause of this patient’s syncope? What should be done next?
The telemetry strip from immediately following the syncopal event (Figure 2) shows an apparent wide complex tachycardia. On closer inspection, native QRS complexes (Figure 2, red triangles) can be seen marching through the wide complex signals (Figure 2, black stars). These findings, coupled with the patient’s stable vital signs, suggested that the wide-complex signal was likely owing to artifact, in this case caused by the fall and postsyncopal myoclonic jerks. The rhythm strip from the moments directly preceding the syncopal episode (Figure 1C) demonstrates progressive sinus bradycardia followed by a sinus arrest of 4.73 seconds, an escape beat, and a secondary pause of 4.68 seconds. This pattern strongly suggests cardioinhibitory vasovagal syncope as the cause of this patient’s syncope.
Telemetry rhythm strip obtained immediately postsyncopal event demonstrating native narrow QRS complexes (red arrowheads) marching through the wide complex signals (black stars).
A neck collar was applied to the patient. Follow-up radiography and computed tomographic (CT) scan results were negative for fractures or intracranial bleed. The following day the patient underwent an electrophysiology study demonstrating an accessory pathway located in the left lateral aspect of the mitral ring. The anterograde refractory period of the pathway was 230 ms. Ablation of the pathway via a transseptal approach was successful. Owing to recurrent syncope associated with head trauma, a dual chamber pacemaker was implanted. The patient was discharged the next day with scheduled follow-up in the cardiac device clinic.
Syncope in the context of Wolff-Parkinson-White (WPW) syndrome raises the specter of rapid conduction of atrial fibrillation (AF) through an accessory pathway with degeneration into ventricular fibrillation and possible sudden cardiac death.1 Indeed, for some patients, the first manifestation of WPW may be syncope or aborted sudden cardiac death.2 Syncope in patients with WPW is considered one of the strongest clinical indicators for an EP study with potential radiofrequency catheter ablation.3 In this case, an EP study confirmed rapid anterograde conduction over the accessory pathway, necessitating ablation. During the witnessed syncopal event, the constellation of a wide complex rhythm in the context of syncope and known WPW immediately led the medical team to believe that the cause of the syncope was preexcited atrial fibrillation or ventricular tachycardia. However, careful analysis of the telemetry rhythm strip revealed that the patient was actually in sinus rhythm. This diagnosis was based on the visualization of narrow QRS complexes at regular intervals marching through the wide-complex artifact. Looking further back through the saved telemetry revealed that the true mechanism of syncope in this patient was likely cardioinhibitory vasovagal syncope based on progressive sinus bradycardia followed by prolonged sinus arrest. The decision to implant a permanent pacemaker in patients with vasovagal syncope is nuanced and requires careful consideration of patient-specific factors. For many patients, lifestyle changes such as hydration or compression stockings and education may be effective. In this case, 2 episodes of syncope resulting in head trauma owing to excessive cardioinhibitory response led to the decision of permanent pacemaker implantation.4
Wide complex tachycardias in patients with WPW are most commonly supraventricular arrythmias conducted by an accessory pathway or, less commonly, ventricular tachycardia; however, artifact should always remain as part of the differential diagnosis.5 Similarly, although syncope in a patient with WPW should appropriately spark concerns of a rapidly conducted supraventricular tachycardia, patients with syncope and known WPW may present with alternative causes of syncope. Although short-term telemetry may not usually provide a good diagnostic yield in patients with syncope of unknown cause, occasionally, hospital monitors can be useful in making the diagnosis.6
Nonprodromal syncope and WPW should raise concern that the etiology of syncope may be an atrial tachyarrhythmia with rapid ventricular preexcitation via the accessory pathway.
Wide complex tachycardias in patients with WPW are usually arrhythmias conducted by the accessory pathway and, less frequently, ventricular tachycardia. However, artifact should always remain a part of the differential diagnosis.
Patients with WPW may also present with alternative causes of syncope in addition to rapidly conducted supraventricular tachycardia.
Most commonly vasovagal syncope does not require a permanent pacemaker; however, significant cardioinhibitory response with head trauma during asystole is an indication for permanent pacemaker implantation.
Corresponding Author: Adrian Baranchuk, MD, FACC, FRCPC, FCCS, Professor of Medicine, Cardiac Electrophysiology and Pacing, Kingston General Hospital, Queen's University, 76 Stuart St, Kingston, ON K7L 2V7, Canada (email@example.com).
Published Online: February 4, 2019. doi:10.1001/jamainternmed.2018.7646
Conflict of Interest Disclosures: None reported.
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Alexander B, Haseeb S, Baranchuk A. Syncope in a Patient With Wolff-Parkinson-White Pattern: Not All That Glitters Is Gold. JAMA Intern Med. 2019;179(3):418–420. doi:10.1001/jamainternmed.2018.7646
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