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A man in his 40s was seen in clinic for a long history of palpitations. He had a history of cardiac arrest after receiving adenosine for sustained supraventricular tachycardia and tachycardia-induced cardiomyopathy. The patient was also noted to have episodes of atrial flutter. Transthoracic echocardiogram displayed a left ventricular ejection fraction of 63% and mild aortic and mitral regurgitation. Cardiac magnetic resonance imaging in sinus rhythm showed mild left ventricle thickening (up to 14 mm) and was otherwise normal. The patient was hospitalized for initiation of sotalol, given that he experienced frequent episodes of atrial arrhythmia. Figure 1A shows sinus rhythm prior to sotalol initiation. Figure 1B shows telemetry during administration of sotalol.
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Latent accessory pathway (Wolff-Parkinson-White syndrome)
B. Electrophysiology study and catheter ablation
Prior to sotalol loading, the 12-lead electrocardiogram (ECG) (Figure 1A) showed sinus rhythm at 57 beats per minute with a normal axis and QT interval. There were no Q waves in the lateral leads. There were inferolateral precordial T-wave abnormalities. With sotalol loading, the telemetry strip (Figure 1B) revealed widening of the QRS complex. The differential diagnosis included (1) rate-related aberrancy, (2) idioventricular rhythm, (3) phase 4 aberrancy, and (4) preexcitation from an atrioventricular pathway. Phase 3 or 4 aberrancy was unlikely because the sinus rate had not changed significantly. An idioventricular rhythm resulting in this finding would have to be perfectly isorhythmic to maintain constant PR intervals. The short, fixed PR interval with wide QRS complex makes ventricular preexcitation from an atrioventricular pathway (Wolff-Parkinson-White syndrome) the most likely diagnosis.1 Electrophysiology study and catheter ablation provide high likelihood of cure. Amiodarone is not indicated in a young patient with Wolff-Parkinson-White syndrome; ST segment changes are due to altered ventricular repolarization owing to preexcitation rather than ischemia. Exercise treadmill testing is not useful with lack of ischemia or exposure to medications with use dependence (class I).
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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.
Corresponding Author: Albert J. Rogers, MD, MBA, Department of Medicine, Stanford University, 780 Welch Rd, MC 5773, Stanford, CA 94305 (email@example.com).
Published Online: January 26, 2022. doi:10.1001/jamacardio.2021.5788
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank the patient for granting permission to publish this information.
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