A man in his early 20s presented with suspected syncope and shaking with no significant medical history. The patient fell asleep and his girlfriend tried to wake him, but he started shaking and slumped over on the ground. He denied confusion afterward but did not feel well with nausea, flushing, chest tightness, and a rapid heart rate. About 10 minutes later, he had a second syncopal episode for 2 to 3 minutes with more than 20 muscle jerks. On presentation at the emergency department, he was afebrile, blood pressure was 120/59 mm Hg, heart rate was 85 beats per min, respiratory rate was 16 breaths per min, and oxygen saturation was 96% on room air. His cardiac examination revealed normal heart sounds with no murmurs.
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Brugada type 1 syndrome with unexplained syncope
C. Implantable cardioverter defibrillator
The key to the correct diagnosis in this case was the ECG that was consistent with spontaneous Brugada type 1 morphology with more than 2-mm coved ST-segment elevation in leads V1 and V2 (Figure). Recognition of the Brugada type 1 pattern as a potential cause of cardio-arrhythmogenic syncope is important.
The incidence of the Brugada type 1 ECG pattern in the US is thought to be as low as 0.03%.1 The proposed Shanghai Score System2 can be used for the diagnosis of Brugada syndrome, which relies on ECG, clinical history, family history, or genetic test results. A score of more than 3.5 points is thought to be probable and/or definite Brugada. Brugada type 1 can present asymptomatically, in which case the management is observation. However, in those with symptomatic features, such as unexplained cardiac arrest or polymorphic ventricular tachycardia or ventricular fibrillation arrest, nocturnal agonal respirations, atrial fibrillation/flutter in patients younger than 30 years of age, or syncope of uncertain etiology, further evaluation is needed.
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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: Asad J. Torabi, MD, Division of Cardiology, Krannert Institute of Cardiology at Indiana University School of Medicine, 1800 N Capital Ave, Indianapolis, IN 46202 (firstname.lastname@example.org).
Published Online: June 8, 2022. doi:10.1001/jamacardio.2022.1313
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank Jeffrey Mossler, MD, Indiana University School of Medicine, Indianapolis, for his assistance in reviewing the manuscript; he did not receive financial compensation for his contribution. We also the patient for granting permission to publish this information.
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