Author + information
- Received October 28, 2016
- Revision received November 11, 2016
- Accepted November 17, 2016
- Published online August 21, 2017.
- aDepartment of Internal Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
- bDepartment of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Benjamin Khazan, Department of Internal Medicine, Thomas Jefferson University Hospital, 723 Bainbridge Street, Apartment B, Philadelphia, Pennsylvania 19147.
A 48-year-old Vietnamese man presented with epigastric pain and pre-syncope. He described a constant pain starting 2 days prior to admission that radiated to his back. One week earlier, he had presented to an emergency department with complaints of dizziness and lightheadedness, typically when going from a lying to a standing position. He denied any history of loss of consciousness, falls, or palpitations, and had no family history of sudden death.
An initial electrocardiogram (Figure 1A) revealed a coved ST-segment elevation and T-wave inversion in V1 with ST-segment elevations also present in V2 and V3 (consistent with a type I Brugada pattern). A narrow QRS duration appeared in the majority of complexes; however, 3 appeared wide due to a delta wave with a negative deflection in aVL and without a left bundle branch morphology, suggesting a left anterolateral wall accessory pathway (1). Subsequent electrocardiograms demonstrated the same Brugada pattern with a narrow QRS interval (Figure 1B), and an atypical Brugada pattern occurring during a delta-wave–induced wide QRS interval (Figure 1C). A transthoracic echocardiogram displayed normal left ventricular functions without valvular disease or any wall motion abnormalities. Other than a mild leukocytosis, laboratory studies, including serum electrolytes and cardiac enzymes resulted within normal limits.
Individually, the presence of a Brugada pattern and that of an accessory pathway remain uncommon entities, with prevalences of roughly 0.05% to 0.1% and 0.15%, respectively (2). The co-occurrence of these 2 phenomenon, therefore, may be as rare as 1 to 15 in 10 million (3). First described by Eckardt et al. (4) in 2001, only a few case reports have described simultaneous electrocardiographic evidence of these anomalies, with several others requiring provocation (by stress testing, utilization of class I antiarrhythmics, or accessory pathway ablation) for concurrent visualization (2–6). This case provides another scarce example of synchronous Brugada and pre-excitation patterns.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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- Received October 28, 2016.
- Revision received November 11, 2016.
- Accepted November 17, 2016.
- 2017 American College of Cardiology Foundation