Key result
Procainamide challenge clarifies suspected Brugada syndrome in two young men with type 2 EKG patterns.
Why the study?
Identifying and working up non-ischemic causes of ST-segment elevation, such as channelopathies and genetic conditions, presents a challenge to primary care providers.
Does procainamide challenge improve diagnostic confirmation of Brugada syndrome in young patients with suspicious EKG findings?
Case Report (n=2)
No
Does procainamide challenge improve diagnostic confirmation of Brugada syndrome in young patients with suspicious EKG findings?
Procainamide challenge is a useful diagnostic tool to risk stratify and confirm Brugada syndrome in patients presenting with suspicious type 2 EKG patterns.
May support procainamide challenge for Brugada diagnosis in select cases; hypothesis-generating and should not yet change practice.
While a large proportion of ST-segment elevation on EKG is related to myocardial ischemia, the differential diagnosis must include pericarditis, channelopathies, and various genetic conditions. Identifying and working up such abnormalities present a challenge to primary care providers (PCPs). We present two clinical cases of young male patients with ST-segment elevation in anteroseptal leads suspicious for Brugada syndrome and show how to risk stratify and manage them. Our first case presents a 23-year-old male with no past medical history with acute onset substernal chest pain, shortness of breath, and palpitations. Initial workup revealed negative serial troponins and normal B-type natriuretic peptide (BNP). The EKG revealed ST elevation in lead V2. An evaluation for Brugada syndrome was pursued. Upon completion of a procainamide challenge, it was determined that he did not have Brugada syndrome and was shortly discharged. Our second case presents a 33-year-old male with no pertinent cardiac medical history who presented to an outpatient cardiology clinic after discovering an incidental ST elevation in V2 on EKG. His family history was negative for early atherosclerotic cardiovascular events or sudden cardiac death. The patient's initial workup was negative. Suspicion for Brugada syndrome leads to performing a procainamide challenge, which was significant for ST changes in the anterolateral leads. He was asymptomatic during the challenge and initial presentation, and no further intervention was indicated. He was advised to avoid sodium channel blocking medications and treat any fevers and was sent for genetic testing. These cases illustrate the importance of maintaining an appropriate suspicion for Brugada syndrome in young patients with minimal ischemic risk factors. We discuss a guideline-directed algorithmic workup for PCPs in suspicious individuals. Stratifying patients based on the presence of symptoms, history of tachyarrhythmias, and EKG findings before and after drug challenge allows physicians to guide further management of these patients.
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Blotner et al. (2022) conducted a case report in Suspected Brugada Syndrome (n=2). Procainamide challenge was evaluated on Conversion to type 1 Brugada pattern on EKG. A procainamide challenge in two young men with suspected Brugada syndrome based on type 2 EKG patterns ruled out the condition in one patient and confirmed it in the other by inducing a type 1 pattern.
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