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Ventricular Fibrillation in an Afebrile COVID-19 Patient Presenting With Transient Type-I Brugada Pattern
Judah A Kreinbrook1, Annalia Foster2, Luis Paulino3
1School of Medicine, Duke University, Durham, USA.
Insights
COVID-19 patients may develop Brugada phenocopies, mimicking Brugada syndrome arrhythmias. This case highlights the risk of ventricular fibrillation in afebrile COVID-19 patients with transient type-I Brugada patterns, emphasizing vigilance.
Area of Science:
- Cardiology
- Infectious Diseases
- Genetics
Background:
- COVID-19 increases arrhythmia risk, including atrial and ventricular arrhythmias.
- Brugada syndrome (BrS) presents a baseline risk for ventricular arrhythmias (VF), particularly during febrile illnesses.
- Brugada phenocopies (BrP) mimic BrS ECG patterns and can be triggered by various conditions, including infections.
Observation:
- A SARS-CoV-2 positive patient presented with type-I Brugada pattern (BP) during acute illness.
- The patient experienced hypoxemia, electrolyte abnormalities, and acute kidney injury.
- Ventricular fibrillation (VF) occurred days later in an afebrile state, despite normalized ECG and electrolytes.
Findings:
- The case demonstrates transient type-I BP in afebrile COVID-19, leading to VF.
- Distinguishing BrS from BrP in acute illness is challenging due to similar ECG presentations.
- ECG normalized post-treatment, but type-I BP recurred, exacerbated by bradycardia.
Implications:
- This case underscores the importance of guideline-directed management and vigilance for arrhythmias in COVID-19 patients with type-I BP.
- Further research is needed to determine the prevalence and outcomes of type-I BP in COVID-19.
- Genetic testing is recommended for definitive BrS diagnosis when possible.
Abstract:
COVID-19 has been associated with an increased risk of both atrial and ventricular arrhythmias. Brugada syndrome (BrS), an inherited sodium channelopathy presenting with a characteristic ECG morphology, confers a baseline risk of ventricular arrhythmias such as ventricular fibrillation (VF), especially during febrile illnesses. However, mimics of BrS, termed Brugada phenocopies (BrP), have been noted in association with fever, electrolyte abnormalities, and toxidromes outside of viral illness. Such presentations manifest the same ECG pattern, the type-I Brugada pattern (type-I BP). Thus, the acute stage of an illness such as COVID-19, when accompanied by a first-time presentation of type-I BP, may not result in a certain diagnosis of BrS versus BrP. Thus, expert recommendations are to anticipate arrhythmia regardless of the presumed diagnosis. Here we demonstrate the importance of these guidelines and a novel report of VF in the setting of a transient type-I BP in afebrile COVID-19. We discuss the potential factors which may have triggered VF, the presentation of isolated "coved" ST elevation in V1, and the difficulty of BrS versus BrP diagnosis in acute illness. In summary, a SARS-CoV-2 positive 65-year-old male without significant cardiac history for BrS presented with type-I BP after two days of shortness of breath. Hypoxemia, hyperkalemia, hyperglycemia, elevated inflammatory markers, and acute kidney injury were present. After treatment, his ECG normalized; however, aborted VF occurred days later while afebrile and normokalemic. Follow-up ECG again revealed a type-I BP, which also became more apparent during an episode of bradycardia, a classic finding in BrS. This case suggests that there is room for larger studies to determine the prevalence and outcomes when type-I BP presents in acute COVID-19. When possible, genetic data should be obtained to confirm BrS, a notable limitation in our case. Regardless, it corroborates guideline-directed clinical management, with heightened vigilance for arrhythmia in such patients until full recovery.
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