Sex: M
Vaccine: HEP, HEP
Symptoms: Electrocardiogram abnormal, Myocardial infarction, Patient isolation, Pyrexia, Respiratory viral panel
Clinical narrative: COVID-19; Fever; Fever; This case was reported in a literature article.   Co-suspect products included Hepatitis B vaccine for prophylaxis.   The patient's past medical history included syncope (Family History) (Notably, the patient's younger brother had a similar episode approximately a year ago). Concurrent medical conditions included brugada syndrome, syncope and loss of consciousness.   On an unknown date, the patient received the 1st dose of Hepatitis B vaccine and the 2nd dose of Hepatitis B vaccine. On an unknown date, not applicable after receiving Hepatitis B vaccine and less than a week after receiving Hepatitis B vaccine, the patient experienced covid-19 (serious criteria GSK medically significant), fever and fever. The patient was treated with paracetamol (Tylenol). (Dechallenge was positive). On an unknown date, the outcome of the covid-19 was unknown and the outcome of the fever and fever were recovered/resolved.   The reporter considered the fever to be related to Hepatitis B vaccine. The reporter considered the covid-19 and fever to be related to Hepatitis B vaccine.  Additional details were provided as follows: This case was reported in a literature article and described the occurrence of fever in a 49-year-old male patient, who was vaccinated with unspecified Hepatitis B vaccine (manufacturer unknown) for prophylaxis. The patient without significant medical history presented after an episode of syncope. A colleague witnessed the patient suddenly lose consciousness while sitting in chair at work. The patient regained consciousness after 1-2 minutes with no postictal symptoms. The patient had previously unrecognized Brugada syndrome. The patient denied similar episodes in the past and also denied recent travel or sick contacts. Notably, the patient's younger brother had a similar episode of syncope approximately a year ago; there was no family history of sudden cardiac death. No information on patient's concomitant medication was provided. On an unspecified date, 48 hours prior to presentation, the patient received 2nd dose of unspecified Hepatitis B vaccine (administration route and site unspecified; batch number not provided). The age of vaccination was not provided but it could be 48 years or 49 years. On an unspecified date, an unknown period after the vaccination, the patient reported a day of subjective fevers, which attributed to hepatitis B vaccination. The patient had experienced a similar reaction after the 1st (first) injection a month prior. Upon presentation, the patient was afebrile with otherwise stable vital signs. An ST-elevation myocardial infarction was called following acquisition of his first electrocardiogram (ECG) and the patient was taken for urgent coronary angiogram, which showed normal coronary arteries. Transthoracic echocardiogram was performed, which showed preserved cardiac function with no anatomic abnormalities. No pericardial or pleural effusions were noted. The patient was admitted for further evaluation. Overnight, the patient spiked a fever of 102 degree F with ECG changes. Given the persistent fevers overnight, the patient was placed on airborne isolation and tested for COVID-19 (UTM: Viral Transport). The patient's fever improved with Tylenol and the patient remained asymptomatic with no respiratory symptoms, including cough and dyspnea. With defervescence, the patient's ECG changes were noted. There were no significant arrhythmic events, including premature ventricular contractions and non-sustained ventricular tachycardia observed on telemetry. The respiratory viral panel and blood cultures were unremarkable. Approximately 24 hours after the viral swab was collected, the patient tested positive for COVID-19. The patient remained in airborne isolation for 7 days owing to persistent fevers but had no respiratory symptoms. The patient was discharged with a LifeVest  with plan for outpatient cardiac magnetic resonance imaging and eventual implantation of a subcutaneous defibrillator when cleared from home quarantine. The medical staff in contact with the patient was screened and high-risk staff members were sent for the COVID-19 tests and quarantined. The author commented, Fever, alcohol, and medications causing sodium channel blockade are well-described provocative triggers that may incite arrhythmia in patients with Brugada syndrome. Patients with the Brugada syndrome, a combination of the Brugada ECG pattern, clinical symptoms, and/or pertinent family history commonly present with an episode of syncope or aborted sudden cardiac arrest from ventricular arrhythmia. Discerning the difference between Brugada syndrome and the Brugada pattern with no relevant clinical features is important for patient management. An implantable cardioverter-defibrillator implantation is a class 1 indication in patients with Brugada syndrome who survived a cardiac arrest and/or who have a history of spontaneous sustained ventricular tachycardia. On the other hand, asymptomatic patients with the Brugada ECG pattern but no clinical signs and family history suggestive of Brugada syndrome do not benefit from a defibrillator. In patients without a clear indication for an implantable cardioverter-defibrillator but presenting with high clinical suspicion for Brugada syndrome, other clues may help guide treatment. Provocative triggers such as fever, alcohol, and medications may unmask a type 1 Brugada ECG pattern. For instance, a patient with a type 2 Brugada ECG pattern at rest presenting with a fever and a "coved" ST elevation resembling a type 1 Brugada ECG pattern may be diagnosed with Brugada syndrome without an antiarrhythmic drug challenge. Fever is shown to precipitate arrhythmia in patients with Brugada syndrome, and 1 study showed that more than half of the study cohort experienced syncope or cardiac arrest in the setting of a fever. The biophysical properties of the cardiac sodium channel worsen at higher temperatures. Although the functional decline in mutated sodium channels in patients with Brugada syndrome from a physiological temperature to a higher temperature may be minimal, the loss of function of the intact sodium channels may clinically translate into a fever-induced arrhythmia. The severe inflammatory response to COVID-19 results in a febrile illness in the vast majority of patients. As shown in our case, COVID-19- induced fever led to symptomatic Brugada syndrome. The author concluded, Symptomatic COVID-19 infection is typified by high fever, a known precipitant of arrhythmia in patients with Brugada syndrome. In addition to standard isolation procedures for patients diagnosed with COVID-19, those with known or suspected Brugada ECG patterns may warrant more aggressive antipyretic therapy and serial screening ECGs. In addition, when managing a febrile patient with syncope, an ECG must be a part of the evaluation. Defibrillator implantation should be strongly considered in individuals with a provoked type 1 Brugada ECG pattern.