Key result
Standard heart failure therapy resolves acute systolic dysfunction from Coxsackie B4 myocarditis and EBV reactivation.
Case Report (n=1)
No
Answers are grounded in this paper and cite their sources.
Highlights that Coxsackie B virus myocarditis can masquerade as meningitis and trigger Epstein-Barr virus reactivation, requiring prompt echocardiographic and serological workup when troponin is elevated despite normal EKG findings.
BACKGROUND Myocarditis, defined as inflammation of myocardial tissue of the heart, is an uncommon cardiac presentation and is due to a variety of causes. It affects 1% of the US population, 50% of which is caused by coxsackie B virus. Cardiac tissue is the prime target, and destruction of myocardium results in cardiac failure with fluid overload. CASE REPORT Our patient was a 57-year-old woman with fever, headache, neck pain, and generalized malaise. Her white blood cell count was 13×10³ cells/mm³. Interestingly, lumbar puncture ruled out meningitis. An echocardiogram to evaluate elevated troponin revealed an ejection fraction of 30% with severe left ventricular global hypokinesis without valvular vegetations consistent with new-onset systolic heart failure. Cardiac MRI showed a small pericardial effusion with bilateral pleural effusion. As she continued to be febrile, a viral panel was ordered, revealing coxsackie B4 antibody titer of 1: 640 (reference: >1: 32 indicates recent infection) with positive Epstein-Barr virus deoxyribonucleic acid by PCR, consistent with viral myocarditis. CONCLUSIONS Coxsackie B virus myocarditis is rarely recognized and reported by the general internist in clinical practice, so we would like present our experience with an interesting clinical presentation of the viral prodrome. An estimated 95% people in the US are infected with Epstein-Barr virus by adulthood, but it remains dormant in memory B lymphocytes. Recirculation of these B cells in lymphoid tissue stimulated by antigens, which in our case is coxsackie B virus; they differentiate into plasma cells, and the production of Z Epstein-Barr replication activator protein (ZEBRA) increases viral replication, thus explaining the positive EBV DNA measured by PCR.
No takes yet. Share an insight, caveat, or question.
Atti et al. (2017) conducted a case report in Coxsackie B4 myocarditis and hepatitis with reactivated Epstein-Barr virus causing new-onset systolic heart failure (n=1). Guideline-directed heart failure medical therapy (metoprolol succinate, lisinopril, furosemide, spironolactone) and supportive care was evaluated on Clinical symptom resolution and recovery from viral myocarditis. Coxsackie B4 virus infection (titer 1:640) with EBV reactivation presented as a meningitis-like prodrome and acute systolic heart failure (LVEF 30%), resolving with standard heart failure therapy.
Synapse has enriched 10 related papers. Consider them for comparative context: