Fulminant Coxsackievirus B3 myocarditis can rapidly progress to severe dilated cardiomyopathy, life-threatening arrhythmias, and critical thromboembolic complications requiring aggressive multidisciplinary management.
Coxsackievirus B3 (CVB3) commonly induces fulminant viral myocarditis (VM), a significant diagnostic dilemma. The onset of fulminant VM is characterized by nonspecific flu-like symptoms that can be misinterpreted as other diseases, such as acute coronary syndrome (ACS) or cardiomyopathy. Fulminant VM is typically described as rapid progression to acute biventricular failure and cardiogenic shock. A low threshold for suspicion, along with a multidisciplinary approach to this condition, is essential for early recognition and aggressive treatment.We present the case of a previously healthy 23-year-old female who presented with fulminant CVB3 myocarditis. The disease progressed to acute, severe dilated cardiomyopathy. Despite maximal therapy, the patient experienced a catastrophic natural history of life-threatening ventricular arrhythmias and complete heart block. Furthermore, she had rapid development of critical thromboembolic complications, such as acute ischemic stroke due to LV thrombosis and acute bilateral pulmonary embolism. Serology was positive for CVB3 (IgM) with a fourfold increase in IgG titers. The diagnosis was supported by an endomyocardial biopsy showing lymphocytic myocarditis and the positivity of myocardium for CVB3 viral RNA.This case highlights the importance of maintaining a high degree of suspicion, which leads to timely diagnosis and individualized immunomodulatory therapy based on tissue diagnosis, along with rapid neurologic intervention to minimize thromboembolic and neurological sequelae. The serious course of the illness became evident when refractory cardiogenic shock occurred on hospital day 28, despite maximal supportive therapy.
Jahoda et al. (Wed,) studied this question.