Title : Not your average heartbreak: a unique case of fulminant myocarditis due to coxsackie b virus in an immunocompetent male
Background:The clinical presentation of viral myocarditis is variable and is an important cause of cardiomyopathy worldwide. In some cases, symptoms are minimal consisting of mild fatigue and chest discomfort, where other cases result in fulminant heart failure, arrythmia and sudden cardiac death. Here, we present a case of fulminant myocarditis an immunocompetent 19-year-old man secondary to coxsackie B virus.
Case:A 19-year-old male with no past medical history presented with malaise and pleuritic chest pain associated with new fevers and chills. He denied any respiratory symptoms. On arrival, he febrile and tachycardic. Computed tomography was negative for acute pulmonary embolism, and a transthoracic echocardiogram (TTE) revealed a structural normal heart with an ejection fraction (EF) of 68%. An infectious workup was started, and he was empirically treated with broad spectrum antibiotics and fluid resuscitation.The following day, the he became hypotensive that was not responsive to fluid resuscitation and developed a new oxygen requirement and bibasilar crackles. A chest x-ray revealed an enlarged cardiac silhouette. This prompted a repeat TTE to be performed, showing a new decline in EF to 32% as well as moderate to severe tricuspid regurgitation. ECG was unremarkable. He was empirically started on colchicine and ibuprofen and was then transferred to our tertiary care center to be managed in the cardiac intensive care unit (CICU).On arrival to the CICU, he was still tachycardic to the 140s and febrile and hypotensive. High sensitivity troponin was elevated to the 700s and a TTE showed a further reduced EF to 20%, with cold extremities and evidence of end-organ dysfunction with poor mentation and new acute kidney injury. Given concern for acute cardiogenic shock, he was started on empiric milrinone therapy.
He underwent a right heart catheterization revealing a cardiac output of 3.7 and cardiac index of 1.8. A cMRI was performed which was showed acute myocarditis. He underwent an endomyocardial biopsy revealing minimal cardiac myocyte hypertrophy with minimal interstitial fibrosis and rare perivascular lymphocytes, notably negative for lymphocytic and giant cell myocarditis. A few days into his course, he developed ulcerated lesions on his right hand and hard palate, concerning for Hand, Foot and Mouth disease secondary coxsackie virus. Positive titers to coxsackie B virus confirmed the diagnosis.
Over the week, he was able to be weaned off milrinone and his cardiogenic shock had resolved. He was initiated on guideline directed medical therapy, with repeat TTE showing improved EF to 54% without evidence of tricuspid regurgitation. He was shortly discharged after his clinical improvement and set up with outpatient advanced heart failure follow up.
Conclusion:Fulminant myocarditis is a very rare and potentially fatal complication of coxsackie virus infection. Elucidating the etiology of myocarditis is challenging and is often critical when there is possibility for lymphocytic or giant cell myocarditis. Although the management is generally supportive when a viral etiology is identified, the prompt recognition of acute heart failure and initiation of advanced therapies may be necessary, even in immunocompetent patients. These patients should be started on GDMT for cardiac recovery and prevention of cardiomyopathy even when EF has recovered.
- Prompt recognition of fulminant myocarditis in immunocompetent patients and the use of ionodilator therapy in the support of acute heart failure
- Understand that viral prodromes may be absent prior to the presentation of fulminant myocarditis when a viral etiology is suspected or identified
- Importance of guideline directed medical therapy after fulminant myocarditis
- Review the role of advanced cardiac imaging and endomyocardial biopsy in the diagnosis and treatment of myocarditis