Fulminant Lymphocytic Myocarditis Possibly Secondary to Rhinovirus Infection in an Adolescent Female

Abstract

Introduction Rhinovirus is responsible for a large number of upper respiratory tract infections annually. While viral infection is a well-known cause of dilated cardiomyopathy (DCM), rhinovirus-associated myocarditis is not well understood. This is a case of a young woman who suffered cardiogenic shock due to fulminant lymphocytic myocarditis and diagnostic testing noting the presence of rhinovirus, suggesting potential causation. Case Description During late autumn, a healthy 19 year old woman noted 1 week of progressive exertional dyspnea associated with a non-productive cough and epigastric pain. She was diagnosed with a new-onset DCM at a community hospital and transferred to our tertiary center for further management. Urgent echocardiography demonstrated severe biventricular systolic dysfunction and chamber dilation but normal wall thickness. Severe tricuspid valve insufficiency was present secondary to torn chordea tendinae causing a flail septal leaflet Cardiac magnetic resonance imaging revealed diffuse biventricular sub-endocardial delayed enhancement concerning for fulminant myocarditis. Viral respiratory testing was positive for rhinovirus alone. Other laboratory diagnostic data was unremarkable. Cardiac catheterization was conducted, demonstrating the absence of coronary artery disease, but severely impaired cardiac output with an index of 1.65 L/min/m2 and moderately elevated left sided filling pressures. An endomyocardial biopsy confirmed lymphocytic myocarditis with extensive necrosis and fibrosis and CD68 positivity indicating macrophage predominate infiltrate. On the night of hospital day 3, hemodynamic instability was noted with an accelerating frequency of ventricular ectopy. Dobutmaine was started and the initiation of temporary mechanical support was attempted with Impella, However, this was aborted due to catheter occlusion of a small diameter femoral artery given her small stature. Therefore, central VA ECMO was placed. An expedited heart transplant evaluation was begun which she received 8 days later. Gross pathology of the explanted heart confirmed the diagnosis, with a mixed T-cell and B-cell lymphocytic infiltrate. Several months post-transplant, she is thriving. In the absence of other compelling causes of DCM, rhinovirus remains a possible culprit. Viral myocarditis is typically characterized by direct myocyte damage causing necrosis and host immune system upregulation leading to molecular mimicry. However, rhinovirus direct cardiac toxicity has not been identified. To date, two other reported cases of unexplained DCM in a 4 and 27 year-old showed the presence of rhinovirus on nasal swab however, myocardial biopsy was not performed. Conclusion This case presents a missed opportunity for confirming the link between rhinovirus and DCM. Confirmatory viral PCR on biopsy tissue should become a practice standard in any suspected cases and as a standard investigation in cases with unclear etiology.