Hydrocarbon Exposure in Myocarditis: Rare Toxic Cause or Trigger? Insights from a Biopsy-Proven Fulminant Viral Case and a Systematic Literature Review

Abstract

Toxic myocarditis (TM) is rare, and no systematic evidence is available regarding its treatment or prognosis. Hydrocarbons even more rarely cause TM, and they are associated with severe extracardiac toxicity. Moreover, a pathogenic interaction between viral and toxic agents in TM has not been studied. We present the first case of biopsy-proven parvovirus B19 (B19V) viral fulminant myocarditis diagnosed after hydrocarbon exposure, along with a systematic literature review of hydrocarbon-TM cases. A systematic literature review was conducted by searching hydrocarbon-TM cases. Clinical and prognostic data were recorded. After screening of 937 records, 7 were included. All cases were male, with a median age of 24 years (IQR 23-25). Chest pain and dyspnea were the main symptoms, but arrhythmic presentation was also reported; endomyocardial biopsy (EMB) was performed in only one case. Overall, treatment was based on supportive measures, such as antiarrhythmic and/or vasoactive therapy. Our example (male, 47 years old) is the first reported fulminant biopsy-proven case diagnosed after a massive exposure to hydrocarbons, in which EMB molecular analysis unexpectedly revealed B19V with a high viral load. Hemodynamic and arrhythmic instability required percutaneous stellate ganglion blockade and temporary wearable defibrillator use. Left ventricular function spontaneously normalized at 3 months. In conclusion, we report the first fulminant B19V myocarditis case temporally associated with aromatic hydrocarbon exposure due to a coexistence of viral and toxic causes. Our case and the systematic review show that promptly performing EMB can provide a definitive diagnosis and guide treatment, especially in severe cases in which infectious agents may contribute to myocardial damage.

Keywords: endomyocardial biopsy; fulminant myocarditis; hydrocarbons; myocarditis prognosis; toxic myocarditis.

Figure 1

Chest CT scan on admission, showing bilateral diffuse consolidation areas, consistent with chemical pneumonitis.

Figure 2

ECG and CMR findings. (1) Panel (A) shows patients’ ECG on day two after admission: sinus tachycardia is present, together with diffuse ST elevation with “shark fin” morphology, as well as ventricular ectopics (blue arrow). Notably, ECG on day one was unremarkable. (2) Panels (B) (short axis) and (C) (four chamber) show CMR T2-weighted sequences: subepicardial edema (non-ischemic pattern) is present at the level of the lateral LV wall (green circles). (3) Panels (D) (short axis) and (E) (four chamber) show CMR T1-weighted post-contrast sequences: subepicardial LGE (non-ischemic pattern) is present at the level of the lateral LV wall, with a corresponding distribution as myocardial edema (red circles).

Figure 3

Histology and immunohistochemistry findings from the endomyocardial biopsy: (A) massive myocyte necrosis (pale areas) associated with diffuse mononuclear cell infiltrates in the absence of giant cells and eosinophils (hematoxylin–eosin stain, bar = 400 micron); (B) higher magnification of B (hematoxylin–eosin stain, bar = 200 micron); (C) immunohistochemistry for CD3+ T-cell (>7 cells/mm²); (D) immunohistochemistry for CD68 macrophages (up to 4 mm²; same field as C, bar = 200 micron).

Figure 4

Timeline of the most relevant clinical and diagnostic findings and therapeutic interventions. Legend: B19V = parvovirus B19; CMR = cardiac magnetic resonance; EMB = endomyocardial biopsy; HF = heart failure; IV = intravenous: OMT = optimal medical therapy. Created with BioRender Version #201.

Figure 5

Systematic literature review flowchart.