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Acute necrotizing eosinophilic myocarditis possibly triggered by an antimigraine drug as an uncommon cause of acute heart failure: a case report.

ABSTRACT:

Background

Epigastric or chest pain with an abnormal electrocardiogram (ECG) in a young, otherwise healthy patient should trigger an investigation to rule out myocarditis. The myocarditis covers a wide spectrum of severity. The search for the aetiologic factor could be definitive for the success of therapy.

Case summary

A previously healthy 29-year-old woman presented to the Emergency Room with epigastric pain, eosinophilia, and an abnormal ECG. A thorough evaluation including cardiac magnetic resonance and endomyocardial biopsy was undertaken. A diagnosis of acute necrotizing eosinophilic myocarditis was made.

Discussion

The case is particularly unique for its suspected predisposing trigger: an antimigraine drug. A possible systemic hypersensitivity reaction, reflected by the occurrence of concomitant severe serum eosinophilia, acute myocarditis, and central nervous system vasculitis, was successfully treated with steroids, further supporting the diagnosis.

SUBMITTER: Beck-da-Silva L

PROVIDER: S-EPMC8350354 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:AimsNecrotizing coronary vasculitis (NCV) is a rare entity usually associated to myocarditis which incidence, cause, and response to therapy is unreported.Methods and resultsAmong 1916 patients with biopsy-proven myocarditis, 30 had NCV. Endomyocardial samples were retrospectively investigated with immunohistochemistry for toll-like receptor 4 (TLR4) and real-time polymerase chain reaction (PCR) for viral genomes. Serum samples were processed for anti-heart autoantibodies (Abs), IL-1β, IL-6, IL-8, tumour necrosis factor (TNF)-α. Identification of an immunologic pathway (including virus-negativity, TLR4-, and Ab-positivity) was followed by immunosuppression. Myocarditis-NCV cohort was followed for 6 months with 2D-echo and/or cardiac magnetic resonance and compared with 60 Myocarditis patients and 30 controls. Increase in left ventricular ejection fraction ≥10% was classified as response to therapy. Control endomyocardial biopsy followed the end of treatment. Twenty-six Myocarditis-NCV patients presented with heart failure; four with electrical instability. Cause of Myocarditis-NCV included infectious agents (10%) and immune-mediated causes (chest trauma 3%; drug hypersensitivity 7%; hypereosinophilic syndrome 3%; primary autoimmune diseases 33%, idiopathic 44%). Abs were positive in immune-mediated Myocarditis-NCV and virus-negative Myocarditis; Myocarditis-NCV patients with Ab+ presented autoreactivity in vessel walls. Toll-like receptor 4 was overexpressed in immune-mediated forms and poorly detectable in viral. Interleukin-1β was significantly higher in Myocarditis-NCV than Myocarditis, the former presenting 24% in-hospital mortality compared with 1.5% of Myocarditis cohort. Immunosuppression induced improvement of cardiac function in 88% of Myocarditis-NCV and 86% of virus-negative Myocarditis patients.ConclusionNecrotizing coronary vasculitis is histologically detectable in 1.5% of Myocarditis. Necrotizing coronary vasculitis includes viral and immune-mediated causes. Intra-hospital mortality is 24%. The immunologic pathway is associated with beneficial response to immunosuppression.