Biomarkers in Acute Myocarditis and Chronic Inflammatory Cardiomyopathy: An Updated Review of the Literature

Abstract

Myocarditis is a disease caused by cardiac inflammation that can progress to dilated cardiomyopathy, heart failure, and eventually death. Several etiologies, including autoimmune, drug-induced, and infectious, lead to inflammation, which causes damage to the myocardium, followed by remodeling and fibrosis. Although there has been an increasing understanding of pathophysiology, early and accurate diagnosis, and effective treatment remain challenging due to the high heterogeneity. As a result, many patients have poor prognosis, with those surviving at risk of long-term sequelae. Current diagnostic methods, including imaging and endomyocardial biopsy, are, at times, expensive, invasive, and not always performed early enough to affect disease progression. Therefore, the identification of accurate, cost-effective, and prognostically informative biomarkers is critical for screening and treatment. The review then focuses on the biomarkers currently associated with these conditions, which have been extensively studied via blood tests and imaging techniques. The information within this review was retrieved through extensive literature research conducted on major publicly accessible databases and has been collated and revised by an international panel of experts. The biomarkers discussed in the article have shown great promise in clinical research studies and provide clinicians with essential tools for early diagnosis and improved outcomes.

Keywords: biomarkers; cardiac sarcoidosis; heart failure; imaging; inflammatory heart disease; myocarditis.

Figure 5

Conditions associated with eosinophilic myocardial injury. Eosinophilic myocarditis exhibits diverse etiologies, ranging from idiopathic to its associated with various systemic disorders. These associated conditions encompass a broad spectrum: (A) Hypersensitivity Reactions to Drugs and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): These reactions are generally characterized by fever and a diffuse skin rash, often with a delayed onset after drug initiation (typically 2–6 weeks); (B) Eosinophilic Granulomatosis with Polyangiitis (EGPA): Often linked with asthma, pulmonary nonfixed infiltrates (indicated by arrows on chest computed tomography in the blue inset), and paranasal sinus abnormalities; (C) Hypereosinophilic Syndromes (HES): Distinguished by persistent peripheral eosinophilia (≥1.5 × 10⁹/L for over 6 months), which can manifest as a complex idiopathic form or a myeloproliferative variant; (D) Infections caused by parasitic agents; (E) rarely, eosinophilic myocarditis may be associated with solid tumors.

Figure 1

Different etiologies implicated in the development of myocarditis. Abbreviations: GCM, Giant cell myocarditis; HIV, Human immunodeficiency virus.

Figure 2

Different types of acute myocarditis. (A) Acute lymphocytic myocarditis with focal inflammatory cell infiltrates (black arrow) and cardiomyocyte necrosis. (B) Cardiac sarcoidosis, with evidence of granuloma (black arrow). (C) Giant cell myocarditis, with presence of giant multinucleated cells (yellow arrows). (D) Eosinophilic myocarditis. Re-used with permission from Dominguez et al. [8].

Figure 3

Characteristic late gadolinium enhancement (LGE) patterns in myocarditis. Characteristic late gadolinium enhancement (LGE) patterns in viral myocarditis (upper left) inferolateral subepicardial LGE), giant cell myocarditis (upper right) complex LGE involving both ventricles including the right ventricular insertion points), cardiac sarcoidosis (lower left) complex LGE involving both ventricles including the inferior right ventricular insertion point), and eosinophilic myocarditis (lower right) diffuse subendocardial LGE with high signal intensity). Re-used with permission from Polte et al. [27].

Figure 4

Pathogenesis of viral and inflammatory cardiomyopathy. Re-used with permission from Dominguez et al. [8].