Acute Myocarditis and Inflammatory Cardiomyopathies: Insights From Cardiac Magnetic Resonance Findings

Abstract

Myocardial inflammation encompasses a broad spectrum of conditions, including acute myocarditis, chronic inflammatory cardiomyopathy, and several overlapping entities that differ in clinical presentation, pathophysiology, and progression. These conditions range from self-limiting acute inflammation to chronic myocardial injury and dysfunction. The etiologic classification of myocardial inflammation highlights the complexity of its pathogenesis, involving direct tissue damage, immune-mediated mechanisms, and environmental triggers. Cardiac magnetic resonance (CMR) imaging has become a central diagnostic tool in the assessment of myocardial inflammation, providing precise characterization of myocardial tissue, assessing cardiac function, and stratifying prognosis. Advanced techniques such as T1 and T2 mapping and extracellular volume quantification have further expanded its diagnostic capabilities. This review highlights the essential role of CMR in diagnosing myocardial inflammation, recognizing various imaging findings associated with different underlying causes, and informing clinical management. The standardization of CMR protocols, along with advancements in imaging techniques and strengthened interdisciplinary collaboration, represents a fundamental step toward improving diagnostic accuracy, patient outcomes, and the understanding of the broad spectrum of myocardial inflammatory diseases.

Keywords: cardiovascular magnetic resonance; chronic inflammatory cardiomyopathy; myocardial inflammation; myocarditis.

FIGURE 1

Etiology of myocardial inflammation.

FIGURE 2

Acute myocarditis in a 21‐year‐old patient presenting with acute chest pain and fever. CMR shows focal edema (a, STIR image) and subepicardial LGE in the LV basal inferolateral and inferior segments (b), (c) corresponding to high myocardial native T1, ECV, and T2 values (d)–(f). CMR, cardiac magnetic resonance; ECV, extracellular volume; LGE, late gadolinium enhancement; LV, left ventricular; STIR, short tau inversion recovery.

FIGURE 3

Acute endomyocarditis in eosinophilic granulomatosis with polyangiitis (EGPA). LGE images display patchy subendocardial LGE (arrows in a, b) in the basal anterolateral wall, mid‐cavity, and apical regions, along with increased T2 signal in STIR sequence (c) and increased T2 values on mapping (d). LGE, late gadolinium enhancement; STIR, short tau inversion recovery.

FIGURE 4

Acute myocarditis in lupus eritematosus (LES). STIR images (a) show increased signal in the LV basal lateral wall with associated focal mid‐wall LGE (arrows in images b, c) and high myocardial native T1, ECV, and T2 mapping values (d)–(f). ECV, extracellular volume; LGE, late gadolinium enhancement; LV, left ventricular; STIR, short tau inversion recovery.

FIGURE 5

Acute myocarditis with pericardial involvement in systemic sclerosis (SSc). STIR images (a) reveal increased signals in the interventricular septum and anterior LV wall. LGE images (b), (c) show focal mid‐wall enhancement (arrows), in the LV basal anterior segment. High myocardial native T1, ECV, and T2 mapping values (d)–(f) are observed on the basal LV septum. Thickening and increased inferior and lateral pericardial sheets signal intensity in STIR and LGE (a)–(c). ECV, extracellular volume; LGE, late gadolinium enhancement; LV, left ventricular; STIR, short tau inversion recovery.

FIGURE 6

Cardiac sarcoidosis. CMR (a) shows a focal area of LGE in the basal infero‐septal wall (arrow), which corresponds to an area of increased uptake of the metabolic tracer at PET‐CT (b). CMR, cardiac magnetic resonance; LGE, late gadolinium enhancement; PET‐CT, positron emission tomography‐computed tomography.

FIGURE 7

Fifty‐nine‐year‐old patient undergoing treatment for B‐cell non‐Hodgkin lymphoma with doxorubicin, vincristine, and cyclophosphamide. STIR images (a) show diffuse hyperintensity with associated elevated global myocardial native T1, ECV, and T2 values (d–f; mean values of the mid‐ventricular segments are shown in the figures). No focal delayed enhancement was observed on LGE imaging (b), (c). ECV, extracellular volume; LGE, late gadolinium enhancement; STIR, short tau inversion recovery.

FIGURE 8

Sixty‐year‐old woman with Takotsubo cardiomyopathy. CMR demonstrates diffuse myocardial edema in the mid‐apical LV walls (a and e, STIR). Mapping reveals elevated global myocardial native T1, ECV, and T2 values (d–f; mean values of the mid‐ventricular segments are shown in the figures). Cine‐SSFP images in the horizontal long‐axis view (f and g) show the typical apical “ballooning” of the LV (* in g) in the end‐systolic phase. No focal delayed enhancement was observed on LGE imaging (h).

FIGURE 9

Genetic cardiomyopathy. Progressive enlargement of subepicardial LGE in a young patient with recurrent chest pain associated with mild troponin elevation. Initially interpreted over the years as recurrent myocarditis, the diagnosis was later revised to desmoplakin cardiomyopathy following genetic testing.