Unmasking Tuberculous Myocarditis: CMR and PET as gatekeepers in a Pediatric Cardiomyopathy

Description of Clinical Presentation: An 11-year-old girl presented with progressive debility and fatigability over several months, followed by cough and orthopnea. She was subsequently admitted with features of congestive heart failure. Laboratory evaluation revealed elevated high-sensitivity troponin I (393 ng/L), markedly raised NT-proBNP (2152–14580 pg/mL), and mildly elevated CPK-MB (4.3 ng/mL), with normal viral markers, liver function, and renal function. Transthoracic echocardiography demonstrated a dilated left ventricle with moderate systolic dysfunction and mild mitral regurgitation, raising concern for a cardiomyopathic process.

Diagnostic Techniques and Their Most Important Findings: Cardiac MRI demonstrated moderate biventricular dysfunction (LVEF 34%, RVEF 37%) with global hypokinesia, reduced LV global longitudinal strain (-9.8%), and dilated LV volumes (LVEDVI 136 mL/m²) (Figure 1). Tissue characterization revealed elevated native T1 (1387 ms), increased extracellular volume (35%), and regionally elevated T2 values in the mid-anterior wall (52 ms). Late gadolinium enhancement showed a heterogeneous pattern: non-territorial subendocardial enhancement at basal segments with variable transmurality, along with subepicardial enhancement of the mid-anterior wall extending toward the apical regions (Figure 2). There was no pericardial effusion, thickening, or enhancement. In addition, enlarged axillary and mediastinal lymph nodes were identified, which were FDG-avid on PET-CT (Figure 3). EBUS-guided biopsy of a mediastinal node tested positive for Mycobacterium tuberculosis by GeneXpert assay, establishing the diagnosis of tuberculous myocarditis. The patient was initiated on anti-tubercular therapy.
On follow-up CMR performed after approximately one year of therapy, there was evidence of reverse remodeling with reduction in LV volumes (LVEDVI 98.4 mL/m²). Systolic function showed mild improvement with LVEF increasing to 40%, RVEF to 60%, and LV global longitudinal strain to -11.6%. The previously noted lymphadenopathy had regressed in size, and the patient reported significant symptomatic improvement, correlating with the imaging findings.

Learning Points from this Case: Tuberculous myocarditis is a rare but important cause of non-ischemic cardiomyopathy, particularly in endemic regions. This case demonstrates the pivotal role of CMR in characterizing myocardial involvement through functional, strain, and tissue parameters, differentiating myocarditis from dilated cardiomyopathy, and revealing extracardiac findings that guided targeted evaluation. Integration of CMR with FDG-PET and biopsy enabled a definitive diagnosis, preventing misclassification as idiopathic myocarditis or primary cardiomyopathy. Follow-up CMR confirmed reverse remodeling and functional recovery under anti-tubercular therapy, underscoring its value not only in diagnosis but also in longitudinal monitoring.

Long axis cine images in 2 chamber, 4 chamber and 3 chamber planes show dilated left ventricle with normal wall thickness and reduced global longitudinal strain -9.8%.
(A) Precontrast and (B) Post contrast T1 mapping shows elevated global native T1 values 1387 ms. (C) T2 mapping shows regional elevation of T2 values at the mid anterior wall ~ 52 ms, Short axis PSIR images at show subendocardial to focal transmural LGE at base (D), subepicardial LGE at mid (E) and apical cavity (F) - blue arrowheads.
Axial PET-CT images show FDG avid enlarged lymph nodes (Blue arrows) at right axillary, right highest mediastinal and subcarinal nodal stations.