Cardiac MRI as a Diagnostic Game-Changer in Pediatric Cardiac Beriberi Mimicking Myocarditis

Description of Clinical Presentation: We describe two adolescent males (aged 13 and 14 years) with global developmental delay, residing in the same orphanage, presented on the same day with progressive dyspnea, peripheral edema, and cardiomegaly following a short febrile illness. Electrocardiogram (ECG) showed sinus tachycardia with T-wave flattening; echocardiography revealed reduced left ventricular ejection function (EF 30% and 50%, respectively) with minimal pericardial effusion. Troponin-T and NT-pro BNP were elevated, and weakly positive Mycoplasma pneumoniae titers (1:40 and 1:80, respectively) initially raised suspicion for myocarditis.

Diagnostic Techniques and Their Most Important Findings: Cardiovascular magnetic resonance (CMR) was performed on a 1.5T scanner using a protocol specifically optimized for non-cooperative pediatric patients. The imaging protocol included steady-state free precession (SSFP) cine imaging, T2-weighted imaging with fat suppression, native T1 mapping, post-contrast T1 mapping for extracellular volume (ECV) quantification, T2 mapping, and single-shot phase-sensitive inversion recovery (PSIR) late gadolinium enhancement (LGE).

CMR revealed mildly dilated left ventricles with mildly reduced systolic function (ejection fraction 45% and 53%, respectively). There was evidence of mild diffuse myocardial fibrosis, as demonstrated by elevated native T1 values ( >1050 ms; 1052 and 1081 ms) and increased ECV ( >26%; 27% and 30.8%), without evidence of LGE on single-shot imaging. Importantly, T2-based imaging showed no myocardial edema (Figure), and the overall findings did not fulfill the 2018 Lake Louise criteria for acute myocarditis. This prompted reconsideration of the initial diagnosis.

The clustering of similar clinical presentations in a shared setting, combined with common dietary risk factors and consistent CMR findings, raised suspicion of a shared underlying etiology. Subsequent laboratory testing confirmed thiamine deficiency (24.73 and 27.59 µg/L; normal range 28–85 µg/L). Both patients were treated with intravenous thiamine alongside standard heart failure therapy. Within 72 hours, symptoms improved markedly, and follow-up echocardiography at one month confirmed full recovery of left ventricular function (EF 55%). No four-fold rise in Mycoplasma pneumoniae titers was detected, excluding active infection.

Learning Points from this Case: These cases highlight the diagnostic power of CMR in pediatric cardiomyopathy, particularly when myocarditis is suspected. The absence of myocardial edema and LGE—failing to meet the 2018 Lake Louise criteria—combined with abnormal tissue mapping values, supported a diagnosis of cardiac beriberi rather than myocarditis. In uncooperative pediatric patients, single-shot LGE sequences provide a valuable tool for obtaining diagnostic-quality imaging without the need for prolonged breath-holding. Tailoring imaging protocols in this way enhances diagnostic accuracy in challenging clinical settings.

Cardiovascular magnetic resonance (CMR) imaging in two patients with cardiac beriberi. The figure shows T2-weighted short tau inversion recovery imaging (T2W STIR), single shot late gadolinium enhancement imaging (LGE), native T1 mapping (nT1 mapping), enhanced T1 mapping (eT1 mapping), and T2 mapping.