Case Report: acute myocarditis in a patient with Duchenne muscular dystrophy (QF_SA_138)

An 11-year-old boy with DMD presented to the emergency department with a 5-day history of persistent nasal congestion, runny nose, and cough. He was regularly taking prednisolone acetate, angiotensin-converting enzyme (ACE) inhibitors, and β-blockers for suspected DMD-associated cardiomyopathy. Upon presentation, a substantially elevated cardiac troponin I (cTnI) level of 19.8 μg/L and abnormal electrocardiogram (ECG) results were detected. Further cardiac magnetic resonance imaging (CMR) showed myocardial inflammation with localized T2 hyperintensity from the basal to middle lateral and inferior walls, as well as late gadolinium enhancement (LGE) from the basal to apical inferior lateral walls, supporting a diagnosis of acute myocarditis. Subsequently, the patient showed clinical improvement in response to combination treatment with intravenous immunoglobulin, oral prednisolone acetate, potassium chloride sustained-release tablets, anti-heart failure medication, and broad-spectrum antibiotics.

Diagnostic Techniques and Their Most Important Findings:

We have presented a rare case of acute myocarditis in a patient with DMD, potentially due to upper respiratory tract infection; the condition was accurately diagnosed by CMR and successfully treated. Considering our experience in this case, we believe that there is a compelling need for further investigation into this condition. CMR, the gold standard for noninvasive diagnosis of myocarditis, is essential for confirming a diagnosis of myocarditis when cardiac troponin levels or ECG findings are abnormal. In the few reported cases of DMD-associated myocarditis, patients often presented with edema in the left ventricular free wall and corresponding LGE on CMR. Abdul et al. found myocardial edema and LGE in both septal and lateral walls, consistent with our CMR results. Notably, our patient already had left ventricular free wall LGE before the onset of myocarditis. During myocarditis, however, the extent of free wall LGE increased; we also observed transmural LGE in the inferior wall and new interventricular septal LGE. The presence of transmural and septal LGE is presumably associated with a poor prognosis. This case report presents a potentially valuable diagnostic tool and effective management strategy for DMD-associated cardiomyopathy complicated by acute myocarditis. Further studies are needed to confirm the efficacy of this approach.

Learning Points from this Case:

To our knowledge, there have been few reported cases of subclinical myocarditis lacking typical clinical manifestations in patients with DMD. Our case emphasizes that, in children with DMD, even mild respiratory infection symptoms deserve clinical attention. In patients with normal cardiac function, markers of myocardial injury and ECG abnormalities may provide valuable information. Further evaluation with CMR is essential to confirm a diagnosis of myocarditis. Our case also highlights the potential for upper respiratory tract infections to induce acute myocarditis, resulting in clinically significant myocardial edema and inflammation that may accelerate the progression of DMD-associated cardiomyopathy and require closer clinical follow-up.