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Progression of Duchenne Cardiomyopathy Presenting with Chest Pain and Troponin Elevation

Kan N Hor1, Pace Johnston1, Kathi Kinnett2

  • 1Nationwide Children's Hospital, Columbus, OH, USA.

Journal of Neuromuscular Diseases
|October 7, 2017
PubMed

Insights

Acute chest pain with elevated troponin I (cTn) in Duchenne muscular dystrophy (DMD) boys may signal worsening cardiomyopathy. This under-recognized presentation indicates acute left ventricular dysfunction and myocardial fibrosis progression in DMD patients.

Area of Science:

  • Cardiology
  • Neuromuscular Disorders
  • Biomarkers

Background:

  • Duchenne muscular dystrophy (DMD) management advances have shifted mortality causes to progressive cardiomyopathy.
  • Troponin I (cTn) levels are typically not elevated in asymptomatic DMD patients despite cardiac imaging findings.

Purpose of the Study:

  • To describe the clinical presentation and cardiac findings in Duchenne muscular dystrophy (DMD) boys experiencing acute chest pain (ACP) with elevated troponin I (cTn).
  • To investigate the association between ACP, cTn elevation, and cardiomyopathy progression in DMD.

Main Methods:

  • Case series of eight boys with DMD presenting with acute chest pain (ACP) and elevated troponin I (cTn).
  • Evaluation included electrocardiograms (ECG), cardiac magnetic resonance imaging (CMR) with late gadolinium enhancement (LGE), and serial cTn measurements.
  • Left ventricular ejection fraction (LVEF) was assessed via echocardiography and CMR.

Main Results:

  • Eight DMD boys presented with ACP and acute cTn elevation (mean peak 44±15.4 ng/mL).
  • CMR revealed increased LGE (12.4% to 36.5%) and decreased LVEF (61% to 47.6%), which remained depressed on follow-up.
  • cTn levels normalized with supportive care; viral studies were negative.

Conclusions:

  • Acute chest pain (ACP) with troponin I (cTn) elevation is a recognized clinical event in Duchenne muscular dystrophy (DMD) boys.
  • This presentation signifies acute left ventricular dysfunction and potential progression of myocardial fibrosis, indicating cardiomyopathy advancement.
  • These events may represent a critical pathophysiological mechanism in DMD cardiomyopathy progression.
Abstract

Keywords:
Duchennecardiomyopathyheart failuretroponin

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