Late Gadolinium Enhancement in Acute Eosinophilic Myocarditis: Correlation of Noninvasive Imaging With Tissue Pathology

An 18-year-old male with one-year history of asthma presented to an allergist with dyspnea, rhinorrhea, and upper respiratory symptoms. His white blood cell count was found to be 25K cells/μL, with 29% eosinophils. He was treated for an asthma exacerbation and given antibiotics. Two weeks later, he then presented in cardiogenic shock with an ejection fraction (EF) of 5% after a cardiac arrest at home. His clinical course was marked by the need for invasive hemodynamic monitoring, intra-aortic balloon pump (IABP) support, ionotropes and tailored advanced heart failure therapy.

Cardiac magnetic resonance imaging (MRI) was performed to assess for evidence of acute myocarditis. Figure 1 (clockwise from the left) displays the following:

  • Plate 1: T2 weighted black blood image in the short axis showing increased signal intensity in the apical inferior wall and inferior septum due to myocardial edema.
  • Plates 2 and 3: T1 weighted post-gadolinium images in the short axis and four-chamber orientation showing corresponding late gadolinium enhancement.

Figure 1

Figure 1

High-dose steroids were then initiated. Due to the focal inflammation seen on MRI in the apical septal endocardium, an RV biopsy was performed to confirm the diagnosis showing numerous infiltrating eosinophilic cytotoxic granules (Figure 2, Plate 2) and evolving fibrosis (Figure 2, Plate 1, Arrow).

Figure 2

Figure 2

Genetic testing revealed a PDGFRA mutation, and he was treated with hybrid anti-IL-5 therapy and steroids. He clinically improved and was placed on guideline-directed medical therapy for chronic heart failure (CHF). Given frequent nonsustained ventricular tachycardia (NSVT) and unclear primary rhythm at the time of his arrest, an automated implantable cardioverter-defibrillator (AICD) was implanted for secondary prevention. His EF normalized, and he was discharged home, returning to college within the month.

This case demonstrates the role of CMRI and its characteristic imaging findings in acute eosinophilic myocarditis. The noninvasive findings correspond to pathologic findings at the cellular level. With targeted therapy against cytotoxic eosinophil degranulation, there is a reasonable chance of reducing inflammatory myocardial necrosis, improving clinical outcome and stopping adverse fibrotic remodeling.


  1. Rothenberg ME, Klion AD, Roufosse FE, et al. Treatment of patients with the hypereosinophilic syndrome with mepolizumab. N Engl J Med 2008; 358:1215-1228.

Clinical Topics: Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Prevention, Implantable Devices, SCD/Ventricular Arrhythmias, Acute Heart Failure, Magnetic Resonance Imaging

Keywords: Diagnostic Imaging, Anti-Bacterial Agents, Asthma, Biopsy, Defibrillators, Implantable, Dyspnea, Edema, Endocardium, Eosinophils, Gadolinium, Heart Failure, Heart Arrest, Hemodynamics, Inflammation, Interleukin-5, Leukocyte Count, Magnetic Resonance Imaging, Myocardial Infarction, Myocarditis, Myocardium, Secondary Prevention, Shock, Cardiogenic, Tachycardia, Ventricular

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