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Case Session
SCMR 22nd Annual Scientific Sessions
Andrew Peters, MD
Cardiology Fellow
Lewis Katz School of Medicine at Temple University
Baidarbhi Chakraborty, MD
Pathology Resident
Lewis Katz School of Medicine at Temple University
Rene Alvarez, MD
Attending Cardiologist
Lewis Katz School of Medicine at Temple University
Yoshiya Toyoda, MD
Cardio-thoracic Surgeon
Lewis Katz School of Medicine at Temple University
Chandra Dass, MD
Professor of Radiology
Lewis Katz School of Medicine at Temple University
Pravin Patil, MD
Attending Cardiologist
Lewis Katz School of Medicine at Temple University
Description of Clinical Presentation:
A 53-year-old woman with a history of polymyositis presented with five days of worsening chest pain and dyspnea. She denied recent illness or sick contacts. Initial vitals were notable for a fever of 38 degrees Celsius, tachycardia at 105 bpm, and a blood pressure of 136/90 mmHg. On exam her breath sounds were normal, there was no pericardial rub, and jugular venous pressure was 8 cm of H2O. Her ECG was notable for sinus tachycardia and low voltage. Labs revealed an elevated cardiac troponin of 22 ng/ml, a creatinine kinase of 1543 U/L, and an erythrocyte sedimentation rate of 58 MM/Hr. Her renal function and complete blood count were normal. An echocardiogram showed a left ventricular ejection fraction (LVEF) of 40-45% with a small pericardial effusion. Over the next 24 hours she developed progressive chest pain and dyspnea with a rise in troponin to 53 ng/ml and diffuse ST-segment elevations on ECG. A repeat echo showed the LVEF decreased to 10-15% and there was moderate pericardial thickening with a moderate sized pericardial effusion.
Diagnostic Techniques and Their Most Important Findings:
Due to the patient’s precipitous decline, a cardiac MR (cMR) was performed. This showed patchy delayed enhancement of the myocardium and pericardium compatible with severe myopericarditis with severe global biventricular hypokinesis (Figure 1). These findings prompted urgent initiation of mechanical support with surgically implanted biventricular CentriMagTM devices. At the time of surgery, a biopsy of the right ventricle was obtained that showed extensive myocyte necrosis with an abundance of eosinophils consistent with necrotizing eosinophilic myocarditis (Figure 2). The patient was treated with high dose intravenous steroids and aggressive supportive measures. Despite prolonged mechanical support the patient did not have significant cardiac recovery and ultimately did not survive hospitalization due to infectious complications.
Learning Points from this Case:
Necrotizing eosinophilic myocarditis is a rare and potentially fatal condition. In an early presentation, before onset of cardiogenic shock, cMR is useful for diagnosis and to guide therapies. In our case, the patient had diffuse myocardial edema on T2-weighted imaging (Figure 3) and extensive late gadolinium enhancement to suggest poor prognosis. Because of this, the decision was made to proceed with early central mechanical support to provide ventricular unloading for an anticipated prolonged course. Prompt triage of patients with myocarditis to mechanical support prior to developing the sequela of cardiogenic shock may result in improved outcomes.