Eosinophilic Myocarditis: The Key is Visualizing the Apex
A 55-year-old Caucasian woman with a history of ulcerative colitis (diagnosed at the age of 24) with no known cardiovascular risk factors was seen in the emergency department after a 1-week history of sharp, right-sided chest pain. The chest pain was atypical, non-exertional and lasted approximately 1 hour at a time. Over the past month, she had been intermittently febrile with occasional night sweats and non-bloody, non-mucoid diarrhea. Review of systems was notable for ongoing chills, fatigue, headache, and weakness but no nausea, abdominal pain, rash, dyspnea, or sick contacts. She had no history of drug, tobacco, or alcohol use.
She was hospitalized 4 months prior during a trip to China for severe nausea, emesis, and diarrhea. She required antibiotics and intravenous hydration. Her last flare of ulcerative colitis was 6 months prior, at which time she was already maintained on mesalamine but was treated successfully with a course of prednisone.
Her blood pressure was 100/58 mmHg, heart rate was 90 bpm, respiratory rate was 18, temperature was 101°F, and O2 saturation was 98% on room air. Her cardiovascular exam and remainder of the physical exam was unremarkable.
The electrocardiogram showed normal sinus rhythm with mild T-wave abnormalities in the anterior leads (Figure 1). The chest X-ray demonstrated no acute processes. Initial laboratory studies revealed a normal basic chemistry, mild transaminitis (aspartate aminotransferase = 43 U/L; alanine aminotransferase = 47 U/L; alkaline phosphatase = 126 U/L), elevated lipase = 721 U/L), and total white blood cell count of 10.7 with 24% eosinophils. The remainder of the complete blood count and coagulation studies were normal. The troponin was elevated at 0.3 ng/mL. The erythrocyte sedimentation rate was 36 mm/h, and C-reactive protein was 1.6 mg/L.
Figure 1: 12-Lead Electrocardiogram With Mild Anterior T-wave Abnormalities
Transthoracic echocardiogram showed normal left ventricle (LV) size and function (ejection fraction = 65%) with mildly increased wall thickness and mild diastolic dysfunction. Right ventricle (RV) size and function were normal. There was no significant valvular disease. An exercise stress echocardiogram during the hospitalization showed no regional wall motion abnormalities but possible apical hypertrophy without evidence of an LV outflow tract gradient.
Computed tomography (CT) of the abdomen and pelvis showed concentric wall thickening and edema suggestive of colitis in the descending colon, sigmoid colon, and rectum. A colonoscopy showed pseudomembranes. Magnetic resonance cholangiopancreatography showed small strictures of the right and left hepatic ducts, suspicious for early sclerosing cholangitis, and mural thickening and mucosal enhancement of the distal descending colon compatible with a diagnosis of ulcerative colitis. She was started on ursodiol and prednisone.
Her blood cultures were negative. Rheumatologic studies (anti-nuclear antibodies, anti-double stranded DNA, anti-neutrophil cytoplasmic antibodies) were normal, and Lyme testing was negative. Stool and antigen testing for C. difficile, ova/parasites, and Giardia were negative. Her chest pain resolved during the admission, and she was discharged.
In the outpatient setting, she saw a cardiologist in consultation. Her gastrointestinal symptoms had completely resolved. However, since being seen in the emergency department, she developed dyspnea, and the episodes of atypical chest pain recurred. Coronary CT angiography (CCTA) was ordered for anatomical assessment of coronary arteries.
The CCTA showed normal coronary origins and minimal non-obstructive coronary artery disease (Figure 2). Thickening of the LV and RV apices was noted again, with hypoperfusion of the central portion of the thickening suggestive of thrombus (Figure 3).
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