A 23-year-old healthy Caucasian male presented to the emergency department (ED) with acute intermittent, severe substernal chest pain radiating to both forearms. He had experienced two similar episodes during the prior week which were of lesser severity and had resolved spontaneously. The day of admission, his symptoms returned with increasing severity, prompting presentation to the ED.
The patient's past medical history included generalized anxiety disorder and seasonal allergies. He denied any personal or family history of cardiac disease. He worked as a landscaper and denied recent illnesses or sick contacts. He consumed alcohol infrequently, chewed tobacco, and did not smoke or use illicit drugs. He had recently returned from a three-day camping trip to Pigeon Forge, Tennessee one day prior to the first episode. He denied any history of international travel or Tuberculosis risk factors. Animal exposures included a pet dog and chickens.
Sublingual nitroglycerin administered en route to the ED improved his pain with complete resolution of symptoms by one hour. Vital signs were temperature 98.5 F, pulse 68, blood pressure 128/75, and SpO2 98% and physical examination was without pertinent findings. Initial differential included acute coronary syndrome, stress-induced cardiomyopathy, myocarditis, pericarditis, and pulmonary embolism.
Initial electrocardiogram (ECG) revealed only subtle lateral ST elevations (Fig. 1). Laboratory work-up revealed an elevated serum troponin of 8.51 ng/mL with peak of 12.8 ng/mL (normal< 0.30 ng/mL), mildly elevated transaminases of aspartate aminotransferase and alanine aminotransferase at 108 and 91, respectively, with otherwise unremarkable complete blood count, basic metabolic panel, erythrocyte sedimentation rate, C-reactive protein, D-dimer, urine drug screen, and chest x-ray. COVID-19 real-time reverse-transcription polymerase chain reaction (PCR) was negative. Urgent coronary angiography showed normal coronary artery anatomy with no acute obstruction. Left ventriculogram showed no wall motion abnormality or changes suggestive of stress cardiomyopathy. Transthoracic echocardiography was normal with left ventricular ejection fraction 60-65% and no structural heart disease or pericardial effusion.
Cardiac magnetic resonance imaging (cMRI) showed evidence of biventricular myocarditis and failure, with LVEF of 45% and RVEF of 41% (Fig. 2). Comprehensive infectious work-up (Table 1) subsequently revealed elevated Toxoplasma gondii IgM and IgG titers (IgM > 160 AU/mL, IgG 36.7 IU/mL).
The patient was initiated on a planned four-week course of pyrimethamine, sulfadiazine and leucovorin plus guideline-directed medical therapy for ventricular systolic dysfunction. He had ophthalmologic evaluation which ruled out ocular involvement. HIV testing, which had been performed and was negative during the initial work-up, was repeated to rule out the possibility of false negative result and was again negative.
As myocardial biopsy was ultimately deferred given clinical improvement with antibiotics, serial toxoplasma serologies were followed to support diagnosis (Table 1): at 5 days, IgM was> 160 AU/mL and IgG 97.6 IU/mL, and at 5 weeks, IgM was> 160 AU/mL and IgG 117 IU/mL.
During follow-up evaluation with cardiology and infectious disease, he only complained of occasional intermittent fatigue with otherwise complete return to baseline without limitation in activity level. Eighteen days into the planned four-week antimicrobial course, he developed significant gastrointestinal intolerance and antimicrobial therapy was stopped. It was not restarted given his symptomatic improvement and return to clinical baseline. Repeat echocardiography performed five weeks after discharge showed normal cardiac function. The patient was instructed to have repeat cardiac MRI in 6 months to ensure sustained resolution of myocarditis.