79-year-old man with a remote history of renal cell carcinoma presented to a community hospital with chest pressure that was nonradiating, nonexertional, and not associated with nausea or diaphoresis. His ECG showed T-wave inversion in leads aVL, V 3 V 6 , and ST depressions V 3 to V 6 (Figure [A]). His troponin peaked at 1.68 ng/mL. The patient underwent cardiac catheterization that revealed angiographically normal coronary arteries. At presentation, the patient also had multiple neurological complaints including a 1-week history of right upper extremity weakness and numbness, difficulty standing, and bilateral lower extremity paresthesia. Computed tomography scan of the head showed multiple small acute infarcts in bilateral frontal, parietal, occipital, and cerebellar areas. Concerned for embolic cause, an echocardiogram was performed, which revealed normal left ventricle (LV) cavity size, ejection fraction 60% to 65%, and prominent LV apical hypertrophy (Figure [B] and Movie I in the Data Supplement). The right ventricle systolic function was normal; however, the right ventricle systolic pressure was elevated at 45 to 50 mm Hg (Figure [C] and Movies II and III in the Data Supplement). Two weeks before admission, the patient was treated for upper respiratory infection with azithromycin, which was broadened to levofloxacin due to lack of symptom resolution. Two months before admission, the patient developed hives after taking an over the counter probiotic. These resolved completely with cetirizine and diphenhydramine. The constellation of septal and apical LV hypertrophy, preserved LV ejection fraction, suspected cardiac source of emboli, and recent drug reaction raised concern for possible eosinophilic myocarditis (EM). The patient was transferred to an academic hospital for cardiac magnetic resonance imaging (CMR) and biopsy. On admission, the serum eosinophilic count was 33.3%, whereas labs 2 days before admission showed no evidence of eosinophilia. Right heart catheterization showed right atrium 9, right ventricle 45/7, pulmonary artery 47/14 (26), and pulmonary capillary wedge pressure 14 mm Hg, and endomyocardial biopsy revealed interstitial eosinophils 14/high-power field (Figure [F]). The patient underwent a CMR showing normal LV chamber size and a preserved LV ejection fraction of 65%. Resting steady-state free precession cine imaging on CMR showed mild hypokinesis involving the apical segments with moderate hypokinesis of the true apex. There were subendocardial perfusion defects at rest involving the apical segments and a subendocardial thrombus along the apical inferoseptal myocardium (Figure [D] and Movie IV in the Data Supplement). Myocardial edema predominantly involved the mid to apical septal and inferoseptal myocardial segments (Figure [E]). The CMR findings were consistent with acute EM. The patient was treated with Solumedrol 40 mg BID IV on day 7 with an improved eosinophil count to 2.7 (day 8). The patient was discharged home on