Abstract

A 56-year-old white man was admitted with palpitations, chest pressure, and dyspnea on exertion. He had an embolic stroke 2 months before admission without a defined embolic source. He had history of well-controlled hypertension and allergic asthma treated with theophylline. On admission, the resting ECG revealed sinus rhythm, right axis deviation, anterolateral ST-segment depression, and a normal QT interval (Figure 1). His cardiac biomarkers were elevated to indicate myocardial injury (troponin I, 2.66 ng/mL; creatine kinase-MB, 5.8 ng/mL). While in hospital, he developed episodes of polymorphic ventricular tachycardia (Figure 2) requiring multiple cardioversions and eventually temporary pacing. The initial peripheral blood count revealed a marked leukocytosis (22 000/μL) with a severe hypereosinophilia (47%, 10 000/μL). A transthoracic echocardiogram showed a normal-size left ventricle (LV) with normal global systolic function. The right ventricle (RV) was mildly enlarged with a mildly decreased systolic function. The LV and RV apexes appeared thickened and hypokinetic (Movie I in the online-only Data Supplement). Subsequent left and right cardiac catheterization demonstrated normal coronary arteries and elevated right and left heart filling pressures (right atrial pressure, 20 mm Hg; capillary wedge pressure, 23 mm Hg) with signs of restrictive physiology (Figure 3). An extensive workup for conditions associated with hypereosinophilia was negative. The patient had no rash or other evidence of vasculitis. Parasitosis was ruled out with serial …

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