Cardiac involvement in hypereosinophilic syndrome
Nakhle A, Nasr Y, Laktineh A, and Parikh S. Cardiac involvement in hypereosinophilic syndrome. J Hosp Med 2017; 12(s2)
Journal of Hospital Medicine
Case Presentation: 70-year-old male with remote past medical history of prostate cancer and COPD presented to the emergency department with new onset left side weakness along with left side facial droop. Patient underwent CT scan of the head which was negative and an MRI of the brain which showed multiple bilateral small strokes that raised suspicion for cardio-embolic origin. Laboratory findings showed elevated troponin and white blood count and he was admitted to the hospital for further work up. A review of the patient’s history was noted that he had chronic elevation of the eosinophilic count >1500 cells/mL for more than one year. He underwent a trans-thoracic echo that showed left ventricle (LV) mass and a trans-esophageal echo (TEE) that could not rule out LV mass vs. thrombus. Anticoagulation was held at first due to concern for hemorrhagic conversion, then patient was started on low dose intensity heparin with bridging to warfarin. Hematology was consulted for possible hypereosinophilia syndrome (HES), and other organs involvement was ruled out with the proper laboratory and imaging studies. Hospital course was complicated by atrial fibrillation with rapid ventricle response and hypoxia that required intubation. Cardiac MRI showed findings consistent with the eosinophilic infiltration within the left ventricular myocardium. He was started on boluses of intra-venous steroids which was tapered weekly, with significant improve of his symptoms. Patient then was extubated and discharged to rehab facility on steroid maintenance dose. Discussion:HES is defined as an absolute eosinophilic count more than 1500 cells/mL in two different occasions separated in time by at least one month and/or pathologic confirmation of tissue (HE) associated with eosinophil-mediated organ damage or dysfunction. Cardiac involvement consists of three stages, acute early necrotic stage which is usually clinically silent, intermediate thrombotic stage, and late fibrotic stage that is characterized by altered cardiac muscle function. Our patient has chronic HE who presented with embolic events, an evidence of LV thrombus on TEE, and negative blood cultures. Cardiac MRI showed diffuse T1 abnormal subendocardial delayed enhancement and T2 hyper-intensity/edema in a similar distribution, all of which are compatible with long standing history of HE. he responded well to steroids and repeat echo after six months showed normal cardiac function. Other myeloproliferative disorders were ruled out as an etiology for HE with negative molecular studies. Conclusions:We present a patient with bilateral multiple stroke due to HE endocarditis. HES should be considered as a reason for aseptic endocarditis. Thrombotic events could be the first presentation of HE endocarditis and treatment is with high doses of glucocorticoid. Electrocardiogram and echocardiogram can be used to monitor late manifestations such as restrictive cardiomyopathy.