P731 When cardiac imaging saves the day - a rare cause of embolic stroke

Abstract INTRODUCTION Hypereosinophilic syndrome (HES) is a rare disorder characterised by infiltration of tissues by eosinophils. Myocardial infiltration occurs in 50-60% of HES and leads to a condition called Loeffler’s endocarditis. Eosinophilic protein toxicity initiates endomyocardial necrosis. This is followed by a thrombotic stage and finally by endomyocardial fibrosis leading to a form of restrictive cardiomyopathy. Thrombosis is often located in the apical region of the ventricles and can result in stroke, which is the most devastating neurological consequence of hyperoesinophilia. We describe a case of a patient that presented with neurological symptoms and was found to have multiple embolic strokes secondary to Loeffler’s endocarditis. CASE A 57-year-old female presented to our institution with new onset confusion and reduced level of consciousness. Initial neurological assessment was consistent with encephalopathy. She had a 2-year history of eosinophilia that had been investigated by the haematology and rheumatology teams with no obvious aetiology identified. Initial haematological investigations showed a raised eosinophil count at 13mmol/L. Her cerebral MRI scan showed multiple embolic infarcts and therefore a transthoracic echo (TTE) was booked. This did not show any obvious intracardiac cause of emboli although the appearances of the LV apex were suspicious of thrombus. This was confirmed later, on contrast imaging (Fig 1). Staphylococcus aureus was grown in a single blood culture specimen raising the suspicion of infective endocarditis and a transoeosophageal echocardiogram (TOE) ruled out vegetations but again illustrated the apical filling defect despite absence of wall motion abnormalities (Fig 2). Finally, a cardiac MRI was arranged and this confirmed the diagnosis of Loeffler’s endocarditis with endomyocardial fibrosis and superimposed LV thrombus (Fig 3). She was treated with anticoagulation and steroids and her eosinophil count normalised before discharge. She remains well with no recurrence at two months post-event. DISCUSSION The diagnosis of Loeffler’s endocarditis depends on the presence high eosinophil count in combination with cardiac involvement on imaging. Transthoracic echocardiography can provide useful information such as apical thickening and thrombus in the left ventricle. As in our case, contrast TTE often provides further detail however contrast-enhanced cardiac MRI remains a key tool in the diagnosis and monitoring of this condition. It provides an assessment of systolic and diastolic function, tissue characterisation and typical features notably endomyocardial fibrosis and thrombosis on late enhancement imaging. CONCLUSIONS We presented a case where cardiac imaging has revealed the diagnosis in a patient presenting with systemic symptoms. We encourage clinicians to use multi-modality cardiac imaging as this has an invaluable role in the diagnostic process of complex patients. Abstract P731 Figure.