P1473 Detection of cardiac sources of cerebrovascular events in patient with systemic lupus erythematosus with neuropsychiatric manifestations

Abstract

Abstract Introduction Systemic lupus erythematosus (SLE) is an idiopathic connective tissue disease, characterized with multiorgan involvement. Central nervous system (CNS) involvement is one of the most frequent manifestation of SLE and is termed as neuropsychiatric SLE (NPSLE) Prevalence of NPSLE varies between 12% and 95% among SLE patients. cerebrovascular accidents (CVA) and/or transient ischemic attack (TIA) represents one of the most frequent neuropsychiatric manifestation in SLE patients. Cerebral embolism may have cardioembolic source. Purpose: we described one case of SLE patient with NPSLE diagnosis and concomitant nonsignificant size of ASD II and tried to find its possible association with cerebrovascular accident. Method: We performed retrospective analysis of SLE (NPSLE) patient who had undergone echocardiographic and brain MRI evaluation. Case-Results: A 63 years old women was diagnosed with SLE in 1996 based on positive ANF, positive anti-cardiolipin IGg , arthritis, discoid lupus, positive coombs test and neurological manifestations (hemiplegia and aphasia). Echocardiographic evaluation showed pericarditis and nonsignificant ASD II (<3mm). Ischemic changes were observed on Brain MRI study. Two years later in 1998 brain MRI showed a white matter defect (suspected vascular nature). Patient received 6 standard course of treatment with Cyclophosphamide ,Prednisone (from 60 mg gradually decreased to 10 mg) and oral anticoagulation drugs. After 9 years from the first diagnosis of SLE patient achieved complete remission, but soon in 2006 patient developed TIA and in 2013 developed lacunar infarct. Cardiac source of embolism was excluded according to performed analysis. In addition myocardial infarction was excluded based on Single-photon emission computed tomography (SPECT) perfusion scan. Since then patient remained under the observation of multidisciplinary team. Conclusion: We demonstrated one case of SLE patient with life threating neurological manifestations developed several times. Transthoracic echocardiographic examination showed small ASD II which was not considered as source of embolism, but we believe that in SLE patients with PFO/ASD, even though the size of defect is not large, cerebrovascular accidents may develop due to underlying inflammatory mechanism predisposing possible thromboembolism and early diagnosis, follow-up and management can be paramount to avoid future complications.