<p>1188 either Cat: Valvular Heart Disease: Mechanisms and Treatment Options</p><p>RHEUMATIC HEART DISEASE IN SICKLE CELL DISEASE IN SUB- SAHARAN AFRICA A.C. Atanda 1, Y. Aliyu1, O.I. Atanda3, A. Babadoko4, A. Suleiman, A. Mamman, Z.Y. Aliyu2,4,5 1. Howard University Hospital, Washington DC, USA 2. Vascular Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA 3. Queens Heart Institute, Rosedale, New York, USA 3. Ahmadu Bello University Teaching Hospital, Zaria, Kaduna, Nigeria 5- Center of Sickle Cell Disease and Department of Medicine, Howard University, Washington, DC; USA Objective: To demonstrate incidence of Rheumatic Heart disease (RHD) in Sickle cell disease (SCD) patients. Background: RHD remains a major public health and clinical concern in Sub-Sahara Africa with about 50% of the world RHD burden. RHD incidence in general population varies from 5-36% with higher incidence in rural areas (where there is limited access to antibiotics and delay in diagnosis of rheumatic fever). This is unlike SCD population where there is paucity of data. Method: Cross-sectional study of 208 hydroxyurea-naive consecutive SCD patients aged 10-52 years at steady state and 94 healthy non-matched controls were studied in Rural sites of a Teaching hospital in Nigeria. SCD patients were required to have electrophoretic and or liquid chromatography documentation of major sickling phenotypes. Control group was required to have non-sickling phenotype. Cardiac measurements were performed with transthoracic echo (TTE) for ventricular functions according to American Society of Echocardiography guidelines. Results: The only valvular disease identified is tricuspid regurgitation in SCD patients who have significantly higher mean±SD values for TRV than controls (2.1±0.6 vs. 1.8±0.5; P=0.001). 0% of SCD patient has any features suggestive of RHD. This was similar in the control. However, the SCD cohorts were mostly of low socioeconomic status with less than 5% likelihood of life-time transfusion and less than 20% life-time access to doctors. This’ unlike control which was largely hospital workers and medical students who mostly have basic understanding and access to medical care. Conclusion: Although the frequency with which RHD and SCD coexist is unknown, it would have been expected that the frequency would have been at least similar to the general population. We propose that as is the case with sickle cell and malaria infection, balanced genetic polymorphism or some other genetic basis leading to evolution of the sickle cell trait may provide some degree of protection to RHD in SCD patients. More research is needed on this.</p>