IJCS | Volume 32, Nº5, September/October 2019

DOI: 10.5935/2359-4802.20190041 435 EDITORIAL International Journal of Cardiovascular Sciences. 2019;32(5):435-437 Mailing Address: Andressa Mussi Soares Rua Papa João XXIII, n.1, apto 1202. Postal Code: 29303-297, Gilberto Machado - Cachoeiro de Itapemirim, ES - Brazil. E-mail: amussisoares@gmail.com Rheumatic Heart Disease - How are We in 2019, Have We Evolved? Andressa Mussi Soares 1,2, 3 Hospital Evangélico de Cachoeiro de Itapemirim, 1 Cachoeiro de Itapemirim, ES - Brazil Faculdade de Medicina da Universidade de São Paulo, 2 São Paulo, SP - Brazil Departamento de Cardiopatia Congênita e Cardiologia Pediátrica - Gestão 2018-19, 3 Rio de Janeiro, RJ - Brazil Rheumatic heart disease; chronic valvular heart disease; control programs; corticosteroids; echocardiography. Keywords Acute rheumatic fever (ARF) is the result of an autoimmune response to pharyngitis caused by infection with the sole member of the group A Streptococcus (GAS), Streptococcus pyogenes . ARF leads to a condition characterized by various combinations of joint pain and swelling, cardiac-valve regurgitation with the potential for secondary heart failure, chorea, skin and subcutaneous manifestations, and fever. Rheumatic heart disease (RHD) is a disease of poverty that affects children and working-age adults. The global economic impact of early death from RHD is still very high. In Brazil, the average cost of RHD-related damage is around 89 million Brazilian reals (close to US$ 28 million) a year. Information from the Brazilian Unified National Health System database (DATASUS) indicates a cardiac mortality rate of about 7.9% from chronic rheumatic fever (RF). 1 RHDcontrol programswere successfully implemented in some low- and middle-income countries during the latter part of the 20th century, prompting the World Health Organization (WHO) and others to downscale their RF (rheumatic fever)/RHD activities by the early 2000s. 2 Cardiac valves have been studied extensively, especially the mitral valve. There is an evident inflammatory process from the VCAM-1 expression on the valve surface endothelium. Further, CD4+ and CD8+ T lymphocytes localize over the valve endothelium as well as in the immediate subendothelial layer. The T lymphocytes (both CD4+ and CD8+) adhere to and extravasate through the valve endothelium, and neovascularization of the diseased valves is associated with the same phenomenon of T lymphocytes adhering to and extravasating through the endothelium of the newly formed blood vessels. 3 Studies have suggested that virulent clones of GAS organisms present in the community have emerged, causing RF. Proteomic/genomic studies on organisms (such as M1, M3, or M18) obtained fromRF epidemics or RF patients, comparedwith the sameM types not causing RF are necessary. These studies would help to identify proteomic/genomic differences (in particular, the antigenic proteins/glycoproteins) between the virulent clone and the non-virulent organism (not causing RF). 4,5 Long-term morbidity and mortality from ARF are mainly caused by RHD, which, in turn, is mostly a function of the extent of the acute cardiac involvement of ARF and the incidence of subsequent episodes of recurrent ARF. 5 In the study “Evolutive Study of Rheumatic Carditis Cases Treatedwith Corticosteroids in a Public Hospital”, 93 cases of rheumatic carditis in patients under 18 years old treated with corticosteroids were evaluated in the period of 2000-2015. 6 In the study, 93.5% developed moderate or severe carditis, andmitral regurgitationwas detected in 100% of the sample. The progress of the cases was favorable in 71%. Comparisons of the initial with posterior valve lesions regarding the use of corticoids showed statistically significant results (p < 0.001). A difference between the ejection fraction medians was observed (p = 0.048). Surgery was performed in 23.7% of patients – mitral, aortic and/or tricuspid valve repair or replacement. Mortality rate was 5.4%.