ABC | Volume 114, Nº2, February 2020

Short Editorial Gowdak Atherosclerosis, inflammation, and genetics Arq Bras Cardiol. 2020; 114(2):273-274 1. Allam AH, Thompson RC, Wann LS, Miyamoto M, Nur El-Din Arl H, El Maksoud GA, et al. Aterosclerose in ancient Egyptian mummies: the Horus study. JACC Cardiovasc Imaging 2011;4(4):315-27. 2. Thomas GS, Wann LS, Allam AH, Thompson RC, Michalik DE, Sutherland MY, et al. Why did ancient people have aterosclerose?: from autopsies to computed tomography to potential causes. GlobHeart. 2014;9(2):229-37. 3. Gimbrone MA, García-Cardeña G. Endothelial Cell Dysfunction and the Pathobiology of Aterosclerose. Circ Res. 2016;118(4):620-36. 4. Bennett MR, Sinha S, Owens GK. Vascular Smooth Muscle Cells in Aterosclerose. Circ Res. 2016;118(4):692-702. 5. Taleb S. Inflammation in aterosclerose. Arch Cardiovasc Dis. 2016;109(12):708-15. 6. Zhu Y, Xian X, Wang Z, Bi Y, Che Q, Han X, et al. Research Progress on the Relationship between Aterosclerose and Inflammation. Biomolecules. 2018;8(3):pii E80. 7. Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM jr, Katelein JJ, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-207. 8. Ridker PM, Everett BM, Thuren T, Mac Fadyen JG, Chang WH, Ballantyne C, et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med 2017;377(12):1119-31. 9. Ridker PM, MacFadyen JG, Everett BM, Libby P, Thuren T, Glynn RJ,et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial. Lancet 2018;391(10118):319-28. 10. Vinkhuyzen AA,WrayNR, Yang J, GoddardME, Visscher PM. Estimation and partition of heritability in human populations using whole-genome analysis methods. Annu Rev Genet 2013;47:75-95. 11. Samani NJ, Erdmann J, Hall AS, Hengstenberg C, Mangino M, Mayer B, et al.Genomewide association analysis of coronary artery disease. NEngl J Med 2007;357(5):443-53. 12. McPherson R, Tybjaerg-HansenA. Genetics of Coronary ArteryDisease. Circ Res 2016;118(4):564-78. 13. Brull DJ, Serrano N, Zito F,Jones L, Montgomery HE, Rumley A, et al. Human CRP gene polymorphism influences CRP levels: implications for the prediction and pathogenesis of coronary heart disease. Arterioscler Thromb Vasc Biol 2003;23(11):2063-9. 14. Rocha LO, Rocha E MI, Succi GM, Brito-Junior RB. Association between Periodontitis, Genetic Polymorphisms and Presence of Coronary Artery Disease in Southern Brazil. Arq Bras Cardiol. 2020; 114(2):268-272. References This is an open-access article distributed under the terms of the Creative Commons Attribution License Investigators from different research facilities have produced a complex, most likely still incomplete picture of the intricate relationship between inflammation-infection, genetics, and atherosclerotic diseases like CAD. In this issue of the Brazilian Archives of Cardiology , Rocha et al., 14 sought to investigate the link between periodontal disease (as a model of chronic inflammatory condition) and two specific polymorphisms in genes knowingly related to inflammation (C-reactive protein and interleukin-6), with the presence of CAD in 80 patients from the South Region of Brazil referred for invasive coronary angiography. They found in the multivariate model that male gender and the CRP gene +1444C > T variant were significantly associated with the presence of CAD. The authors should be congratulated for their contribution to the field, because replicating the finding of a significant association between a specific SNP and clinical outcomes in different populations strengthens the finding’s relevance to the occurrence of the measured outcome. Nevertheless, the study would benefit from providing the levels of hsCRP in the population study (as a measurement of chronic inflammatory status) and further detailing the extension of the obstructive pattern, rather than only a dichotomous classification of CAD present/absent based on the medical report. Additionally, I would be very cautious in dismissing the possible association between the IL-6 gene variant and the presence of CAD because of the small number of patients included in the study, which yielded a marginal statistical significance in the multivariate model (p-value = 0.06), given that this association has been validated in previous studies mentioned by the authors. Despite its limitations, the work by Rocha et al. 14 draws clinical cardiologists’ attention to the fact that genetics has gone beyond the laboratory and is currently making its way into clinical practice, at least as a tool to help us better understand how different our patients are, even if they are exposed to the same risk factors with which we are all too familiar. We will have to learn how to apply genetic risk scores that may improve our ability to predict the risk of CAD 14 beyond what is estimated based on traditional risk factors alone. Gregor Mendel would be delighted to see how far we have come from his early experiments with pea plants more than 150 years ago, but the road to fully understanding the role of genetic factors in complex diseases such as atherosclerosis or hypertension is a long, albeit fascinating one. 274