ABC | Volume 110, Nº5, May 2018

Original Article Salmazo et al Frequency of subclinical atherosclerosis in Brazilian HIV-infected patients Arq Bras Cardiol. 2018; 110(5):402-410 1. Brasil. Ministério da Saúde. Vigilância, Prevenção eControle das IST, doHIC/ Aids e das Hepatites virais. Boletim Epidemiológico HIV/Aids-2013;2(1). Brasília; 2013. 2. Global report: UNAIDS report on the global AIDS epidemic 2013. Geneva: UNAIDS; 2013. 3. Maggi P, Perilli F, Lillo A, Gargiulo M, Ferraro S, Grisorio B, et al. Rapid progressionofcarotidlesionsinHAART-treatedHIV‑1patients.Atherosclerosis. 2007;192(2):407-12. doi: 10.1016/j.atherosclerosis.2006.05.026. 4. Bonilla H, Mcshannic J, Goldberg E, Chua D, Conner R, Fiorentino M, et al. Impact of human immunodeficiency virus infection on measures of cardiovascular disease in long-term nonprogressors. Infect Dis Clin Pract. 2013;21(3):177-80. doi: 10.1097/IPC.0b013e31828262f3. 5. Barbaro G. HIV infection, highly active antiretroviral therapy and the cardiovascular system. Cardiovasc Res. 2003;60(1):87-95. doi: https://doi. org/10.1016/S0008-6363(02)00828-3. 6. Hulten E, Mitchell J, Scally J, Gibbs B, Villines T. HIV positivity, protease inhibitor exposure and subclinical atherosclerosis: a systematic review and meta-analysis of observational studies. Heart. 2009;95(22):1826-35. doi: 10.1136/hrt.2009.177774. 7. Xavier HT, Izar MC, Faria Neto JR, Assad MH, Rocha VZ, Sposito AC, et al. [V BrazilianGuidelines on dyslipidemias and prevention of atherosclerosis]. ArqBras Cardiol. 2013;101(4 Suppl 1):1-20. doi: http://dx.doi.org/10.5935/ abc.2013S010. 8. Goodman A. Accelerated atherosclerosis in HIV-positive patients may be due to disease, not treatment. 50th Interscience Conference on Antimicrobial Agents andChemotherapy (ICAAC); 2010 Sept 12-15; Boston (Massachusetts). Abstract H-220. 9. ZamanAG,HelftG,WorthleySG,Badimon JJ.Theroleofplaqueruptureand thrombosis incoronaryarterydisease.Atherosclerosis.2000;149(2):251-66. doi: http://dx.doi.org/10.1016/S0021-9150(99)00479-7. References This result, associated with the presence of PL in almost 20% of the low-risk patients classified by the FCRS, would indicate that they are at risk of developing atherosclerosis. Thus, the group with such characteristics would be exposed to major cardiovascular events, such as myocardial infarction and stroke, even without symptoms. The IV Brazilian Guidelines on Dyslipidemia and Atherosclerosis Prevention recommend that evaluation of cardiovascular risk in HIV-infected patients should be performed assessing lipid profile and FCRS. 12 Patients classified as low-risk have normal lipids and are not using HAART, and should undergo cardiovascular reevaluation in 2 years. In those with HAART, reevaluations are recommended one month after initiation of therapy and then every three months. It is thus noted that the criteria established by the guidelines fail to consider the risks of this particular HIV-infected population, and that these patients have not been properly and specifically assessed for early CVD detection. Limitations There are some limitations in this study. The data are only observational. There is a gap between this study population and the population from Framingham in the original description of the risk score. The pathophysiological determinants of multifactorial conditions involved in the association between HIV-infection or HAART use and atherosclerosis were not analyzed in this study. Information on previous CVD and other causes of immunosuppression were obtained by medical record review only, without specific evaluation for each condition. Conclusions The data suggest that HIV-infected patients are at increased risk of atherosclerosis in association with the classical cardiovascular risk factors. In addition, HAART interacts with time since HIV infection diagnosis and patient age to modify lipid levels, but is not associated with higher PL frequency and does not promote functional changes in the arteries. Smoking, more prevalent in the HIV-infected population, influences the effect of age on the mechanical properties of arteries and may have an additional atherogenic effect in those patients. The FCRS may be inappropriate for this population. Author contributions Conception and design of the research: Salmazo PS; Acquisition of data: Salmazo PS, Shiraishi FG; Analysis and interpretation of the data: Salmazo PS, Bazan SGZ, Shiraishi FG, Bazan R, Okoshi K, Hueb JC; Statistical analysis: Bazan SGZ, Bazan R; Writing of the manuscript: Salmazo PS, Bazan SGZ, Shiraishi FG, Bazan R; Critical revision of the manuscript for intellectual content: Okoshi K, Hueb JC. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding There were no external funding sources for this study. Study Association This article is part of the thesis of Doctoral submitted by Péricles Sidnei Salmazo, from Faculdade de Medicina de Botucatu. Experimental work involving human beings This study was approved by the Ethics Committee of the Faculdade de Medicina de Botucatu under the protocol number CEP 3451-2010. All the procedures in this study were in accordance with the 1975 Helsinki Declaration, updated in 2013. Informed consent was obtained from all participants included in the study. 408