ABC | Volume 110, Nº5, May 2018

Original Article Frequency of Subclinical Atherosclerosis in Brazilian HIV‑Infected Patients Péricles Sidnei Salmazo, Silméia Garcia Zanati Bazan, Flávio Gobbis Shiraishi, Rodrigo Bazan, Katashi Okoshi, João Carlos Hueb Faculdade de Medicina de Botucatu (UNESP), Botucatu, SP – Brazil Mailing Address: Silméia Garcia Zanati Bazan • Faculdade de Medicina de Botucatu - Unesp - Departamento de Clínica Médica. Distrito de Rubião Jr., s/n. Postal Code 18618-687, Botucatu, SP – Brazil E-mail: sgzanati@fmb.unesp.br, sgzanati@cardiol.br Manuscript received June 03, 2017, revised manuscript October 17, 2017, accepted December 12, 2017 DOI: 10.5935/abc.20180058 Abstract Background: AIDS as well as atherosclerosis are important public health problems. The longer survival among HIV-infected is associated with increased number of cardiovascular events in this population, and this association is not fully understood. Objectives: To identify the frequency of subclinical atherosclerosis in HIV-infected patients compared to control subjects; to analyze associations between atherosclerosis and clinical and laboratory variables, cardiovascular risk factors, and the Framingham coronary heart disease risk score (FCRS). Methods: Prospective cross-sectional case-control study assessing the presence of subclinical atherosclerosis in 264 HIV-infected patients and 279 controls. Clinical evaluation included ultrasound examination of the carotid arteries, arterial stiffness by pulse wave velocity (PWV) and augmentation index (AIx), laboratory analysis of peripheral blood, and cardiovascular risk according to FCRS criteria. The significance level adopted in the statistical analysis was p < 0.05. Results: Plaques were found in 37% of the HIV group and 4% of controls (p < 0.001). Furthermore, carotid intima-media thickness was higher in the HIV group than in controls (p < 0.001). Patients with carotid plaque had higher fasting glucose, total cholesterol, low-density lipoprotein cholesterol, and triglycerides than those without plaques. The presence of HIV, adjusted for age, overweight/obesity, and smoking increased by almost fivefold the risk of atherosclerotic carotid plaque (OR: 4.9; 95%CI: 2.5‑9.9; p < 0.001). Exposure to protease inhibitors did not influence carotid intima-media thickness, was not associated with carotid plaque frequency, and did not alter the mechanical characteristics of the arterial system (PWV and AIx). Conclusions: HIV-infected patients are at increased risk of atherosclerosis in association with classical cardiovascular risk factors. Treatment with protease inhibitors does not promote functional changes in the arteries, and shows no association with increased frequency of atherosclerotic plaques in carotid arteries. The FCRS may be inappropriate for this population. (Arq Bras Cardiol. 2018; 110(5):402-410) Keywords: Atherosclerosis / complications; HIV; Cardiovascular Diseases / mortality; Carotid Intima Media Carotideo; Vascular Stiffness; Risk Factors. Introduction By the end of 2012, about 35 million people were HIV positive worldwide. By June 2012 in Brazil, 656,701 cases had been identified since the first one detected in São Paulo in 1980; this includes 253,706 lethal cases between 1980 and 2011. 1,2 In the mid-1990s rates were increasing, but the current situation indicates a stable epidemic, 2 with signs of a reduction in mortality rate in the last decade. 1 The most important contributing factors were the introduction and easy access to highly active antiretroviral therapy (HAART). However, over the years, observations have shown that HAART may alter the patient’s lipid profile, thereby accelerating atherosclerosis. 3-8 Despite this, cardiovascular disease (CVD) is the leading cause of death worldwide (World Health Organization, 2013) and represents the foremost cause of preventable death. There is some indication of a possible direct effect from viral protein particles or infected cells liberating proteins in the receptors present in the vascular endothelium, thus favoring the presence of pro-coagulants, platelet activation, reduced nitric oxide production from the destruction of CD4 T lymphocytes (CD4 + cell), and the production of inflammatory cytokines. 4,9,10 Recent publications have indicated that viral effect on the vascular endothelium can contribute to a reduction in the number of primary endothelial cells, which leads to endothelial dysfunction and atherosclerosis. 11 Nevertheless, there is no consensus on the relationship between HAART and atherosclerosis; this may be due to the complexity of the factors involved. 4-6,8,10,11 In light of these facts, new strategies have been suggested to prevent cardiovascular events, including subclinical atherosclerosis research. 6,12-16 402