Open AccessFactors associated with subclinical atherosclerosis in HIV infected patients from northeast of Brazil
Author(s) -
Úrsula Maria Moreira Costa Burgos,
Enaldo Vieira de Melo,
Ângela Maria da Silva,
Antônio Carlos Sobral Sousa,
Willams de Matos,
Maria Aline Moura Reis,
Lucas Alves Bezerra,
Dalmo Correia Filho,
Joselina Luzia Menezes Oliveira
Publication year - 2021
Publication title -
research, society and development
Language(s) - English
Resource type - Journals
ISSN - 2525-3409
DOI - 10.33448/rsd-v10i12.20484
Subject(s) - medicine , hazard ratio , subclinical infection , viremia , diabetes mellitus , incidence (geometry) , human immunodeficiency virus (hiv) , gastroenterology , multicenter aids cohort study , viral load , immunology , antiretroviral therapy , endocrinology , confidence interval , physics , optics
AIDS has changed its morbidity curve, rising cardiovascular diseases. HIV-infected patients have increased cardiovascular event rates but data on the prevalence of subclinical atherosclerosis are not uniform. Methods: HIV-infected patients underwent to coronary tomography for CACs assessement. We performed a comparison between 97 HIV-infected patients and 129 seronegative healthy controls. The univariable analysis matched the association of HIV infection, cardiovascular risk profile, and HIV-related factors with subclinical atherosclerosis. Results: HIV-infected patients with CACs above zero were older (54.8±7.0 vs. 43.3.5±11.0 years; p<0.001) and more likely to have hypertension (36.7% vs. 12.5%; p=0.07) than HIV(-) CACs zero ones. Factors associated with altered CACs in unadjusted hazard ratio were age (HR=1.13; 95%CI=1.07-1.20; p<0.0001) and hypertension (HR=4.05; 95%CI=1.42-11.60; p=0.0009). When adjusted hazard ratio was constructed age, male gender and protease inhibitors (PI) use appeared as factors associated with coronary calcification. HIV-infected patients were less likely to have hypertension (20.2% vs 50.4%; p<0.001) and diabetes (5.3% vs 23.3%; p<0.001) than HIV uninfected ones. Conversely, both groups have same CACs level. Among HIV-infected patients altered CACs was 30.9%, vs 42.3% among control. Most of HIV-infected patients showed undetectable viremia and high CD4+ count, in parallel with lipid profile disturbances. Conclusion: Increased CAC incidence was associated with age, male gender and PI use among HIV-infected patients. Despite younger, fewer traditional risk factors and with controlled disease, the PLHIV had similar CAC scores compared with controls. Besides viruses itself, antiretroviral drugs play a role, mainly because control viruses at expense of worsening in lipid profile.