Effects of aging and smoking on carotid intima-media thickness in HIV-infection

aMassachusetts General Hospital (MGH) Program in Nutritional Metabolism bMGH Cardiovascular Division, MGH cBiostatistics Center. *These authors contributed equally to this work.
AIDS (London, England) (Impact Factor: 5.55). 08/2012; 27(1). DOI: 10.1097/QAD.0b013e328358b29c
Source: PubMed


To investigate the effects of aging and smoking on carotid intima-media thickness (cIMT) among patients with and without HIV.

Data from a community sample of HIV-infected and HIV-uninfected participants were analyzed. Carotid intima-media thickness was measured via carotid ultrasound and smoking history was obtained via patient interview.

Data on 166 male and female participants with stable HIV-infection and 152 healthy HIV-uninfected participants were analyzed. Among the HIV-infected and HIV-uninfected participants, a significant association was observed between age and cIMT [r = 0.51, P < 0.0001 (HIV), r = 0.39, P < 0.0001, (non-HIV)], and between smoking burden and cIMT [r = 0.42, P < 0.0001 (HIV), r = 0.24, P = 0.003 (non-HIV)]. In multivariate regression modeling among all participants (HIV and non-HIV), a significant three-way interaction was observed between age, smoking burden, and HIV status with respect to cIMT (P < 0.010), controlling for sex, race, and traditional cardiovascular disease (CVD) risk factors, such that increased cIMT was associated with increased smoking burden and age to a greater degree among HIV-infected vs. HIV-uninfected participants. Among HIV-infected participants a significant interaction between smoking burden and age with respect to cIMT was seen (P = 0.027) controlling for race, sex, CVD risk factors, immunological function, and antiretroviral therapy use.

A significant interaction between HIV, age, and smoking on cIMT was observed, suggesting that HIV-infection modifies the relationship of age and smoking on cIMT in this population. These findings emphasize the need to encourage smoking cessation in this population, due to its deleterious effect on subclinical atherosclerosis in older HIV-infected patients.

11 Reads
  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE:: As survival with human immunodeficiency virus (HIV) infection improves, HIV-infected individuals appear to be susceptible to development of chronic diseases, including restrictive and obstructive lung diseases. We sought to determine the independent association of HIV infection on lung function decline. DESIGN:: Longitudinal analysis of the AIDS Linked to the Intravenous Experience study, an observational cohort of current and former injection drug users METHODS:: Generalized estimating equations were used to determine the effects of markers of HIV infection on adjusted annual change in FEV1 and FVC. RESULTS:: A total of 1064 participants contributed 4555 spirometry measurements over a median follow-up time of 2.75 years. The mean age of the cohort was 48 years, nearly two-thirds were male and 85% current smokers. After adjustment, the overall annual decline of FEV1 and FVC between HIV-infected and uninfected persons did not differ. However, there was a 76 ml/yr greater rate of decline in FEV1 and 86 ml/yr greater rate of decline in FVC among HIV-infected participants with viral load >75,000 copies/ml compared to HIV-uninfected individuals (p < 0.01). Similarly, HIV-infected individuals with CD4 < 100 cells/mm had a 57 ml/yr more rapid decline in FEV1 and 86 ml/yr more rapid decline in FVC than HIV-uninfected participants (p = 0.018 and p = 0.001, respectively). CONCLUSIONS:: Markers of poorly controlled HIV disease are independently associated with accelerated annual lung function decline, with decrements in both FEV1 and FVC. These findings highlight the need for optimized HIV antiretroviral therapy in addition to smoking cessation among HIV-infected individuals with tobacco dependence.
    No preview · Article · Jan 2013 · AIDS (London, England)
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The increased immune activation and inflammation of chronic HIV-infection and the characteristic dyslipidemias associated with HIV infection and antiretroviral therapy (ART) contribute to an increased risk of atherosclerotic vascular disease among HIV-infected adults. There is an emerging need to understand determinants of cardiovascular disease (CVD) among individuals aging with HIV in sub-Saharan Africa. We determined the prevalence of subclinical atherosclerosis [carotid intima media thickness (CIMT) ≥0.78 mm] and its correlation with traditional CVD risk factors among HIV-infected adults.
    Full-text · Article · Feb 2014 · PLoS ONE
  • [Show abstract] [Hide abstract]
    ABSTRACT: The objective of this review is to appraise recently published literature that describes the relationship between HIV, biologic and environmental risk factors, and cardiovascular disease (CVD) risk with particular emphasis on the aging HIV population and to demonstrate that these biologic and environmental factors may interact to increase the risk of CVD in the HIV population. The mechanisms linking HIV and CVD are multifactorial and encompass biological and 'environmental' modalities including multimorbid conditions that co-occur with HIV, immunologic alterations associated with HIV, polypharmacy (which affects adherence and increases likelihood of adverse drug-drug interactions) and healthcare disparities in CVD risk reduction by HIV status. Data regarding optimal treatment strategies that balance immunological restoration and CVD risk reduction are needed.
    No preview · Article · May 2014 · Current opinion in HIV and AIDS
Show more