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Carotid Plaques Develop More Often With vs Without HIV in Metabolic Syndrome Patients
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4th International Workshop on HIV and Aging, October 30-31, 2013, Baltimore
Mark Mascolini
Carotid artery intima-media thickness (cIMT) progressed at a similar rate in HIV-positive people and metabolic syndrome patients without HIV, according to results of 575-person prospective study in Canada [1]. But carotid artery plaque prevalence and incidence were significantly greater in the HIV group in this 3.6-year study.
cIMT offers a noninvasive marker that predicts development of atherosclerosis, but methods of measuring cIMT differ from study to study, and cIMT findings in people with HIV vary because of differences in study populations and other factors. Researchers at McMaster University in Hamilton, Ontario conducted this prospective study of cIMT and plaque formation in 145 HIV-positive people from the Canadian HIV Vascular Study and 430 presumed HIV-negative controls from the international 2003-2006 Study of Atherosclerosis with Ramipril and Rosiglitazone (STARR).
All participants of both studies had 12-segment carotid artery ultrasound with computer-assisted image reading at the same center. Each 35-or-older HIV-positive person was matched by age and gender to 3 presumed-HIV-negative people in STARR. Everyone in STARR had metabolic syndrome, with fasting glucose from 110 to 126 mg/dL, and all were participating in a randomized trial of cardiovascular disease and diabetes prevention; 39% of participants were from North America. The Canadian HIV Vascular Study is a multicenter cohort study assessing the relationships between HIV medications, metabolic abnormalities, and vascular disease among HIV-positive subjects. Viral load is undetectable in a large majority of cohort members.
HIV-positive study participants averaged 46.1 years in age (+/-8.3), compared with 46.4 years (+/- 8.24) in STARR controls. Most study participants, 83.5%, were men, and an average 3.6 years elapsed between first and final cIMT measurements. Compared with STARR controls, the HIV group included a higher proportion of smokers (31% versus 13.5%), and people with HIV had a lower body mass index (25.2 versus 29.7 kg/m2). The groups did not differ significantly in fasting glucose, history of high cholesterol, or statin use.
Average yearly cIMT change barely differed between the HIV group (0.019 mm +/-0.039) and STARR controls (0.017 mm +/-0.036) P = 0.63). At the baseline visit, a significantly higher proportion of HIV-positive people than controls had plaque (cIMT greater than 1.5 mm): 41.2% versus 12.3% (P < 0.001). Plaque incidence was also significantly higher in the HIV group, as plaques developed in 15.8% of people with HIV and 6.2% of controls (P < 0.001).
Multivariate analysis determined that HIV infection raised the odds of new plaque development more than 7 times (adjusted odds ratio [aOR] 7.69, 95% confidence interval 4.16 to 14.28). Other factors independently associated with plaque development were current smoking (aOR 1.95, 95% CI 1.22 to 3.12), higher fasting glucose (aOR 1.17, 95% CI 1.01 to 1.37), history of high cholesterol (aOR 2.00, 95% CI 1.29 to 3.11), high systolic blood pressure (aOR 1.02, 95% CI 1.01 to 1.03), and longer follow-up time.
The researchers proposed that incident arterial plaque is a candidate outcome for future intervention trials.
A recent US study comparing common carotid cIMT in 85 antiretroviral-naive people with HIV and 45 HIV-negative people found a 0.0177-mm 48-week increase in the HIV-negative group and a 0.0046-mm decrease in the HIV-positive group, after adjustment for cardiovascular risk factors [2]. A US study of 389 HIV-positive people, 78% of them on antiretroviral therapy, measured a median 2-year common carotid cIMT increase of 0.016 mm [3], similar to the 0.019-mm 1-year increase in HIV-positive Ontario study participants [1]. In the US study [3] people with an undetectable baseline viral load and those who maintained viral suppression throughout follow-up had declines in median cIMT (-0.009 and -0.011 mm per year).
References
1. Mbuagbaw L, Lonn EM, Smaill FM, Smieja M. Matched cohort analysis of carotid artery intima media thickness progression and carotid artery plaque amongst HIV-infected and uninfected adults. 4th International Workshop on HIV and Aging, October 30-31, 2013, Baltimore. Abstract 8.
2. Hileman CO, Carman TL, Longenecker CT, et al. Rate and predictors of carotid artery intima media thickness progression in antiretroviral-naive HIV-infected and uninfected adults: a 48-week matched prospective cohort study. Antivir Ther. 2013 Jun 11. doi: 10.3851/IMP2651. Epub ahead of print.
3. Baker JV, Henry WK, Patel P, et al. Progression of carotid intima-media thickness in a contemporary human immunodeficiency virus cohort. Clin Infect Dis. 2011;53:826-835. http://cid.oxfordjournals.org/content/53/8/826.long
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