Carotid intima-media thickness course in HIV-infected patients: beyond classical cardiovascular risk factors

Abstract

The study of atherosclerosis in HIV-infected patients is highly relevant due to the longer life expectancy and disturbances observed in metabolic parameters. A previous issue of AIDS included a very interesting study by Currier et al.[1], which investigated atherosclerosis in HIV-infected patients. This work is especially warranted because the course of carotid intima-media thickness (IMT) is a well validated marker of atherosclerosis progression, and provides us with a precise view of the risk of suffering from future cardiovascular events [2]. Currier et al.[1] conclude that neither HIV infection, nor the antiretrovirals prescribed, significantly influence the rate of carotid IMT increase. These results deserve further consideration because they are not in line with published literature. The rate of IMT increase reported by Currier et al.[1] is far more diminished compared to similar studies (Table 1) [3–5]. It is even significantly lower than the considered normal rate of carotid IMT increase (0.01 mm/year). Furthermore, most of these studies showed a significantly higher rate of IMT increase in HIV-infected patients compared to a non-infected population [3,4].Table 1: Summary of studies addressing the course of IMT in HIV-infected patients.These apparently discordant results may be due to several reasons. First, considering technical issues, Currier et al.[1] scanned the common carotid artery (CCA) of 90 HIV-infected patients. The anatomic and physiologic conditions of the CCA (laminar flux) make it unlikely to find significant differences between groups, especially in young participants. Larger studies or, alternatively, more complex IMT acquisition protocols (including data from bulb or internal carotid arteries) should be more informative. Second, HIV-infected patients are chronically inflamed, and this condition might influence the carotid IMT values. Accordingly, Hsue et al.[6] reported a significant influence of cytomegalovirus specific CD4 cell responses and concentrations of C-reactive protein in the development of atherosclerosis in HIV-infected patients. Furthermore, it should be noted that up to 38% of the IMT variability might be attributed to genetic conditions [7]; therefore, the study of genetic polymorphisms in this scenario may be of great interest [8]. In summary, the assessment of atherosclerosis should not be limited to the study of the CCA and the assessment of environmental factors (antiretroviral therapies). We should strengthen its scope by incorporating nonclassical cardiovascular risk factors, such as genetics, immune responses, and so on, to go beyond classical markers or antiretroviral therapies. Sponsorship: Financially supported by FIS (PI041752), RC/MN (C03/08). Blai Coll is awarded by Instituto de Salud Carlos III.