In studies from Europe and the USA, HIV has been associated with a ∼50% increased risk of myocardial infarction after adjustment for traditional coronary heart disease (CHD) risk factors
CHD incidence and prevalence among patients infected with HIV is expected to rise in resource-constrained countries as access to life-extending combination antiretroviral therapy (cART) broadens
Traditional CHD risk factors and HIV-specific immune activation jointly promote atherogenesis in individuals infected with HIV
Some cART regimens exacerbate metabolic CHD risk factors, through induction of lipodystrophy or more-direct mechanisms, but seem to lessen, albeit without fully normalizing, many indices of proatherogenic HIV-specific immune activation
cART regimens with the fewest adverse metabolic effects should be selected and traditional risk factors should be carefully managed
Tailored CHD risk-prediction paradigms are needed, and agents that synergistically decrease proatherogenic immune activation are being studied
The lives of individuals infected with HIV who have access to combination antiretroviral therapy (cART) are substantially prolonged, which increases the risk of developing non-AIDS comorbidities, including coronary heart disease (CHD). In Europe and the USA, individuals with HIV infection have a ∼1.5-fold increased risk of myocardial infarction relative to uninfected individuals. In Africa, the relative risk of myocardial infarction is unknown, but broadened access to life-extending cART suggests that rates of CHD will rise in this and other resource-constrained regions. Atherogenesis in HIV is affected by complex interactions between traditional and immune risk factors. cART has varied, regimen-specific effects on metabolic risk factors. Overall, cART seems to lessen proatherogenic immune activation, but does not eliminate it even in patients in whom viraemia is suppressed. Current strategies to decrease the risk of CHD in individuals infected with HIV include early initiation of cART regimens with the fewest metabolic adverse effects, and careful management of traditional CHD risk factors throughout treatment. Future strategies to prevent CHD in patients with HIV infection might involve the use of HIV-tailored CHD risk-prediction paradigms and the administration of therapies alongside cART that will further decrease proatherogenic HIV-specific immune activation.
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M.V.Z. has worked on investigator-initiated research projects supported by scientific grants from Gilead Sciences and Immunex. J.S. has received travel grants from Boehringer-Ingelheim, Gilead Sciences, and ViiV Healthcare. S.K.G., through his institution, has received scientific grant support from EMD Serono Inc., Gilead Sciences, and Immunex. In addition, S.K.G. has received travel support and consulting fees from Novo Nordisk, and consulting fees from AstraZeneca and Navidea. P.R. has received independent scientific grant support from Bristol-Myers Squibb, Gilead Sciences, Janssen Pharmaceuticals, Merck & Co, and ViiV Healthcare, and travel support from Gilead Sciences, all through his institution. In addition, P.R. has served on a scientific advisory board for Gilead Sciences and currently serves on a data safety monitoring committee for Janssen Pharmaceuticals, for which his institution has received remuneration.
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Zanni, M., Schouten, J., Grinspoon, S. et al. Risk of coronary heart disease in patients with HIV infection. Nat Rev Cardiol 11, 728–741 (2014). https://doi.org/10.1038/nrcardio.2014.167
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