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Atazanavir and Cardiovascular Risk Among Human Immunodeficiency Virus-Infected Patients: A Systematic Review
Dominic Chow1, Cecilia Shikuma2, Corey Ritchings3
1Hawaii Center for AIDS, John A. Burns School of Medicine, University of Hawaii Mānoa, Honolulu, HI, USA. dominicc@hawaii.edu.
Insights
This systematic review found no increased cardiovascular disease risk in HIV patients taking ritonavir-boosted atazanavir (ATV). ATV also showed benefits in slowing atherosclerosis progression, suggesting a favorable cardiovascular profile.
Area of Science:
- Cardiology
- Infectious Diseases
- Pharmacology
Background:
- Human immunodeficiency virus (HIV) infection elevates cardiovascular disease (CVD) risk.
- Certain antiretrovirals, including protease inhibitors, may increase CVD risk.
- Ritonavir-boosted atazanavir (ATV) has shown potential for a favorable cardiovascular profile, possibly due to hyperbilirubinemia.
Approach:
- A systematic literature review was conducted using PubMed and Embase databases.
- Searched for studies on atazanavir (ATV), HIV, and CVD, including randomized-controlled and observational studies in adult humans.
- Primary outcome was CVD incidence; surrogate markers of CVD were also included.
Key Points:
- Ten studies were analyzed, reporting on CVD outcomes, atherosclerosis (carotid intima-media thickness), and endothelial function.
- Atazanavir (ATV) was not associated with an increased risk of myocardial infarction or other adverse cardiovascular events.
- ATV demonstrated beneficial effects on carotid intima-media thickness progression compared to non-ATV regimens.
Conclusions:
- No increased risk of adverse cardiovascular events was observed in HIV patients receiving atazanavir (ATV).
- Markers of atherosclerosis improved, suggesting a potential antioxidant effect of ATV.
- Endothelial function remained unaffected by atazanavir (ATV) treatment.
Introduction:
Patients with human immunodeficiency virus (HIV) infection have an increased risk of cardiovascular disease (CVD). While viral suppression with antiretroviral therapy decreases CVD risk overall, several studies have suggested that certain antiretrovirals, particularly certain protease inhibitors, may be associated with an increased relative risk of CVD. In AIDS Clinical Trials Group 5260 s, ritonavir-boosted atazanavir (ATV) was associated with slower atherosclerosis progression compared to ritonavir-boosted darunavir and raltegravir, potentially due to hyperbilirubinemia. Although hyperbilirubinemia may lead to increased rates of treatment discontinuation, it may also contribute to a favorable cardiovascular (CV) profile for ATV. To fully elucidate the effect of ATV on CVD risk among HIV-infected patients, a systematic review of the literature was performed.
Methods:
A systematic search of the PubMed and Embase databases was conducted on August 26, 2015, using terms to identify papers that discuss ATV, HIV, and CVD. Articles were limited to English-language publications of randomized-controlled or observational studies investigating adult humans. The primary outcome was the incidence of CVD. Articles describing surrogate markers of CVD were also included.
Results:
Ten studies were included in this qualitative analysis: six reported CVD outcomes, two reported data on atherosclerosis as assessed by carotid intima-media thickness (cIMT), and two reported outcomes related to endothelial function. The studies reporting the incidence of myocardial infarction (MI) among HIV-infected patients showed that ATV (boosted and unboosted) was not associated with an increased risk of acute MI. Other CV endpoints were similarly unaffected by treatment with ATV. Compared with non-ATV-based regimens, ATV had beneficial effects on cIMT progression in the publications identified, with no apparent impact on endothelial function.
Conclusions:
This analysis showed that there was no increased risk or occurrence of adverse CV events among HIV-infected patients receiving ATV. Markers of atherosclerosis were improved, suggesting a possible antioxidant effect of ATV, and endothelial function was not affected.
Funding:
Bristol-Myers Squibb (article processing charges and medical writing support).
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