Six months of the combined ART regimen Stribild did not reduce arterial inflammation among treatment-naive patients with HIV, a study recently published in JAMA Cardiology found, leading researchers to conclude that other strategies may be necessary to reduce arterial inflammation in patients with the virus.
“Arterial inflammation is a marker of [cardiovascular disease (CVD)] risk in the general population and is increased among individuals with HIV infection who receive ART,” Markella V. Zanni, MD, of Harvard Medical School, and colleagues wrote. “We hypothesized that initiation of ART in treatment-naive persons would reduce arterial inflammation as well as systemic immune activation/inflammation.”
The risk for heart attack in patients with HIV is 50% greater than in uninfected individuals, and Zanni and colleagues noted that the “effects of ART on myocardial infarction risk are not fully understood.”
For their study, conducted from July 24, 2012 to May 7, 2015, Zanni and colleagues initiated Stribild (elvitegravir, cobicistat, emtricitabine, tenofovir disoproxil fumarate, Gilead Sciences; combined ART) in treatment-naive men (n = 12; mean age, 35 years) with no known CVD at the General Research Center at Massachusetts General Hospital. Twelve men without HIV were included as controls.
The researchers studied the effects of initiating combined ART on arterial inflammation in the men with HIV using fludeoxyglucose F 18 ([18F]-FDG-) PET scan. The patients were assessed at baseline and after 6 months of ART. Three participants had their assessments delayed past 6 months, and one did not complete [18F]-FDG-PET scanning at the end of the study.
The researchers found a “strong association” between increasing aortic target-background ratio and an increase in lipoprotein-associated phospholipase A2 (n = 10; r = 0.67; P = .03). Plaque volumes, both calcified and noncalcified, were greater in the three HIV patients who had plaque at baseline.
“Studies are needed to examine longer-term, comparative effects of different ART regimens on arterial inflammation,” Zanni and colleagues wrote. “In addition, future studies are needed to elucidate the relationship between arterial inflammation, atherogenesis, and myocardial infarction in HIV.”
James H. Stein, MD, the Robert Turell Professor of Cardiovascular Research at the University of Wisconsin School of Medicine and Public Health, and Priscilla Y. Hsue, MD, professor of medicine at the University of California, San Francisco, wrote in an accompanying editorial that the study showed decreases in lymph node inflammation and “underscores how little we understand about the effects of HIV and ART on arterial injury and function.”
Priscilla Y. Hsue
“Because of the complexity of the effects of ART on inflammation and immune regulation and because of the inconsistent results of the ART initiation studies, we need to continue to harness the power of large, randomized clinical trials to better characterize the effects of ART and inflammation on arterial injury,” Stein and Hsue wrote. “By doing so, we eventually will be able to provide effective [atherosclerotic cardiovascular disease (ASCVD)] risk-reducing treatments to the growing population of individuals who are living with HIV infection but now face dying of ASCVD.” – by Andy Polhamus
Disclosure: The researchers report no relevant financial disclosures. Please see the full editorial for a list of all authors’ relevant financial disclosures.