Boston—Antiretroviral therapy (ART) alone is not enough to reduce the elevated arterial inflammation linked to an increased risk of cardiovascular disease in HIV-infected patients.

That’s according to a study published in JAMA Cardiology, which noted that initiation of ART soon after diagnosis of an HIV infection did not prevent the progression of significant arterial inflammation in a small group of previously untreated patients.

The follow-up investigation was led by researchers from Massachusetts General Hospital (MGH).

“Our previous studies have found that persistent arterial inflammation may predispose people living with HIV to the development of high-risk coronary artery plaques that are potentially more likely to rupture and cause a heart attack,” explained lead author Markella Zanni, MD. “Our findings suggest that additional strategies geared toward reducing arterial inflammation among HIV-infected patients receiving ART may be needed.”

Background information in the article notes that a number of studies have suggested that HIV-infected patients have a 50% to 75% increased risk of heart attack and stroke compared with uninfected individuals who have the same traditional risk factors.

A previous study by some of the same researchers found levels of inflammation within the aortas of HIV-infected individuals that were comparable to those seen in patients with established cardiovascular disease, although it was not known whether the inflammation had developed before or during the participants’ 3 months of ART treatment.

Recognizing that ART reduces several measures of immune system activation, the current study was designed to investigate whether it could suppress or reduce arterial inflammation.

For the study, 12 previously untreated HIV-infected men at an average of 11 months after diagnosis who began ART with a currently used combination of four antiviral medications were compared to 12 uninfected, age-matched control participants. None of the participants had a prior history of coronary artery disease or autoimmune or inflammatory disease other than HIV infection, and none had significant cardiovascular risk factors.

Imaging was used at the beginning of the study and 6 months later to assess effect. Results indicate that, while ART suppressed viral loads and increased levels of CD4 T cells in HIV-infected participants, 80% of them developed increased inflammation of the aorta during the 6-month study period.

Inflammation was reduced significantly in lymph nodes and somewhat in the spleen, but arterial inflammation was found to have increased to levels similar to those seen in the earlier study of patients already receiving ART.

In addition, coronary artery plaque initially identified in a quarter of the HIV-infected participants had enlarged and new plaque developed in one HIV-infected patient during the study period.

“Further research is needed to better understand the relationship between persistent immune activation, arterial inflammation and plaque development in HIV infection,” said senior author Steven Grinspoon, MD, in a MGH press release. “We need to compare the effects of different antiretroviral therapy regimens on arterial inflammation over time. Moreover, we need to investigate the important question of whether administering immune-modulatory strategies along with ART can help suppress arterial inflammation, stabilize coronary plaques and reduce cardiovascular risk in HIV-infected patients.”

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