Taking a cholesterol-lowering statin, combined with antiretroviral (ARV) therapy, further reduced the risk of death by 67 percent in a cohort of people living with HIV, according to a new report published by PLoS One. Though the data are from an observational cohort study and need to be confirmed in a prospective clinical trial, the results add to a growing body of evidence supporting therapeutic strategies aimed at minimizing inflammation in people living with HIV. 

HIV is associated with chronic inflammation and immune activation. Though ARV therapy reduces inflammation, it often fails to reduce markers of inflammation to levels seen in people not living with HIV or other chronic infections.

Statins, technically called HMG-coenzyme A reductase inhibitors, are typically used to lower harmful cholesterol levels, thereby reducing the risk of cardiovascular disease (CVD). But research suggests that their lipid-lowering activity in the body doesn’t fully explain their effect on CVD risk—statins also appear to reduce inflammation, which has also been shown to be a CVD risk factor.

Based on these observations, along with the fact that many people living with HIV require cholesterol-lowering drugs to manage the lipid gains that often accompany ARV treatment, statins remain a logical therapy to assess for disease-reducing and life-saving effects in HIV-positive people.

Richard Moore, John Bartlett and Joel Gallant, all of Johns Hopkins University School of Medicine in Baltimore, explored this possibility by evaluating patients enrolled in the Johns Hopkins HIV Clinical Cohort who achieved undetectable viral loads within six months of starting ARV treatment after January 1, 1998. Assessment was continued until death in patients who maintained undetectable viral loads, or until their viral loads became detectable again and went above 500.

Roughly 15 percent of the 1,538 individuals who qualified for the analysis took a statin. Two thirds of study participants were men. Those who took a statin tended to be somewhat older (46 versus 42 years old) and to have started ARV treatment with a higher CD4 cell count (270 versus 200 cells).

Of the 85 people who died during the average 1.5-year follow-up period, seven used statins, whereas 78 did not. Cancers, non-AIDS-defining infections, liver failure and CVD were the main causes of death.

After adjusting for a variety of factors—CD4 cell count, viral load, hemoglobin, cholesterol levels when ARV therapy was started, age, race, hepatitis coinfection, the length of ARV therapy and the different types of ARVs used—the risk of death among those using statins was a third of that seen among those who didn’t use a statin. This was highly statistically significant, meaning it wasn’t due to chance, and translated into a 67 percent reduction in the risk of death among those who used statins in combination with HIV-suppressive ARV treatment.

“In summary,” the researchers write, “we found that patients who maintained virologic suppression on effective [ARV treatment] appeared to derive additional survival benefit from the use of a statin. If additional observational data support this finding, a randomized clinical trial would be warranted to confirm this association.”