POZ - Treatment News : Is HIV Itself a Risk Factor for Heart Disease?

Even HIV-positive patients with undetectable viral loads and not on antiretroviral (ARV) therapy have thicker carotid arteries than HIV-negative patients, according to a study published in the June 1 issue of AIDS. While these data confirm that people living with HIV may be at a higher risk for cardiovascular disease (CVD) as they age, the findings also raise important questions about the underlying cause of the increased CVD risk among HIV-positive people.

Several studies have documented that people living with HIV, on average, have increased carotid intima-media thickness (IMT)—thicker carotid artery walls—compared with HIV-negative individuals. Researchers initially attributed this to the lipid-increasing effects of certain ARVs. Then they found that HIV-positive people not on therapy had increases in IMT compared with HIV-negative people, suggesting that an inflammatory response to high levels of virus caused arterial wall problems.

To explore these theories, Priscilla Hsue, MD, and her colleagues from the University of California in San Francisco performed ultrasound tests of the carotid arteries of 494 HIV-positive and 93 HIV-negative patients. What set this study apart from the rest was that it enrolled 33 “elite controllers”—HIV-positive individuals who maintain undetectable viral loads without using ARV treatment and who show little or no signs of HIV disease progression.

Hsue’s team found that the elite controllers had significantly greater arterial thickness than the HIV-negative patients, debunking theories that unchecked viral loads, low CD4 counts or ARV treatments are solely to blame. In fact, the difference in IMT between the elite controllers and the HIV-negative patients was nearly as great as that between the HIV-negative patients and HIV-positive patients with higher viral loads who were on ARV therapy.

Hsue’s team also found that the elite controllers had levels of an inflammatory protein called high-sensitivity C-reactive protein (hsCRP) that were nearly as elevated as people with uncontrolled HIV who were taking ARVs, suggesting that the mere presence of HIV in the body—even at very low levels—is enough to trigger an inflammatory response to the virus.

The authors acknowledge that future studies will be needed to confirm their results. If similar results are found, they argue, providers may need to be even more aggressive in how they manage heart disease risk in people with HIV who are 50 and older.