September 12, 2010
Cardiovascular risk may be slightly higher even among HIV-positive people whose immune systems are able to keep HIV at bay without the help of antiretrovirals, according to a small study by U.S. researchers presented at ICAAC 2010. The findings are far from the last word on the issue of whether HIV treatment or HIV itself is the greater culprit for heart problems. But they appear to lend additional weight to arguments that regardless of whether a person is on HIV treatment, HIV does indeed play its own role in cardiovascular risk.
The study involved just 26 people: 13 HIV-negative volunteers were matched by age, race and sex to 13 HIV long-term nonprogressors (LTNPs), a small proportion of HIV-positive people who have never taken HIV medication, but have nonetheless had a stable CD4 count, stable viral load and no sign of HIV disease progression for at least five years. The study recruited volunteers from two HIV clinics in Illinois. (Results were presented by Hector Bonilla of Summa Health System in Akron, Ohio.)
For each volunteer, the researchers took measurements that are thought to be gauges of cardiovascular risk: Carotid artery intima-media thickness (i.e., the thickness of the internal carotid artery wall) was examined, as well as a number of inflammatory markers, including C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM1) and tumor necrosis factor receptor-II (TNF RII). Of these measurements, only TNF RII levels were found to be significantly higher among LTNPs than HIV-negative volunteers; VCAM1 showed a trend toward being worse for LTNPs, but the findings fell short of statistical significance, meaning there is a possibility the trend was due to chance. The researchers also noted that HDL cholesterol levels tended to be much lower among LTNPs than the HIV-negative volunteers, further supporting the trend toward a worse cardiovascular profile among LTNPs. Carotid artery intima-media thickness was similar between the two groups, but a measurement taken at the bulb of the internal carotid artery, right where the artery begins, showed a trend toward being thicker among LTNPs, although this too fell a bit short of statistical significance.
The researchers assert that taken together, the findings suggest that ongoing HIV replication is causing increased levels of inflammation and atherosclerosis, which can in turn increase a person's risk for developing cardiovascular problems. That conclusion is in line with a number of earlier studies on inflammation and cardiovascular risk, but what makes this study intriguing is that it found signs of these problems even in people whose immune system appears to keep HIV replication under control naturally. (Although a few of the LTNPs in this study had a viral load that hovered in the 10,000 to 20,000 range, most had a viral load below 2,000, and four had a viral load below 400, technically making them "elite controllers.")
According to study author Hector Bonilla, these findings support his view that a person who has been diagnosed with HIV should generally begin antiretroviral therapy as soon as possible, regardless of CD4 count or viral load. Although that opinion is shared by many HIV clinicians, it remains a subject of intense debate. Some clinicians still support an upper CD4 limit to starting treatment, while many others feel that a wide range of risks and benefits (as well as an HIV-positive person's mental readiness) should be taken into account before a decision is made to start treatment, at least for people with a CD4 count above 350.
Myles is the editorial director of TheBody.com and TheBodyPRO.com.
Bonilla H, McShannic J, Chua D, Conner R, Mark F, McComsey G. Cardiovascular disease and inflammatory markers in long term non-progressors. In: Program and abstracts of the 50th Interscience Conference on Antimicrobial Agents and Chemotherapy; September 12-15, 2010; Boston, Mass. Abstract H-220.
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