San Francisco, CA - A study tracking progression of carotid intima-media thickness in HIV-positive patients should spur physicians to consider HIV an independent risk factor for cardiovascular disease, researchers say. Writing in the March 16, 2004 rapid access issue of Circulation, Dr Priscilla Y Hsue and colleagues say that immunodeficiency, coexisting risk factors, and chronic inflammation all likely contribute to the accelerated atherosclerosis seen in HIV patients.1
"Our findings and data accumulating from other sources suggest that it would be reasonable to count HIV infection itself as a coronary risk factor," the authors write.
"I don't think this is such a radical idea," Hsue told heartwire. "We now think of atherosclerosis as an inflammatory disease, and since HIV patients have chronic infection and in our study were noted to have a much higher CRP than age-matched controls, I think it's not too surprising that they would also be at increased risk of atherosclerosis."
Atherosclerosis progression and HIV
Hsue et al's study measured carotid intima-media thickness (IMT) in 148 HIV-infected adults and in 63 age- and sex-matched non-HIV-infected controls, then compared these with follow-up measurements taken one year later. They report that mean IMT was significantly greater in HIV+ patients than in noninfected controls at baseline and that IMT increased in HIV+ patients over one year but remained the same in the control patients. When all patients were included in the analysis, HIV infection, age, LDL cholesterol level, smoking, and Latino race were all independent predictors of thicker IMT.
Atherosclerosis, inflammation, and HIV status|
Measure |
HIV+ |
Controls |
p |
|
Baseline IMT (mm) | 0.91 | 0.74 | 0.0001 |
|
Presence of carotid plaque (%) | 45 | 24 | 0.0034 |
|
Mean progression of IMT over one year (mm) | 0.074 | -0.006 | 0.002 |
|
Baseline CRP (mg/L) | 1.6 | 0.8 | <0.01 |
"Because increasing carotid IMT is an independent predictor of stroke and MI in other populations, the findings of this study suggest that the rate of vascular events is likely to increase substantially in HIV patients," Hsue et al write.
The study was not able to determine whether there was any direct link between atherosclerosis progression and antiretroviral medication, but as Hsue pointed out, HIV+ patients on antiretroviral therapy in the study had been on medication only for roughly three years. Longer studies are necessary to pinpoint any direct link between antiretrovirals and atherosclerosis risk, she says.
A different disease?
In the meantime, however, Hsue believes there is ample evidence for physicians to consider switching HIV+ patients with existing CVD risk factors to drugs that do not increase cholesterol and hypertension, as do many of the commonly prescribed HIV medications. A recently FDA-approved protease inhibitor, atazanavir sulfate (ReyatazTM, Bristol-Myers Squibb), does not appear to have the same detrimental effects on lipids as many of its predecessors, for example.
As well, physicians treating HIV+ patients should appreciate that the mechanisms of atherosclerotic disease progression may differ in HIV+ patients from that in the general population. If HIV itself is considered as a risk factor, control of other risk factors is that much more critical.
"Their physicians have to think about aggressively treating hypertension, aggressively addressing risk factors like smoking, putting these patients on aspirin, and so on. In the past, this hasn't been rigorously followed. It just wasn't a concern," Hsue says.
Times are changing, however. At San Francisco General, Hsue's group has started a new HIV cardiology clinic "just to recognize the special population and address their needs," she says. "It's actually one of the first specialty clinics of its kind in the country."
- Progression of atherosclerosis as assessed by carotid intima-media thickness in patients with HIV infection2004; :DOI: 10.116101.CIR.0000124480.32233.8A Available at: http://www.circulationaha.org







