HIV can cause damage to the arteries and blood vessels predictive of future cardiovascular disease when a person has been infected with the virus for as little as two years, investigators report in the journal Atherosclerosis. None of the HIV-positive individuals in the study were taking antiretroviral therapy and all had a normal metabolic profile.
“Our investigation provides compelling evidence that HIV infection is atherogenic independent of the other determinants of the vascular risk that may operate in HIV patients”, write the investigators.
An increased risk of cardiovascular diseases such as heart attack and stroke has been observed in HIV-positive patients taking antiretroviral therapy. It is possible that this could be due to the effect of some anti-HIV drugs on blood fats and sugars. An alternative explanation is that HIV itself causes vascular damage, irrespective of the use of HIV therapy.
Because this issue is still poorly understood, investigators in Italy designed a case controlled study, the aim of which was to see if HIV had an independent effect on vascular function and structure. Brachial flow-mediated vasodilation and carotid intima-media thickness were measured. These are two validated indicators of vascular function.
The study involved 38 HIV-positive patients with a normal metabolic profile and no history of antiretroviral therapy. These patients were matched with 41 HIV-negative controls of the same age, sex, who also had a similar metabolic profile and smoking history to the HIV-positive patients.
The mean duration of infection with HIV was 26 months, with mean viral load being 46,000 copies/ml and mean CD4 cell count 385 cells/mm3.
Carotid intima-media thickness was significantly higher in the HIV-positive patients than the controls (common carotid artery, 0.85 vs. 0.62mm, p
Baseline brachial artery diameter was comparable in the HIV-positive patients and the controls (mean, 3.73 vs. 3.64mm). Therefore flow mediated dilation was monitored. This was significantly poorer in HIV-positive patients than controls (9% vs. 12%, p
Next the investigators restricted their analysis to the HIV-positive patients to see if markers of HIV disease progression (viral load, CD4 cell count, and tumour necrosis factor-alpha) were associated with changes in vascular function.
Their results showed that flow-mediated dilation was significantly poorer (p = 0.001) in patients with a viral load above 23,000 copies/ml compared to those with a viral load below this level. Furthermore, patients with a tumour necrosis factor-alpha above 16pg/ml also had poorer flow-mediated dilation (p = 0.001).
Further analysis showed that changes in carotid intima-media thickness were associated with longer duration of HIV infection (p
“Our results support the concept that HIV infection itself can trigger atherogenic mechanisms at an early stage of the infection”, comment the authors.
“We have found evidence of cardiovascular abnormalities, namely endothelial dysfunction and carotid-media thickening, in HIV-infected patients who had never received antiviral treatment”, comment the authors. They add, “Our results support the concept that HIV infection itself can trigger atherogenic mechanisms at an early stage of the infection.”
Oliviero U et al. Human immunodeficiency virus per se exerts atherogenic effects. Atherosclerosis 204: 586-89, 2009.