Human Immunodeficiency Virus Per Se Exerts Atherogenic Effects

June 2009

Human Immunodeficiency Virus Per Se Exerts Atherogenic Effects
Oliviero U, et al.. Atherosclerosis 2009;204:586-589. [PubMed Abstract]

Background: Premature atherosclerosis with HIV infection has been attributed to both HIV disease and its treatment. The purpose of the study was to determine the role of HIV infection in promoting atherogenesis.

Methods: The authors studied 38 patients with HIV infection for comparison with 41 controls who were matched by age, BMI, blood pressure, lipid profile, and smoking. All participants were excluded if they had prior cardiovascular events, diabetes, hypertension, prior or current antiretroviral drugs, any OI, or hepatitis B or C. The evaluation was based on thickness of carotid intima measured by ultrasound of both the common and internal carotid arteries. Vascular reactivity was measured with the same imaging system of the brachial artery. Endothelial-dependent vasodilation was determined by measuring the maximum increase in brachial artery diameter during reactive hyperemia produced by blood pressure cuff inflated to 250 mmHg for 5 minutes with sudden cuff deflation and measurement of brachial based on brachial artery diameter measurements four times in the following 90 seconds. These measurements were repeated after sublingual nitroglycerin to determine endothelial-independent vasodilatation.

Results: Baseline data for HIV-infected patients and controls are summarized in the Table below. Also shown are results of the study for the mean carotid and internal carotid artery intima-media thickness. Of particular interest was the observation that changes in carotid intima correlated with the duration of HIV infection (P<0.001) and the CD4 cell count (P=0.04). Also shown was impairment in the brachial endothelial–dependent vasodilatation. The results of this assay correlated with the HIV viral load (P<0.001).

HIVn=38

Controlsn=41

Baseline Age median BMI (kg/km)

Hs-CRP (mg/L)

Current smoker

40 yrs22

126/79

0.7

45%

38 yrs22

114/76

0.4

41%

HIV Data (median) Duration (months) Viral load (copies/mL)

CD4 count (cells/mL)

26 + 2646,312

45%

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Carotid intima measurements IMT* (common carotid) IMT*(internal carotid artery)

FMD* (%)

NMD (%)

0.85 + 0.180.82 + 3.0

8.8 + 3.0

21 + 5

0.62 + 0.12**0.64 + 0.13**

12.2 + 3.0**

22 + 5

*IMT = intima-media thickness; FMD = endothelial dependent vasodilation, NMD = endothelial – independent vasodilation.
**P value for difference <0.001.

Conclusion: The authors conclude that HIV infection causes cardiovascular abnormalities in endothelial function and carotid intima-media thickness, these effects occur early in the course of infection, they are independent of antiretroviral therapy or metabolic factors, and some of the changes are related to the duration of infection and viral load.

Comment: Some of these observations have been previously reported (Hue PY. Circulation 2004;109:1603; Blum A. Clin Cardiol 2005;28:149; Charakida M. Circulation 2005;112:103). This paper is reviewed because the scientific methods are particularly strong and the message is worth emphasis.