HIV type 1 infection, and not short-term HAART, induces endothelial dysfunction.
OBJECTIVE
Ischemic cardiovascular events increasingly occur during long-lasting HIV infection and are attributed either to the infection itself or to the use of HAART. Endothelial dysfunction and platelet activation are markers of atherosclerosis. Our aim was to assess whether patients with chronic HIV infection present endothelial dysfunction and whether this is the consequence of infection or of HAART.


METHODS
Fifty-six HIV-infected patients were studied in a retrospective cohort study before and 3, 6, 12 and 24 months after starting HAART with protease inhibitors (n = 28) or nonnucleoside reverse transcriptase inhibitors (n = 28), and compared with 28 age-matched and sex-matched healthy controls, and with 10 naive HIV-infected patients studied at diagnosis and after 12 months of untreated infection.


METHODS
Soluble endothelial and platelet activation markers were measured in plasma by flow cytometry.


RESULTS
Soluble P-selectin, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor were significantly higher in HIV-infected patients than in healthy controls, whereas soluble CD40 ligand and tissue type plasminogen activator were within normal range. During follow-up, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor but not soluble P-selectin decreased progressively, without significant differences between protease inhibitors and nonnucleoside reverse transcriptase inhibitors treatment. In naive, untreated patients, increased plasma markers of endothelial dysfunction were confirmed at diagnosis, with no changes upon follow-up.


CONCLUSIONS
Chronic HIV infection, and not its pharmacological treatment, induces alterations of markers of endothelial function. Short-term treatment with HAART reduces some markers of endothelial dysfunction, with no differences between protease inhibitors and nonnucleoside reverse transcriptase inhibitors.
Francisci
Daniela
D
Division of Infectious Diseases, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia 06126, Italy.
Giannini
Silvia
S
Baldelli
Franco
F
Leone
Mario
M
Belfiori
Barbara
B
Guglielmini
Giuseppe
G
Malincarne
Lisa
L
Gresele
Paolo
P
D000328:Adult; D019380:Anti-HIV Agents / Q000009:adverse effects / Q000494:pharmacology; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects*; D050197:Atherosclerosis / Q000139:chemically induced / Q000821:virology*; D015415:Biomarkers / Q000097:blood; D018791:CD4 Lymphocyte Count; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D004812:Epidemiologic Methods; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology / Q000821:virology; D017320:HIV Protease Inhibitors / Q000009:adverse effects / Q000494:pharmacology; D015497:HIV-1 / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology; D012367:RNA, Viral / Q000097:blood; D018894:Reverse Transcriptase Inhibitors / Q000009:adverse effects / Q000494:pharmacology; D019562:Viral Load; D055815:Young Adult
D019380:Anti-HIV Agents; D015415:Biomarkers; D017320:HIV Protease Inhibitors; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors