ObjectivesAntiretroviral therapy (ART) in HIV-infected patients is associated with increased cardiovascular risk. Circulating markers of endothelial dysfunction may be used to study early atherogenesis. The aim of our study was to investigate changes in such markers during initiation of ART. MethodsIn 115 HIV-positive treatment-naïve patients, plasma lipids, E-selectin, soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), tissue-type plasminogen activator inhibitor 1 (tPAI-1) and high-sensitivity C-reactive protein (hsCRP) were measured before and after 2 and 14 months of ART. A control group of 30 healthy subjects was included. Values are mean AE standard error of the mean. ResultsPrior to treatment, HIV-infected patients had elevated levels of sICAM-1 (296 AE 24 vs. 144 AE 12 ng/mL), tPAI-1 (18 473 AE 1399 vs. 5490 AE 576 pg/mL) and hsCRP (28 060 AE 5530 vs. 6665 AE 2063 ng/mL) compared with controls (Po0.001). In contrast, sVCAM-1 and E-selectin did not differ between the groups. Initiation of ART resulted in significantly lower levels of E-selectin (15.1 AE 0.8; Po0.01), sICAM-1 (248 AE 12 ng/mL; Po0.05), sVCAM-1 (766 AE 33 ng/mL; Po0.001) and hsCRP (14 708 AE 2358 ng/mL; Po0.001) after 2 months, which remained reduced at 14 months. tPAI-1 was not influenced by initiation of ART. ConclusionsMarkers of endothelial dysfunction were elevated in treatment-naïve HIV-infected patients and were related to HIV RNA viral load. Initiation of ART reduced the levels of the majority of these markers. The positive effect of ART initiation was dependent on the duration of HIV infection prior to treatment.

Objective The aim of the study was to determine the incidence of myocardial dysfunction in an HIV‐infected population receiving state‐of‐the‐art treatment. Methods Between April 2001 and July 2002, 91 HIV‐infected patients had a radionuclide ventriculography performed with determination of right ventricular ejection fraction (RVEF) and left ventricular ejection fraction (LVEF), as well as measurement of brain natriuretic peptide (BNP). Between July 2005 and January 2007, 63 patients (69%) agreed to participate in a follow‐up study with a mean follow‐up of 4.5 years. Results All patients had normal LVEF at both examinations. A minimal increase in mean LVEF of 0.02 was observed at follow‐up (P=0.01). At the initial visit, four patients [6%; 95% confidence interval (CI) 2–15%] had a reduced RVEF, and at follow‐up two patients (3%; 95% CI 0–11%) had slightly reduced RVEF. No significant change in mean RVEF was found. No patients had increased BNP and no change in mean plasma BNP was found. Conclusions HIV‐related cardiomyopathy appears not to constitute a problem in closely monitored, well‐treated HIV‐infected patients. Compared with pre‐highly active antiretroviral therapy (HAART) studies, it seems that the improvement in immunocompetency and viral load has removed the problem of HIV‐related cardiomyopathy. Although HAART has been suggested as a possible new cause of cardiomyopathy, we did not find any evidence of this.

Coinfection with cytomegalovirus (CMV) may be involved in cardiovascular disease in HIV-infected patients. We found that higher level of CMV immunoglobulin G (IgG) was independently associated with an increased risk of coronary artery calcium and higher intima-media thickness in HIV-infected patients but not in healthy controls after adjustment for other cardiovascular risk factors and levels of herpes viridae IgG.