Acute systemic inflammation induced by influenza A (H1N1) vaccination causes a deterioration in endothelial function in HIV-infected patients.

OBJECTIVES: Vaccination of HIV-infected patients against the influenza A/H1N1 subtype was proposed as a mandatory precautionary measure during the 2009 pandemic. The immediate cardiovascular effects of the novel vaccine have been largely unexplored. We investigated the impact of vaccination on indices of endothelial function in a cohort of HIV-infected patients. METHODS: We included 24 HIV-infected patients in a study with a randomized, sham procedure-controlled design. A monovalent, adjuvanted vaccine against influenza A/H1N1 was used in the vaccine arm (n=16); patients in the control group (n=8) were subjected to a sham procedure. Endothelial function, as assessed by flow-mediated dilatation (FMD), and inflammatory markers were assessed prior to and 8 and 48 h post vaccination. RESULTS: FMD deteriorated following vaccination (baseline, 6.5 ± 1.1%; 8 h, 1.1 ± 1.5%; 48 h, 2.0 ± 1.4%; P=0.04). The white blood cell count increased at 8 h and remained elevated at 48 h. Soluble intercellular adhesion molecule-1 levels decreased after vaccination; the maximum decrease was noted at 48 h. Conversely, the sham procedure did not induce changes in endothelial function or inflammatory markers, apart from a reduction in the white blood cell count at 48 h. CONCLUSIONS: Acute systemic inflammation induced by vaccination against the influenza A/H1N1 virus resulted in a deterioration in endothelial function in HIV-infected patients, and this effect was sustained for at least 48 h. Our findings may have important implications in view of the high cardiovascular risk that HIV infection carries. The effect of the novel vaccine on endothelial function should be weighed against the immunological protection that it confers.

Association of resistin and adiponectin with different clinical blood pressure phenotypes.

We investigated whether the resistin (Res) and adiponectin (Adp) levels are associated with different clinical blood pressure (BP) phenotypes. Among 465 consecutive never-treated white subjects, we excluded those with diabetes mellitus; impaired glucose metabolism; history of any cardiovascular disease or other concurrent medical condition; secondary hypertension; ongoing vasoactive treatment. Three separate clinic BP measurements and ambulatory BP monitoring were implemented to divide 328 subjects (aged 48±6 years; 172 males) into hypertensives (n=105), masked hypertensives (n=41), white-coat hypertensives (n=52) and normotensives (n=130). Participants underwent echocardiography and oral glucose tolerance testing, whereas, from fasting venous blood samples metabolic profile, plasma Res and Adp levels were assessed. Hypertensives and masked hypertensives showed higher log(10)(Res) and lower log(10)(Adp) levels compared with normotensives, whereas white-coat hypertensives had similar levels of these adipokines compared with normotensives. Common correlates for both of the adipokines were 24-h systolic BP, standing/sitting difference of both diastolic BP and heart rate, and waist circumference. Hypertensive and masked hypertensive compared with normotensive phenotype were independently associated with log(10)(Res) with odds ratios of 1.24 (1.08-1.44), and 1.16 (1.09-1.34) and log(10)(Adp) with 0.74 (0.65-0.87), and 0.81 (0.67-0.95), respectively. Increased Res and decreased Adp plasma levels are associated with out-of-clinic hypertension, whereas they did not determine white-coat hypertension.