Residual adverse changes in arterial endothelial function and LDL oxidation after a mild systemic inflammation...

Several clinical studies have suggested possible increase in cardiovascular risk during and in the first weeks after an acute inflammatory disease. Using influenza vaccine as inflammatory stimulus, we investigated whether arterial endothelial dysfunction could persist beyond the inflammatory state, and whether amplified oxidative modification of low-density lipoprotein (LDL) accompanies this vascular disturbance.

The brachial artery responses to hyperemia (flow-mediated dilatation (FMD), and to sublingual glyceryl trinitrate (GTN), and the carotid intima-media thickness were assessed by external ultrasound in eight healthy male volunteers (age 17-30 y) before, and 2 and 14 days after intramuscular administration of influenza vaccine. Plasma levels of high-sensitivity C-reactive protein (CRP), fibrinogen, cyclic guanosine monophosphate (cGMP), and antibodies against oxidized LDL (oxLDL) were measured at each time point. Data are means+/-standard errors of the mean (SEM).

Influenza vaccination caused a slight elevation in CRP (from 0.5+/-0.1 at baseline, to 2+/-0.6 mg/L, P = 0.01) and fibrinogen (from 2.3+/-0.1 to 2.7+/-0.1 g/L, P = 0.01) at 2 days, which completely resolved at 14 days (CRP: 0.6+/-0.2 mg/L, P = 0.9, and fibrinogen: 2.3+/-0.1 g/L, P = 0.8 versus baseline). OxLDL antibody levels rose significantly at 2 days (from 1+/-0.1 at baseline to 2+/-0.4, P = 0.04), and remained elevated at 14 days (1.7+/-0.3, P = 0.1 versus baseline). FMD of the brachial artery decreased at 2 days (from 8.3+/-1.2% at baseline, to 5.4+/-1%, P = 0.05) with a further decrease at 14 days (4.9+/-0.8%, P = 0.03 versus baseline). The dilatory responses to GTN and the carotid IMT remained unchanged throughout the study period (P>0.5).

Abnormalities in arterial function and LDL oxidation may persist for at least 2 weeks after a slight inflammatory reaction induced by influenza vaccination. These could explain in part the earlier reported increase in cardiovascular risk during the first weeks after an acute inflammatory disorder.