Abstract
Background: Acute systemic inflammation or infection transiently increases risk of cardiovascular events, but the underlying mechanisms are not fully understood. Although observational studies suggest that inflammation is positively associated with arterial stiffness and blood pressure, the causal relationship of this is not clear. Because increased inflammation could be related to vascular dysfunction, we tested the hypothesis that an acute inflammation causes an increase in arterial stiffness and blood pressure. Methods: Using a randomized double blind sham placebo-controlled cross over design, 19 healthy subjects (male 10, female 9; age 24 4 yrs) were injected with an influenza vaccine (0.5 m/L) as a model to generate systemic inflammation, and a sham vaccine (normal saline). C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-a) were measured as a markers of inflammation. Brachial arteryflow mediated vasodilatation (FMD) was measured using B-mode ultrasound. Aortic augmentation index (AIx), carotid-radial pulse wave velocity (PWV), and central blood pressure were measured using applanation tonometry. These variables measured at baseline before each vaccination, 24 hours and 48 hours after each vaccination. Results: Compared with sham placebo, the influenza vaccination caused a significant increase in CRP (1.42 0.6 at baseline, 2.81 1.0 after 24 hours, 5.0 1.3 mg/L after 48 hours, p<0.05) and IL-6 (1.12 0.3, 2.56 0.4, 2.26 0.6 pg/mL, p<0.05). Central systolic blood pressure (98.0 7.4, 104.5 10.8, 100.7 8.4 mmHg, p<0.05) and PWV (7.8 0.9, 8.6 1.5, 8.7 1.3 m/s, p<0.05) were significantly increased after an influenza vaccination but not sham vaccination. FMD was significantly decreased after acute inflammation (6.91 2.5, 3.22 2.8, 3.30 2.5%, p<0.05). Conclusion: These findings show that acute inflammation caused a temporary increase in arterial stiffness and central blood pressure, and acutely reduced endothelial function. This offers insight into the noted increased risk of cardiovascular events associated with acute inflammation.
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