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- Liuba, Petru, et al.
(författare)
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Residual adverse changes in arterial endothelial function and LDL oxidation after a mild systemic inflammation induced by influenza vaccination
- 2007
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Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 39:5, s. 392-399
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Tidskriftsartikel (refereegranskat)abstract
- Background. 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. Methods and subjects. 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). Results. 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). Conclusion. 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.
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| 3. |
- Pesonen, Erkki, et al.
(författare)
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Mannose-binding lectin as a risk factor for acute coronary syndromes.
- 2009
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Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 41, s. 591-598
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Tidskriftsartikel (refereegranskat)abstract
- Background. Mannose-binding lectin (MBL) is a multifunctional protein involved in innate immunity. We tested whether MBL and elevated viral and bacterial antibodies were risk factors for acute coronary events. Design. Controlled cohort study. Methods. A total of 354 patients with unstable angina pectoris (UA) or acute myocardial infarction (AMI) were compared with 334 paired controls. Results. Enterovirus titres were associated with increased risk of UA (odds ratio 10.04, P<0.001) and AMI (odds ratio 3.18, P=0.003), but titres did not correlate with either MBL concentration or genotype. Chlamydia pneumoniae heat shock protein 60 IgG concentrations were also associated with increased risk of UA (odds ratio 1.63, P=0.049). Compared to asymptomatic controls, patients had lower complement C3 serum concentrations (P<0.001), higher MBL serum concentration, and more frequently had MBL genotypes that determined high MBL levels (P<0.001). High MBL genotypes had odds ratios of 1.16 (P=0.010) for UA and 1.12 (P=0.007) for AMI. The elevation of MBL concentrations in the acute phase correlated with MBL concentrations after recovery (r=0.85, P<0.001). Conclusions. Elevated microbial titres, indicating an on-going inflammation, were associated with cardiovascular events. MBL might have a dual role both decreasing susceptibility to infections and increasing the risk of acute coronary syndromes.
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