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Peter Bruins

Publications and source records attributed to Peter Bruins.

3 recordsLinked to original sources
PubMed2005

C-reactive protein is a risk indicator for atrial fibrillation after myocardial revascularization.

BACKGROUND: Activation of the complement system after coronary artery bypass graft surgery involves C-reactive protein (CRP). This inflammatory response is related to baseline CRP levels and associated with postoperative arrhythmia, in particular atrial fibrillation (AF). We investigated whether baseline CRP levels are a risk indicator for the occurrence of AF and whether this phenomenon is cardiopulmonary bypass dependent. METHODS: C-reactive protein was measured in perioperative blood samples of patients of the Octopus Study (coronary artery bypass graft surgery with [n = 73] or without cardiopulmonary bypass [n = 79]). Baseline CRP was dichotomized into a low and a high baseline group, using a cutoff value of 3.0 mg/L. RESULTS: After coronary artery bypass graft surgery with cardiopulmonary bypass 11 of 53 patients (21%) with low preoperative CRP levels had AF versus 11 of 20 patients (55%) with high baseline CRP levels (p = 0.01). In the off-pump group AF occurred in 4 of 52 patients (8%) who had low baseline CRP levels, versus 8 of 27 patients (30%) with high preoperative CRP levels (p = 0.002). After adjusting for age, the odds ratio (95% confidence interval) was 4.6 (1.4 to 15.3) with cardiopulmonary bypass, 3.7 (0.93 to 14.7) in the off-pump group, and 3.3 (1.4 to 7.6) for both groups together. Continuous baseline CRP was an independent predictor for AF in a multivariate logistic regression model (p = 0.02). CONCLUSIONS: Patients with high baseline CRP levels are at higher risk of having postoperative AF in both on-pump and off-pump surgery.

Aged↗
PubMed2005

Complexes between C1q and C3 or C4: novel and specific markers for classical complement pathway activation.

Classical pathway activation is often assessed by measuring circulating levels of activated C4. However, this parameter does not discriminate between activation through the classical or the lectin pathway. We hypothesized that during classical pathway activation, complexes are formed between C1q and activated C4 or C3. Using ELISA, we investigated whether such complexes constitute specific markers for classical pathway activation. In vitro, C1q-C3d/C4d complexes were generated upon incubation of normal recalcified plasma with aggregated IgG or an anti-C1q mAb that activates C1 (mAb anti-C1q-130). In contrast, during incubation with C1s or trypsin, C1q-C3d/C4d complexes were not generated, which excludes an innocent bystander effect. Additionally, C1q-C3d/C4d complexes were not generated during activation of the alternative or the lectin pathway. Repeated freezing and thawing did not influence levels of C1q-C3d/C4d complexes in recalcified plasma. To measure C1q-complement complexes in plasma samples, we separated unbound complement proteins from C1q-C3d/C4d complexes in the samples prior to testing with ELISA. In samples from patients undergoing cardiopulmonary bypass surgery or suffering from rheumatoid arthritis, we found higher levels of C1q-C4 complexes than in samples from healthy individuals. We conclude that complexes between C1q and C4 or C3 are specific markers of classical complement pathway activation.

Arthritis, Rheumatoid↗