Association between telomere length and C-reactive protein and the development of coronary collateral circulation in patients with coronary artery disease.
We identified amino acid residues involved in CRP peptide 201-206-FcγRII (CD32) interactions, which mediate potent antineutrophil and antiplatelet adhesion actions, and these findings open up new perspectives for limiting inflammation and thrombosis underlying coronary artery disease.
These methods are demonstrated in a simulation study and then applied to estimate the causal relation between C-reactive protein and each of fibrinogen and coronary heart disease, based on 3 SNPs in British Women's Heart and Health Study participants assessed at baseline between May 1999 and June 2000.
A weighted genetic risk score that was developed to summarize the effect of risk alleles was strongly associated with CRP levels and explained ≈5% of the trait variance; however, there was no evidence for these genetic variants explaining the association of CRP with coronary heart disease.
Apolipoprotein E genotypes, circulating C-reactive protein and angiographic coronary artery disease: the Ludwigshafen Risk and Cardiovascular Health Study.
Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals.
Based on the recent genetic findings as well as delineation of the role of HNF1-alpha in regulating the expression of the CRP gene, it appears that this transcription factor may play a key role in linking metabolic and inflammatory pathways underlying the pathogenesis of coronary heart disease.
For the other loci associated with CRP levels, we selected the most closely associated SNP for testing against coronary heart disease among 14,365 cases and 32,069 controls.
CRP concentration is partly under genetic control as a higher concentration in young siblings of probands with proved coronary atherosclerosis was documented.
C-reactive protein gene polymorphisms affect plasma CRP and homocysteine concentrations in subjects with and without angiographically confirmed coronary artery disease.
Randomised controlled trials were not available for depression, exercise, or C reactive protein in relation to incidence of coronary heart disease, but trials in patients with diabetes showed some preventive effect of glucose control on risk of coronary heart disease.
The association of C-reactive protein and CRP genotype with coronary heart disease: findings from five studies with 4,610 cases amongst 18,637 participants.
Diagnostic performance of plasma high sensitive C-reactive protein in detecting three-vessel coronary artery disease: modification by apolipoprotein E genotype.