A high level of red blood cell (RBC) aggregation has been consistently found in patients with coronary artery disease (CAD) in case-control studies. Plasma fibrinogen has been shown to promote RBC aggregability. The purpose of this study was to investigate the influence of the genetic variability of the beta-fibrinogen gene on RBC aggregation in patients with CAD.
The genotype of the beta-fibrinogen gene locus was determined by polymerase chain reaction using the restriction enzyme HaeIII for a G to A substitution at position -455 upstream from the transcriptional start site in 135 French Canadians with premature CAD (age: 51+/-7 years). Indices measuring the RBC aggregation kinetics (S10) and shear resistance of the aggregates (gammaS) were obtained by laser reflectometry. Patients were separated into groups by using the medians of S10 and gammaS. Using chi2 analyses, the distribution of the -455GG, -455GA, and -455AA genotypes in the groups with high levels of S10 (0.43, 0.49, and 0.08) and gammaS (0.45, 0.49, and 0.06) were found to be significantly distinct from those in the groups with low levels of S10 (0.67, 0.27, and 0.06; p