ABSTRACT
Many authors have shown an association between Chlamydia pneumoniae (CPn) infection and coronary artery disease (CAD). However, whether CPn infection demonstrated by CPn DNA presence in the artery wall plays an important role in pathogenesis of CAD and acute coronary events (i.e. unstable angina) remains to be elucidated. One hundred and fifteen consecutive patients with CAD (51 with unstable angina and 64 with stable angina) were compared with 52 control subjects with aortic valve disease without angiographic evidence of CAD. The presence of CPn DNA in the aortic wall was assessed with nested polymerase chain reaction (PCR), and the IgM, IgG and IgA anti-CPn titres were assessed with microimmunofluorescence test. CPn DNA presence in the artery (i.e. aortic) wall was associated with 3.7-fold increased risk of CAD (95% CI 1.2-11.3, P < 0.01); however, no statistically significant difference in CPn DNA presence was demonstrated between unstable and stable angina (17.6% vs. 25%). In the CPn DNA positive group more often than in the CPn DNA negative group, serological signs of chronic infection (55.2% vs. 27%, P = 0.004) were demonstrated, whereas no statistically significant differences were demonstrated in prevalence of either acute infection (9.3% vs. 0%) or reinfection (0% vs. 0%). In conclusion, CPn DNA presence in the artery (i.e. aortic) wall was associated with CAD, therefore may be used as a biomarker for CAD. Moreover, no statistically significant differences in CPn DNA presence in the artery wall and in serology were present between unstable and stable angina; therefore, CPn infection does not seem implicated in triggering an acute coronary event.
Subject(s)
Aorta/microbiology , Biomarkers/analysis , Chlamydophila pneumoniae/isolation & purification , Coronary Artery Disease/microbiology , DNA, Bacterial/analysis , Angina, Unstable/immunology , Angina, Unstable/microbiology , Chlamydophila pneumoniae/genetics , Chlamydophila pneumoniae/metabolism , Humans , Male , Middle AgedABSTRACT
Platelets and fibrinogen might be involved in the pathogenesis of thrombus formation and MI. The Bgl II gene polymorphism of the alpha2beta1 integrin, which is a platelet collagen receptor, and the -455G/A polymorphism in the beta fibrinogen gene have been suggested as genetic risk factors for MI. The aim of this study was to look for a relationship between the -455G/A polymorphism in the beta fibrinogen gene and the development of MI in Caucasians with type 2 diabetes. One hundred and forty-two subjects with type 2 diabetes and MI were compared to 234 diabetic subjects with no history of coronary artery disease. There were no significant differences in the frequency of the Bgl II gene polymorphism or of the -455G/A polymorphism in the beta fibrinogen gene in the patients with MI compared to the patients without MI: Bgl II (+/+) genotype was found in 19.7% of patients with MI and 15.4% of controls and -455GG genotype was found in 58.4% of patients with MI and 57.7% of controls. The present study demonstrates that neither the Bgl II gene polymorphism nor -455G/A polymorphism in the beta fibrinogen gene is a genetic marker for MI in Slovene population (Caucasians) with type 2 diabetes.
