Background. Clinical evidence supporting a causal role of Chlamydia pneumoniae in the process of atherosclerosis is limited. It is also uncertain if the organism participates in the inflammatory response in stable angina pectoris. The current study investigates C. pneumoniae IgG and markers reflecting the inflammatory response in stable angina pectoris. The data were subsequently compared with the extent of coronary atherosclerosis.
Setting. Department of Cardiology, Linköping University Hospital, Linköping, Sweden.
Experimental protocol. We investigated 92 patients with stable angina pectoris subject to coronary angiography to assess chest pain Before angiography C. pneumoniae IgG, neutrophil count and plasma levels of myeloperoxidase and interleukin 6 were analysed. The number of major coronary arteries (1-3) having at least one diameter narrowing(=> 50%) stenosis was determined. The patients were divided into two equal sized groups according to C. pneumoniae IgG levels.
Results. Subjects with higher antibody concentrations had a more severe disease. The number of diseased arteries was 2.1±0.8(SD) and 1.4±0.6(SD) for the two groups, respectively. The difference proved to he highly significant (p<0.0001). The groups did not differ with respect to inflammatory parameters.
Conclusion. This study with 92 consented individuals with stable angina pectoris suggests a causative relationship between C. pneumoniae IgG seroreactivity and the degree of coronary atherosclerosis. It does not, however, prove causality. Thus, it is likely that C. pneumoniae participates in the progression of atherosclerosis.