The theories formulated to explain atherogenesis have been evolving from vessel wall lipid accumulation to endothelial dysfunction with vascular wall remodelling. The progress in basic and experimental science have shown that inflammatory and immunological processes, cell and molecular machanizm can initiate atherogenesis. High frequency of cardiac and vessel disease creating on the ground of atherosclerosis caused that prevention is one of major aim of medicine. Estimating the risk of coronary artery disease and coming of clinicals incidents is the basic aim of intervention work. Markers of endothelian demage and activation inflammatory response have a prognostic value independent of clasic risk factors. Diagnostic these markers, although still limited, shought become the basic way of identification patients, that are the most danger with aterosclerosis complications. In the study tried to estimate the level of anti-hsp60 antibody, C-reactive protein, fibrinogen, leucocytes and anti-Ch.p. in class IgG and IgA in group with stable coronary artery disease (CAD) and in group with healthy subjects. In the research comperized the level of anti-hsp60 antibodies, C-reactive protein, fibrinogen, leucocytes and anti-Ch.p. in class IgG and IgA in depending on amount of vessels involved in atherosclerosis and progressing atherosclerosis according to classyfication of Canadian Cardiologic ; al Assocation. Additionally examined correlation between anti-hsp60 antibody, seropositivity to Ch.p. infection (the level of IgG and IgA antibodies) and the level of C-reactive protein, fibrinogen, leucocytes in patients with CAD and in group with healthy volunteers and also in group in CAD depending on amount of vessels involved in atherosclerosis and progressing atherosclerosis according to classyfication of Canadian Cardiological Assocation. The study group consisted of 71 patients aged 37-53 (47,07 ± 4,23 years) from the 2ndDepartment of Cardiology at the Medical College of Jagiellonian University in Cracow, with stable CAD. The control group consisted of 31 healthy volunteers aged 37-53, (44,97 ± 5,38 years) matched according to sex and age, non-smokers, with normal lipid levels, blood pressure and body mass. The exclusion criteria from the study were: an active inflammatory process hypertension diabetes mellitus obesity (BMI<30kg/m2), and lipids disorders, absence of autoimmunological states and neoplasms. In all patients according to the medical history excluded active (the last 8 weeks) and chronic inflammatory and infective disease, autoimmunological states and neoplasm, diabetes, endocrinological disorders and liver disease. All patients had proper blood pressure values (systolic pressure < 140mmHg, diastolic pressure < 90mmHg), non-smokers at least since 2 years. In ; this way excluded part of factors involving in research results. To confirm the diagnosis by all participants medical history, patient examination, clinical measurments, ecg, exercise ecg, coronarography were made. In examined patients percutaneous angioplasty were made (PTCA) and biochemical paramets were taken 6 months after succesful coronary angioplasty. 65% of patients with CAD demonstrated symptoms of CCS I a 35% CCS II according to classyfication of Canadian Cardiological Assocation. By 60% patients with CAD confirmed one vessel coronary disease and by 40% patients multi-vessel disease. Patients were treated with standard farmacological therapy according obligatory guidlines (aspirin, ACE- inhibitor, beta-blocer, statin). The study protocol was approved by the Jagiellonian University Medical College Ethics Committee and informed consent was obtained from all participants. Venous blood samples were drawn after an overnight fast to measure the level of anti-hsp60 antibody, high sensitive C-reactive protein, fibrinogen, leucocytes and anti-Ch.p. in class IgG and IgA antibodies. The level of anti-hsp60 and anti-Ch.p. ; antibodies were measured by, an immunoenzymatic method (ELISA), high sensitivity CRP levels were measured using the immunonephelometric method and using modified Klauss method the level of fibrinogen were measured. The level of leucocytes were measured using ; automatic analyzer. The following statistical tests were performed: parametic tests (Student’s t-test) and non-parametic teats - chi-square, Spearman’s rank correlation. Mann-Whitney’s. Patients with confirmed coronary artery disease had significantly higher levels of hs-CRP (2,07 ± 2,34ng/ml vs 1,37 ± 1,41ng/ml, p = 0,003), fibrinogen (3,96 ± 0,99g/l vs 3,1 ± 0,36g/l, p = 0,0002), and leukocytes (6,89 x103 ± 1,38 vs 5,2x103 ± 0,86, p < 0,00001) as compared with healthy subjects. In examined study men group 30% patients with CAD and 6,4% healthy volunteers presented hsCRP concetrations > 3mg/l, that cause an elevated coronaro-artery risk in that group. The statistical significant difference in levels of anti-hsp60 antibodies and IgG and IgA anti-Ch.p. antibodies has not been proved between study groups. The positive correlation between the level of fibrinogen and hsCRP in patients with CAD and control group was observed (r = 0,63, p < 0,001 and r = 0,69, p < 0,001). The level of anti-hsp60 antibodies did not corelate with presence of elevated level of inflammatory markers and Ch.p. infection. Influence of Ch.p. infection on elevated inflammatory markers in patients with CAD and in healthy subjects was not proved. There was no difference between the level of anti-hsp60 antibodies, hsCRP, fibrinogen, leucocytes and IgG i IgA anti-Ch.p. antibodies in patients with CCS I and CCS II ; as well in patients with CAD and one-vessel disease or multi-vessel disease. Type of used method (PTCA vs PTCA + stent) did not influent on level of anti-hsp60 antibodies, inflammatory and infection markers in study group of patients. In patients with stable CAD undergoing percutaneous angioplasty in comperison to healthy subjects is confirmed, persistant inflammatory reaction iniciates the whole body activation inflammatory response with subclinical view demonstreted with higher level of C-reactive protein, fibrinogen and leukocytes. There is no clearly evidence for cause reason for chronic and persistent infection of Ch.p. in developing of atherosclerosis and describing role of Ch.p. infection in atherosclerotic leasions needs futher clarifications. Futher study needs also describing role oh anti-hsp60 antibodies in etiology of atherosclerosis that can cause to new way of immuno-inflammatory response using immunotherapy and measure in future anti-hsp60 antibodies can help to estimate to develop atherosclerosis. Examined inflammatory markers are useful for estimating immuno-inflammatory process developing in an artery, may have a prognostic value in chosing group with elevated coronary-artery risk and may cause have change therapy used so far in estimated group of patients.