C-reactive protein and the severity of atherosclerosis in myocardial infarction patients with stable angina pectoris.

BACKGROUND: Recent findings provide evidence for the importance of inflammatory processes in the pathogenesis of atherosclerosis. C-reactive protein was elevated in patients with peripheral artery disease, coronary heart disease and myocardial infarction compared to normal subjects. METHODS: In 1112 male and 299 female survivors of myocardial infarction (mean age +/- SD, men, 50.4 +/- 9.5, women, 56.1 +/- 9.3), we investigated whether plasma C-reactive protein concentration is associated with the severity of coronary heart disease and generalized pre-clinical or clinically manifest arteriopathy. The control group consisted of 326 male and 138 female individuals matched for age without clinical symptoms of coronary disease. The severity of arteriosclerotic changes was determined for the extra-cranial brain-supplying arteries, abdominal aorta, pelvis and leg arteries. In myocardial infarction patients coronary angiography was performed. Laboratory analyses included determination of C-reactive protein, fibrinogen, D-dimer, HDL-cholesterol, LDL-cholesterol and triglycerides. RESULTS: The following ranking of C-reactive protein concentrations was found: controls < or = patients after myocardial infarction without atherosclerosis < or = patients with myocardial infarction and pre-clinical atherosclerosis < or = patients with myocardial infarction and clinically manifest atherosclerosis. Additionally, our data showed a significant association between C-reactive protein concentrations and the angiographically detected degree of coronary heart disease. CONCLUSIONS: As C-reactive protein is a marker of inflammatory processes, our results in patients with clinically manifest and early pre-clinical atherosclerosis support the hypothesis that inflammatory processes in the vessel wall participate in atherogenesis. Moreover, they support the hypothesis of a causal relationship between an acute phase reaction and the pathogenesis of atherosclerosis in coronary arteries and other parts of the arterial vessel system.