| Abstract: | C-reactive protein (CRP) is a unique risk marker and plays a role in the pathogenesis of inflammation and atherosclerosis. It is synthesized and secreted mainly by hepatocytes in response to interleukin-6 (IL-6) and either IL-1 or tumor necrosis factor-alpha. The average plasma half life of CRP is 19 hours. CRP activates complement, increases phagocytic activity of neutrophils, increases respiratory burst of neutrophils, and induces expression of adhesion molecules, synthesis of tissue factor, cytokines from monocytes and platelet aggregation. CRP is involved in development of atherosclerosis and thrombosis. High sensitive-CRP (hs-CRP) is a very novel biochemical marker. It is elevated in various conditions including: inflammation both acute and chronic, acute myocardial infarction, unstable angina, peripheral vascular diseases, diabetes, renal disease, hypertension, and cardiopulmonary bypass. A positive association has been reported between CRP levels and age, smoking, body mass, total cholesterol, lipoprotein a [Lp(a)], homocysteine and fibrinogen. It has a predictive value for the development of peripheral vascular disease, restenosis following percutaneous coronary interventions with or without stent implantation, and complications following cardiopulmonary bypass. Preprocedural high levels of plasma CRP are associated with high incidence of late adverse events (composite of cardiac death, nonfatal myocardial infarction, clinical occurrence of symptoms, progression of significant coronary lesion in vessels other then treated ones) after successful coronary stenting. Baseline levels of CRP predict risk of future myocardial infarction, and stroke in apparently healthy middle-aged men and women. CRP levels predict atherosclerotic vascular disease in patients with end-stage renal disease. Increased pretransplant CRP levels are associated with higher risk of acute rejection in transplant recipients. Various strategies to reduce the adverse effects of CRP have been discussed. |
