The Role and Clinical Significance of High-Sensitivity C-Reactive Protein in Cardiovascular Disease

Atherosclerosis, the leading cause of cardiovascular disease, is characterized by chronic inflammation in the artery wall. It has been considered for decades that this disease is associated with hypercholesterolemia and the accumulation of macrophage-derived foamy cells in the arterial wall. While inflammation is involved in initiation, progression, and complication of the atherosclerotic process, the exact mechanisms underlying this inflammatory process remains unclear as yet. C-reactive protein (CRP) is a homopentameric acute-phase protein produced by the liver and binds specifically to phosphorylcholine in a Ca-dependent manner. Its levels rise dramatically during inflammation that occurs in the body. This increment of CRP is due to a rise in the plasma concentration of interleukin-6 (IL-6), produced predominantly by macrophages and adipocytes. During the acute phase response, CRP levels increased rapidly within 2 hours of acute insult, rise above normal limits within 6 hours, and peak at 48 hours. With resolution of the acute phase response, CRP declines with a half-life of 18 hours. CRP can rise up to 50000-fold in acute inflammation, such as during infection. Its level is mainly determined by its rate of production because of its constant half-life. One exception is that the CRP elevations in the absence of clinically significant inflammation can occur in renal failure. Editorial