By DrRich
An elevated blood level of CRP (C-reactive protein) has been shown to predict a high risk of future cardiovascular events, such as heart attack and stroke. CRP is a protein released into the bloodstream any time there is active inflammation in the body. (Inflammation occurs in response to infection, injury or various chronic inflammatory conditions such as arthritis.)
It is now thought that atherosclerosis itself is at least partly an inflammatory process. The association of elevated CRP levels with an increased risk of cardiovascular events supports this relationship between inflammation and atheroscleosis (coronary artery disease.) ( Click here for a discussion of CRP as a risk factor.)
However, scientists do not know whether CRP is merely a marker for increased risk (that is, merely an indication that inflammation is present), or is instead a factor that actually produces increased risk. Now, evidence from a new study in mice suggests that CRP may be a causative agent for the progression of atherosclerosis.
In a study published last week in Circulation, scientists from the Baylor College of Medicine examined the effect of CRP on the progression of atherosclerosis in mice. One group of mice was genetically manipulated to produce human CRP, and another group was not. In the mice with CRP, arterial plaques due to atherosclerosis were 48% larger than in mice without CRP. The presence of human CRP made atherosclerosis progress significantly faster.
This study provides the first real evidence that CRP itself accelerates atherosclerosis - and the heart attacks and strokes caused by atherosclerosis. This information should motivate doctors to measure CRP levels more routinely in assessing their patients' risk, and should stimulate industry to develop drugs that will reliably reduce elevated CRP levels. Click here for a description of recent guidelines for testing CRP levels.
