CRP Identified as Cause of Blood Clots

The study appears in the January 25, 2003, issue of Circulation.

The research demonstrates that CRP causes human aortic endothelial cells to produce higher levels of plasminogen activator inhibitor-1 (PAI-1), a strong marker for heart disease. The researchers, from the University of California, Davis (Sacramento, USA), used a variety of techniques to show how CRP activates PAI-1 in aortic cells, causing lesions in the arteries that lead to the formation of plaques and blood clots. Individuals can have normal cholesterol levels but high levels of CRP, which shows the limitations of cholesterol screening to assess the risk of heart disease.

"The study provides further conclusive evidence that CRP, until now viewed as an ‘innocent bystander' in the formation of heart disease, is in fact a key culprit that causes inflammation in the arteries, resulting in the formation of clots and plaque that lead to heart attacks and strokes,” said Ishwarlal Jialal, professor of pathology at the UC Davis School of Medicine. "By relying on cholesterol alone, a physician could significantly underestimate a patient's risk level.”




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