Two large new studies published in JAMA shed important new light on CRP and other biomarkers, but are unlikely to result in significant changes in clinical practice.
In the first report, a large genome-wide association and replication study, followed by a mendelian randomization study, failed to find a causal role for CRP in coronary heart disease. The researchers, led by by Paul Elliott, said that the “this study suggests that development of therapeutic strategies targeting specific reductions in plasma levels of CRP are unlikely to be fruitful.”
In a comment to CardioBrief, leading CRP expert and proponent Paul Ridker responded: “I have always felt that CRP is a terrific clinical biomarker for inflammation (and high vascular risk) but that it is inflammation that is likely to be causal for atherosclerosis, not CRP itself.” [Ridker’s full comment is published in full below.]