Key result
Elevated hs-CRP acts as a non-causal bystander rather than a direct driver of CAD.
Why the study?
The causal role of hs-C-reactive protein in atherosclerosis and coronary heart disease remains unclear despite numerous mechanistic, genetic, population-based studies, and clinical trials.
Is hs-C-reactive protein part of the causal pathway of atherosclerosis and coronary heart disease or a bystander?
Key points are not available for this paper at this time.
Design
Review of mechanistic, genetic, population-based studies and clinical trials
hs-CRP is a bystander, not causal, in atherosclerosis; supports risk-marker use but leaves direct targeting unproven.
A large number of studies have evaluated the association of hs-C-reactive protein with atherosclerosis and coronary heart disease (CHD) in mechanistic, genetic, population-based studies, as well as clinical trials. This paper reviews the collective evidence to determine if hs-C-reactive protein is part of the causal pathway of atherosclerosis and CHD or whether it is a bystander.
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Anand et al. (2010) studied this question. High-sensitivity C-reactive protein acts as a non-causal bystander rather than a direct causal factor in the pathogenesis of atherosclerosis and coronary heart disease.