C-reactive protein: just a biomarker of inflammation or a pathophysiological player in myocardial function and morphology?

In response to inflammatory stress, C-reactive protein (CRP) is predominantly secreted from the liver and adipose tissue(s), and an independent relationship exists between different markers of overweight/obesity and elevated high sensitive (hs) CRP levels (Figure). Higher hsCRP levels predict incident myocardial infarction (MI), stroke, peripheral arterial disease, sudden cardiac death, and all-cause mortality in healthy individuals with no history of cardiovascular disease.1,2 hsCRP at admission predicts in-hospital outcome, and hsCRP at discharge predicts 6-month event rate and 30-day mortality (Global Utilization of Strategies To Open occluded arteries [GUSTO] IV) in patients with an acute coronary syndrome. Indeed, adding hsCRP levels to the Global Registry in Acute Coronary Events (GRACE) acute coronary syndrome risk model improves the prediction of 30-day mortality. In patients with non-ST-elevated MI, an increased hsCRP level predicts the death rate even at 20-month follow-up but does not predict stent-related complications. The question of whether CRP, apart from serving as a biomarker, acts as a causal factor in vascular/coronary artery disease has been addressed in animal models, in which CRP was injected or genetically overexpressed, and in Mendelian randomization studies.