C-Reactive Protein

Abstract

See related article, pp 208–215 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). Figure. CRP is predominantly secreted from the liver and adipose tissue(s) in response to inflammatory stress resulting from plaque rupture and subsequent microembolization. High levels of CRP induce endothelial dysfunction, activate platelets, and aggravate stress-induced alterations in cardiac function and morphology (ie, cardiomyocyte apoptosis and hypertrophy, fibrosis, and LV dilatation). NFkB indicates nuclear factor κB; iNOS, inducible nitric oxide synthase; LV, left ventricle; IL-6, interleukin 6. 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 …