Biomarkers in acute coronary syndrome 5

Previous

Biomarkers in acute coronary syndrome 5

Biomarkers in acute coronary syndrome 5:

CRP vs hs-CRP

C-reactive protein (CRP) is an acute-phase protein produced by the liver in response to tissue injury, inflammation, or infection. Standard CRP tests determine levels which are increased up to 1,000-fold in response to infection or tissue destruction. These assays are not sensitive enough to assess the normal range of CRP values. High-sensitivity CRP (hs-CRP) assays detect levels of CRP within the normal range and have been proven to predict future cardiovascular events.

Is CRP a risk factor or risk marker?

CRP is previously known to be a marker of high risk in cardiovascular disease. But recent data implicate CRP as mediator of atherogenesis as well. Multiple hypotheses have been put forth including endothelial dysfunction via modulation of synthesis. CRP-stimulated macrophages can cause deposition of low density lipoprotein (LDL) cholesterol in atherosclerotic plaque.

Different types of biomarkers for acute coronary syndrome

There are different types of potential biomarkers of high risk in acute coronary syndrome. They could be inflammatory cytokines like interleukins, cellular adhesion molecules like integrins, selectins, NCAM (neural cell adhesion molecule), VCAM (vascular cellular adhesion molecule), acute-phase reactants like CRP, markers of plaque destabilization and rupture like myeloperoxidase (MPO) and possibly matrix metalloproteinase-9 (MMP-9), those of of ischemia like ischemia modified albumin, markers of myocardial stretch like Brain type natriuretic peptide (BNP) and biomarkers of myocardial necrosis (Troponin, CK-MB, Myoglobin).

Myeloperoxidase

Myeloperoxidase present in white blood cells (WBC) help in destroying bacteria and viral particles. It catalyzes conversion of hydrogen peroxide and chloride into hypochlorous acid, which 50 times more potent anti-microbial than hydrogen peroxide. Myeloperoxidase is released in response to infection and inflammation. Elevation of myeloperoxidase has been shown to identify those at increased risk of cardiovascular events in the six months following a negative troponin in those presenting acute coronary syndrome.

Myeloperoxidase causes oxidation of LDL cholesterol and the oxidized LDL is phagocytosed by macrophages producing foam cells. It causes consumption of nitric oxide, the endothelium dependant relaxing factor. This leads to vasoconstriction and endothelial dysfunction. Endothelial denudation and superficial platelet aggregation follows. Presence of elevated myeloperoxidase levels indicates the presence of activated immune cells. Activated immune cells and inflammation lead to unstable plaque. Inflammatory plaque is inherently less stable and the thin fibrous cap gets fissured/denuded and a nidus for thrombotic occlusion.