Acute coronary syndrome. An Acute Inflammatory Syndrome

Abstract

Atherosclerosis begins with the accumulation of small lipoprotein particles within arterial intima. These particles coalesce together and are modified and then they induce localized endothelial inflammation, thereby attracting leukocytes. Scavenger receptors over the surface of monocytes bind to the modified low density lipoprotein particles, which transform into foam cells that become a source for further inflammatory cytokines. The level of inflammation is heightened in ruptured coronary plaques. In patients dying of an acute myocardial infarction, the level of inflammation is heightened in all lesions in the coronary tree. The inflammatory reaction in acute coronary syndrome is not confined to cellular immunity, but also encompasses humoral immunity. High sensitivity CRP hs-CRP measures systemic inflammation, and at low levels it has emerged as a strong predictor of adverse cardiovascular events. It is mainly used to further stratify the intermediate-risk patients. Many other molecules have shown promise as markers for increased inflammation and increased risk of adverse cardiac events. That risk may be additive in nature, and some studies suggest that inflammatory markers can also predict response to various treatment strategies during acute coronary syndromes.