Immune and inflammatory responses in subjects with stable angina and acute myocardial infarction.

Abstract

associated with systemic inflammation also appear to increase the likelihood of clinically manifest atherosclerotic vascular disease. Acute myocardial infarction (AMI) triggers an intense acute inflammatory response both locally and systemically. However, the differences in systemic immune and inflammatory response between AMI and chronic phase of atherosclerosis are not fully understood. Two papers in the current issue of the journal by Wang and colleagues have used genome wide gene expression in peripheral leukocytes to examine the differences in several inflammation and immunologic related genes between subjects with and without atherosclerosis and, for those with atherosclerosis between those with and without AMI. In the paper by Yan, et al, [2] there was evidence of impaired regulation of T cell activation and proliferation in the AMI group compared with a group of well matched subjects with stable angina (SA), suggesting disregulated immune response in AMI. Given the cross-sectional nature of the study, it is not clear whether any of these changes preceded the acute event. Genes related to mitochondria, electron transport chain, and cellular cation homeostasis were down-regulated, indicating an impaired energy metabolism in leukocytes. In contrast, genes related to inflammatory response, macrophage activation, neutrophil mediated immunity and response to bacterium and DNA damage stimulus were up-regulated in the AMI group compared to the SA group, suggesting an increased inflammatory response and an intense response to tissue damage in AMI. In addition, the up-regulation of positive regulation of the IκB kinase (IKK)/nuclear factor (NF) κB cascade found in the study