Inflammatory markers in coronary artery disease

Abstract

Coronary artery disease (CAD) is one of the most common manifestations of atherosclerosis. Inflammation is considered one of the major processes that contribute to atherogenesis. Inflammation plays an important role not only on the initiation and progression of atherosclerosis but also on plaque rupture, an event that leads to acute vascular events. Various biomarkers express different pathways and pathophysiologic mechanisms of cardiovascular disease, and inflammatory biomarkers express different parts of the atherogenic process, regarding the initiation and progression of atherosclerosis or the destabilization of the atherosclerotic plaque. Therefore, inflammatory biomarkers may prove to be useful in the detection, staging, and prognosis of patients with CAD. Furthermore, the fact that inflammatory processes are essential steps in the course of the disease offers future therapeutic targets for the interruption of the atherogenic process or for the management of acute events.

Ischemic and non-ischemic dilated cardiomyopathy

“…As demonstrated in the literature, inflammation plays a major role in coronary heart disease: multiple pro-inflamatory cytokines and chemokines such as interleukin IL-1β and IL-6 are higher in patients with coronary heart disease [21][22][23][24]. Hence, in line with literature and our observations we can infer that the activation of pro-inflammatory cytokines may now be considered as a marker of coronary artery diseases.…”

FOXP3 genetic variant and risk of acute coronary syndrome in Chinese Han population

“…It suggests that genetic susceptibility may play a vital role in the pathogenesis of coronary heart disease including ACS. Inflammatory processes have been found in at all stages of atherosclerosis including the formation of the fatty streak, the formation of the fibrous plaque and the complicated lesion . Dendritic cells, regulators of innate and adaptive immunity, have also been demonstrated to take part in atherosclerosis .…”

“…Inflammatory processes have been found in at all stages of atherosclerosis including the formation of the fatty streak, the formation of the fibrous plaque and the complicated lesion. 7 Dendritic cells, regulators of innate and adaptive immunity, have also been demonstrated to take part in atherosclerosis. 8 Given the evidence earlier, common variants of gene coding for transcription factors involved in the process of inflammation and autoimmune may be responsible for individual susceptibility to coronary heart disease including ACS.…”

How to use and integrate bioinformatics tools to compare proteomic data from distinct conditions? A tutorial using the pathological similarities between Aortic Valve Stenosis and Coronary Artery Disease as a case-study

“…Such molecules disorganize extracellular matrix and in combination with increased secretion of collagen by fibroblasts are responsible for increased valve or artery stiffness, in AVS and CAD, respectively. Angiogenesis is also observed in both conditions [7,8,[12][13][14][15][16][17].…”