Curbing Inflammation in the Ischemic Heart Disease

Abstract

A modern concept considers acute coronary syndrome as an autoinflammatory disorder. From the onset to the healing stage, an endless inflammation has been presented with complex, multiple cross-talk mechanisms at the molecular, cellular, and organ levels. Inflammatory response following acute myocardial infarction has been well documented since the 1940s and 1950s, including increased erythrocyte sedimentation rate, the C-reactive protein analysis, and the determination of serum complement. It is surprising to note, based on a wide literature overview including the following 30 years (decades of 1960, 1970, and 1980), that the inflammatory acute myocardium infarction lost its focus, virtually disappearing from the literature reports. The reversal of this historical process occurs in the 1990s with the explosion of studies involving cytokines. Considering the importance of inflammation in the pathophysiology of ischemic heart disease, the aim of this paper is to present a conceptual overview in order to explore the possibility of curbing this inflammatory process.

Untitled

“…This is in accordance with those of Khaki-khatibi F et al, high TBARS levels might be resulted from increase lipid peroxidation that's marker of OS 22,24 .…”

“…Elevated hs_CRP level was detectable during significant inflammation in most patients which is associated with an increase risk of IHD 9 . Hypertension, diabetes mellitus, older age, hyperlipidemia seems to be responsible for the elevation of hs_CRP levels 21,22 .…”

Serum Level of suPAR and YKL-40, a New Biomarker in Patients with Acute Myocardial Infarction?

“…These foam cells generate the initial lesions leading to advanced atherosclerosis (5). Foam cells secrete pro-inflammatory cytokines, growth factors, matrix metalloproteinases and tissue factor (3). Neutrophils, lymphocytes, monocytes, and macrophages initiate the inflammatory response through the secretion of numerous growth factors, cytokines (including tumor necrosis factor-α (TNF-α) and interleukin-1β) (2), proteolytic enzymes, integrins and cell adhesion molecules in patients with unstable angina and myocardial infarction (3,4).…”

“…Foam cells secrete pro-inflammatory cytokines, growth factors, matrix metalloproteinases and tissue factor (3). Neutrophils, lymphocytes, monocytes, and macrophages initiate the inflammatory response through the secretion of numerous growth factors, cytokines (including tumor necrosis factor-α (TNF-α) and interleukin-1β) (2), proteolytic enzymes, integrins and cell adhesion molecules in patients with unstable angina and myocardial infarction (3,4). Proteolytic enzymes, including metalloproteinases and cysteinyl cathepsins can degrade extracellular matrix proteins (4-6) and convert a stable atherosclerotic plaques to unstable plaques called "vulnerable" plaque (2,5,7).…”