2001) and, in humans, by the presence of adaptive intimal thickening (Schwartz et al. 2012), the presence of subendothelial dendritic cells (Millonig et al. Before development of atherosclerosis, these predilection sites are characterized by changes in endothelial turnover and gene expression (Wentzel et al. Sites with low or oscillatory endothelial shear stress, located near branch points and along inner curvatures, are the most susceptible (Wentzel et al. The first step in the development of atherosclerosis is the exposure of vascular cells to excess lipid with concomitant endothelial activation/dysfunction and the internalization and deposition of lipids in the intima (Badimon and Vilahur 2014). Most of the biomarkers associated with atherosclerosis are indicators of inflammatory response and will also be used for medical purposes.Ītherosclerosis is a chronic lipid-driven inflammatory disease characterized by a complex endocrine, paracrine and juxtacrine cross-talk between immune and vascular cells as well as several tissues and organs, including the liver, heart, kidney, adipose tissue, adrenal, pancreatic, pituitary and sex glands (Badimon et al. Short conclusionĪtherosclerotic plaques are the battlefield between an unbalanced immune response and lipid accumulation in the intima of arteries. A human atherosclerotic lesion also expresses lipoprotein-associated phospholipase A 2. Oxidized low-density lipoprotein receptor 1 provides a route of entry for oxidized low-density lipoprotein into the endothelium.

Myeloperoxidase has been proposed as a marker of plaque instability. There are also overproductions of matrix metalloproteinases in the rupture-prone regions and promote lipid-necrotic core formation in the atherosclerotic plaque. Osteopontin, acidic phosphoprotein, and osteoprotegerin have emerged as novel markers of atherosclerotic plaque composition. Cluster of differentiation 40 receptor and its ligand have been also detected in atherosclerotic plaques. High rates of protease activated receptor expression are also induced by interleukin-6 secretion in atherosclerotic lesions and areas of vascular tissue injury. Cytokines have been implicated in atheroma formation and complications. Higher leukocyte count is associated with a greater cardiovascular risk. Fibrinogen was demonstrated to be elevated among patients with acute thrombosis. C Reactive Protein plays a direct role in promoting the inflammatory component of atherosclerosis. Various biomarkers are implicated in different stages of the pathophysiological mechanism of plaque formation and evolution. AHA Type III lesion is the earliest of progressive lesions, while AHA Type IV lesion consists of an acellular necrotic core. AHA Type II lesion is primarily composed of abundant macrophages. In the classification of atherosclerosis made by American Heart Association (AHA), AHA Type I lesion is the earliest vascular change described microscopically. It also provides a summary of current biomarkers other than the traditional risk factors so that new treatment modalities can emerge and reduce the morbidity and mortality associated with atherosclerosis. The aim of the review is to get into the fine details of pathophysiologic mechanisms responsible for atherosclerosis with atherosclerotic lesion classification. Atherosclerosis is a chronic lipid-driven inflammatory disease with infiltration of low-density lipoprotein and is considered as the pivotal step in plaque formation.

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