STUDY OF VISFATIN AS A CLINICALBIOMARKER IN CORONARYARTERY DISEASE

Abstract

C oronary artery disease (CAD), and its acute form acute coronary syndrome (ACS), have been considered as a major health problem andone of the most common leading causes of death all over the world. The WHO has estimated that the global number of deaths from CAD will rise from 7.2 million in 2002 to 11.1 million in 2020. ACS is the umbrella term of clinical signs and symptoms of myocardial ischemia including unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI) & ST-segment elevation myocardial infarction (STEMI). The extend of the disease burden and the rate of its increase directed the attention to the imperative need to investigate any potential serum surrogate marker for atherosclerosis which holds a high risk for myocardial infarction. In this regards, visfatin could be a good candidate; owing to its obvious role in the pathophysiology of different forms of cardiovascular diseases. Adipose tissue (AT) is no longer considered an energy storing depot but a real endocrine organ that synthesizes and secretes a wide range of diverse bioactive factors, collectively called adipokines.Visfatin a protein of 491 amino acids with a molecular mass of 52 kDa,is one of the recent identified Adipokines. Visfatin is strongly expressed within symptomatic atherosclerotic carotid plaques and is localized to areas with lipid loaded macrophages,whereit is also implicatedin atherosclerotic plaque instability. Additionally, visfatin is involved in endothelial dysfunction which causes progression of atherosclerosis to MI. Visfatin also act as a growth factor for B-lymphocyte-precursors, produced by different lineages of immune cells and induces expression of variety of cytokines. The researchers concluded that visfatin is considered as a pro-inflammatory adipocyte, associated with pro-inflammatory state that contribute to a number of diseases rather than CAD such as type 2 diabetes mellitus. In addition to its obvious role in inflammation Visfatin increased matrix metalloproteinase-9 (MMP-9) known by its role in matrix degradation. It was also reported that visfatin could induce angiogenesis in human umbilical vein endothelial cells (HUVECs), whereas progressive angiogenesis in atherosclerotic lesions has been considered one of thecauses of plaque expansion and vulnerability.