Vol. 3, Issue 7 (2014)

Author(s):
Revathy. K, Dhananjayan. R and Swaminathan. S

Abstract:
Available statistics and research reveal that most patients with diabetes die from cardiovascular diseases, mainly due to markedly advanced and untreated atherosclerosis. Although the risk of cardiovascular disease increases additively with the number of conventional risk factors, including diabetes, hypertension and dyslipidemia, these conventional risk factors cannot fully account for the risk of cardiovascular diseases. Atherosclerosis is a complex multifactorial and polygenic disorder resulting from interactions among individual genetic and various environmental risk factors. Of late research field has been focusing on arterial calcifications in setting of atherosclerosis. Many features of atherosclerosis-related calcification provide useful clinical information. Several mechanisms leading to calcification associated with atherosclerosis have been proposed; however, no direct testing of proposed mechanisms has yet been reported. Studies in genetically altered animals and in humans have shed light on potential genetic determinants, which in turn could form the basis for more comprehensive understanding of the factors affecting calcification within plaque and the associated pathobiologic implications. Understanding the molecular and genetic determinants of specific structural plaque components such as calcification can provide a solid foundation for the development of novel therapeutic approaches. Although it is possible that some of these atherosclerosis-susceptibility gene polymorphisms are synergistically responsible for advanced atherosclerosis, few studies have reported on the involvement of a combination of potentially susceptible genes in cardiovascular diseases. The objective of the present review is to identify Single Nucleotide Polymorphisms associated with carotid atherosclerosis of type 2 diabetic patients, which can be considered as a surrogate end point of cardiovascular events.