Introduction According to the American Heart Association, in US a total of 869,724 people died due to various cardiovascular diseases in 2004, of which coronary artery disease (CAD) caused the death of more than four hundred thousand people. In comparison, total cancer related deaths in the same year add up to little over 550 thousand. CAD is the single leading cause of death in the US currently (Cardiovascular disease statistics, 2008). CAD is caused by the narrowing of the coronary arteries due fat deposition in them, eventually leading to either complete obstruction of the artery lumen or dislodgment of the plaque embolism. It can lead to complications such as myocardial infarction or stroke. Therefore a sound knowledge of its patho-physiology enables us to understand the disease in better light and leads us to find means of prevention and treatment. Discussion The initiation point of atherosclerosis is usually the deposition of fat in blood vessels. Usually, fatty steaks on the vessel lumen appear. These have been seen in children as young as 9 year old. Fatty streaks are lipids are deposited under the damaged endothelium and which have been ingested by macrophages. The macrophages are now called foam cells. Gradual and ongoing deposition of foam cells leads to the formation of yellow white fibrous plaques. These plaques either grow large in size and occlude the lumen of arteries completely causing ischemia to the organ or can dislodge and rupture from its place causing platelet aggregation and thrombus at the site, and form emboli of the plaque which was dislodged with the potential to get stuck in the narrow arteries (Schoen, F.J. 2004). The arteries most frequently affected are the coronary arteries, carotid arteries and the aorta, where non laminar or turbulent blood flow is present. The process of atherosclerosis and plaque formation is a dynamic, progressive and ongoing process, which can start at an early age given that the risk factors for the disease are present. These include family history, male gender, and high blood levels of LDLs, sedentary life style, obesity, cigarette smoking, Diabetes mellitus, infection and chronic inflammation infection (The Merck Manual, 2005). And (Mallika V, 2007) It has been seen that intimal-medial wall thickness (IMT) is particularly relevant, when looking at complications of atherosclerosis. It ha been seen that IMT is a strong predictor of ischemic attacks. Studies of amongst families, siblings etc have shown that there is a hereditary link to IMT which in turn plays a role in determining the risk of atherosclerosis related complications (Humphries SE, 2004). In atherosclerosis, from the initiation stage of fatty streaks, through the growth stage of deposition of foam cells and even till the occurrence of complications, all are considered to be an inflammatory response to injury. The multiple factors involved in the process include endothelium lining integrity. Nitrous oxide availability, macrophage migration, inflammatory response, smooth muscles and connective tissue deposition. These all have a role to play in the progression of the disease (The Merck Manual). Endothelium “According to (Mitchell ME, et al, 1998,) Injury to the endothelial cell of the artery