It is well known that very low high density lipoprotein is a known risk factor for coronary artery disease. Most of the recent studies have shown that Statins which are included in the treatment do not effect HDL. Also most of the therapies and the recent clinical trials with CETP inhibitors though have increased HDL levels, failed to show clinical benefits and also failed so far to reduce the mortality.

       Pathologic conditions associated with inflammation show an inverse correlation between High density lipoprotein and inflammatory biomarker levels. Atherosclerosis is a multistep disease and the chronic inflammation play a role in its every stage from its onset, progression and finally to plaque rupture. Many markers of inflammation appear during this process, which are used for risk prediction, particularly c- reactive protein.

       In the absence of acute or chronic inflammation High density lipoprotein is anti inflammatory. However the onset of systemic inflammation state such as Acute coronary syndrome, might alter the HDL-components and function such that it becomes pro inflammatory

       It is also recognized that increased inflammation attenuates the protective actions of high HDL levels.

       So it is still unclear whether the changes in plasma levels of HDL-Cholesterol are primary events or secondary to the inflammation. Thus understanding the correlation of inflammatory response in Acute coronary syndrome and the levels of HDL-Cholesterol may lead to new therapeutic interventions