The development of
atherosclerotic plaque is a highly regulated and complex process which occurs as a result of structural and functional alterations in endothelial cells, smooth muscle cells (SMCs), monocytes/macrophages, T-lymphocytes and platelets. The plaque formation in the coronary arteries or
rupture of the plaque in the peripheral vasculature in latter stages of
atherosclerosis triggers the onset of acute ischemic events involving myocardium. Although
lipid lowering with
statins has been established as an important
therapy for the treatment of
atherosclerosis, partially beneficial effects of
statins beyond decreasing
lipid levels has shifted the focus to develop newer drugs that can affect directly the process of
atherosclerosis. Blockade of renin angiotensin system, augmentation of
nitric oxide availability, reduction of Ca(2+) influx, prevention of oxidative stress as well as attenuation of
inflammation, platelet activation and SMC proliferation have been recognized as targets for drug treatment to control the development, progression and management of
atherosclerosis. A major challenge for future drug development is to formulate a combination
therapy affecting different targets to improve the treatment of
atherosclerosis.