Asymmetric dimethylarginine, NO and collateral growth.

Atherosclerosis is a chronic inflammatory disease, which selectively involves the arteries in the vascular system. Atherosclerosis develops because of reactions occurring in vessel wall beginning with response to endothelial injury. Endothelial dysfunction is characterized with impairment and loss of monolayer cells covering the inside of the vessels, which is endothelium. Endothelial dysfunction is the first stage in atherosclerosis. Coronary angiogenesis and collateral growth are chronic adaptations to myocardial ischemia to restore coronary blood flow and salvage myocardium in the ischemic region. Nitric oxide (NO) which represents the status of endothelial health plays a major role in collateral vessel development. Asymmetric dimethylarginine (ADMA) which is endogenous inhibitor of NO synthesis may impair the effective coronary collateral vessel development. Increased plasma ADMA levels are related with poor coronary collateral development. ADMA may be responsible for the difference in coronary collateral vessel development among similar patients with coronary artery disease. Nitric oxide inhibitors have a determinative relation with endothelial cell functions which may be integral prerequisite in all steps of collateral development. The aim of this review is to evaluate the interrelations between ADMA and collateral growth.