Free radicals in blood: evolving concepts in the mechanism of ischemic heart disease.

There has been a considerable debate over past decade on how reactive oxidant species (ROS) in blood augment the cell signaling processes involved in the pathogenesis of coronary heart disease. In particular, it is not clear whether ROS is an important component of the cross-talk between blood and elements of the vasculature during the initial and latter stages of vascular injury and development of atherosclerotic lesions. Features like the recruitment of the circulating activated monocytes, T cells and granulocytes occur extensively in patients with acute coronary syndromes. It is not known what drives the infiltration of these cells into the vessel wall in the active stages of atherosclerosis and whether ROS plays an intermediate part. Currently, the thinking is that although inflammatory processes may be prompted by different etiological factors from that of coronary heart disease, the presence of ROS in circulating blood is the key intermediary related to vascular injury and organ dysfunction. We review, the clinical and experimental data of the mechanisms involved, and evaluate the wider implications of this concept.