Role of oxidative stress and cardiovascular risk factors in ischemic heart disease

Abstract

Ischemic heart disease (IHD) is a major cause of mortality and disability and is the most common type of cardiovascular disease (CVD). Reduced myocardial perfusion by obstruction in coronary arteries due to progressive accumulation of fibrotic material/plaque in the vessel wall leads to the development of IHD. Cardiovascular risk factors such as atherosclerosis, hypertension and thrombosis promote the occurrence of oxidative stress and thus widely contribute to the genesis of tissue necrosis and ischemia-reperfusion (I/R) injury to the heart. Furthermore, the production of reactive oxygen species (ROS) during myocardial ischemia results in subcellular abnormalities and cardiac dysfunction. Particularly, ROS produced by NADPH oxidases, xanthine oxidase, mitochondrial cytochromes and uncoupled nitric oxide synthase have been documented to affect vasculature and play a role in the occurrence of atherosclerosis, thrombosis and hypertension. Accordingly, inhibition of ROS-producing enzymes as well as mitochondrial reverse electron transport can be seen to normalize endothelial vascular function and prevent the development of cardiovascular risk factors for IHD. This article is intended to describe the mechanisms of oxidative stress-induced changes involved atherosclerosis, thrombosis and hypertension, and to summarize the contribution of ROS in the genesis of cardiac dysfunction due to I/R injury.