The Effect of Cardiac Rehabilitation on Oxidative DNA Damage and Inflammation in Patients With Coronary Artery Disease

Coronary artery disease (CAD) is a significant global health issue and the leading cause of cardiovascular mortality. Recent research has focused on the impact of oxidative stress, genetic damage, and inflammation in CAD development. Chronic inflammation and oxidative stress can cause cellular damage by increasing the formation of free oxygen radicals. Oxidative stress leads to endothelial dysfunction, inflammation of the vessel wall, and the formation of atherosclerotic plaques. Atherosclerosis is the most common pathological process associated with cardiovascular diseases, and the disease is characterized by a high oxidative stress state, which causes lipid and protein oxidation. Oxidative stress and an imbalance between oxidants and antioxidants can damage important biomolecules such as DNA, lipids, and proteins. Cardiac rehabilitation (CR) programmes are a recommended therapy with demonstrated efficacy in the treatment of patients with CAD. CR is a holistic approach that combines medical and exercise interventions to improve patients' cardiovascular health and general well-being. Exercise is the foundation of CR. While the literature describes it extensively, there is still some controversy surrounding oxidative stress and exercise. It has been suggested that exercise may increase the production of reactive oxygen molecules associated with oxidative stress, which is a factor in the pathogenesis of CAD. Regular and moderate exercise can have a positive impact on the body by balancing the production of antioxidants, reducing inflammation and oxidative stress. However, it is important to note that exercise should be approached in moderation to avoid any negative effects on the body. Previous studies have focused on risk factors associated with physical fitness, the fibrinolytic system, or lipid profile in cardiac patients. However, there have been relatively few investigations of induced changes in blood. This study aims to investigate the role of oxidative stress and inflammation in the pathogenesis of CAD and the effects of KR on these pathophysiological processes.