Introduction. Despite the known risks of myocardial damage as a result of reperfusion, current treatment strategies often focus only on immediate recanalization of the coronary arteries. At the same time, a lot of experimental and clinical data confirms that this procedure can provoke additional ischemic reperfusion injury to the myocardium. Objective. Analysis of the existing literature on ischemia-reperfusion syndrome in percutaneous coronary intervention in order to systematize knowledge about the mechanisms of its development. Material and methods. The study was conducted in collaboration with international organizations to analyze PRISMA (Preferred Reporting Articles for Systematic Reviews and Meta-analyses). The search for users was conducted in the PubMed, Google Scholar, and eLibrary.ru. Results. A total of 4,268 initial results were found, including PubMed — 2,134 publications, Google Scholar — 1,280 and eLibrary. ru — 854 publication. Only 1,523 papers turned out to be relevant, after studying which only 70 full-text publications were selected for the review, which met all the selection criteria and were included in the analysis. Most studies describe the pathophysiological mechanisms contributing to the development of ischemia-reperfusion syndrome during percutaneous coronary intervention. Conclusion. Ischemia-reperfusion syndrome causes activation of various pathophysiological mechanisms, among which endothelial dysfunction, oxidative stress, inflammatory response, and energy exchange disorders play a leading role. This is the basis for the development of new therapeutic strategies to prevent myocardial damage during percutaneous coronary interventions and improve treatment outcomes in patients with coronary artery disease.