THE ROLE OF ENDOTHELIAL DYSFUNCTION IN THE MECHANISM OF GASTROESOPHAGEAL REFLUX DISEASE DEVELOPMENT IN PATIENTS WIThisCHEMIC HEART DISEASE

Abstract

Ischemic heart disease (IHD) and gastroesophageal reflux disease (GERD) are among the most common diseases worldwide, which in a considerable percentage of cases occur together, thus complicating symptoms, posing problems for timely diagnosis and hindering development of a comprehensive treatment regimen for both diseases. Research has shown that endothelial dysfunction is one of the major pathophysiological mechanisms in the development of IHD. Endothelial dysfunction also affects regional perfusion of the esophagus, thus compromising esophageal tissue defense mechanisms. The aim of our study was to investigate the role of endothelial dysfunction in the mechanisms of GERD development in patients with IHD. For the purpose of this study, we collected data on serum levels of endothelin-1, nitric oxide metabolites and lipid peroxidation products, gastric pH, parameters of regional blood flow, and quality of life assessment. Study results revealed that in IHD patients with concomitant GERD, endothelial dysfunction manifested by a significant increase in the levels of endothelin-1 and lipid peroxidation products, with decreased levels of nitric oxide metabolites, regional blood flow and quality of life. These findings suggest that hypoxia of the esophageal mucosa, caused by endothelial dysfunction, leads to a decrease in the esophageal tissue resistance and to esophageal lower sphincter dysfunction, which, in turn, are the leading factors in the development of GERD.