Deficiency of Klotho protein as a cause of linked angina in young patients with thoracalgic phenotype of gastroesophageal reflux disease

Gastroesophageal reflux disease (GERD) is one of the most common diagnoses in therapeutic practice. Different manifestations of GERD represent different phenotypes of the disease with unique predisposing cofactors and individual pathophysiology. In the continuum of the proposed paradigm, chest pain syndrome in patients with gastroesophageal reflux stands out as a separate phenotype of GERD. Traditionally it was believed that the chest pain in young patients with GERD was not angina. Objective — to study the levels of Klotho protein and nitric oxide in the blood serum of patients with GERD and chest pain (thoracalgic phenotype of GERD). Materials and methods. 64 patients with GERD were prospectively examined, including 27 patients with the thoracalgic phenotype of GERD. The Klotho protein was determined in blood serum by the enzyme immunoassay, the metabolism of NO in the blood plasma was assessed by the Griess test. All patients underwent video esophagogastroscopy, transthoracic echocardiography and 24­Hour Holter electrocardiographic monitoring. Descriptive and nonparametric statistics methods were used in the study. Results. An evaluation of the chest pain syndrome in young patients with GERD revealed a high incidence of linked angina — 25.9%. A decrease in the Klotho protein and NO levels in the blood of patients with GERD and linked angina was observed compared to patients with uncomplicated GERD with pseudo­­coronary pain. The obtained result showed a direct relationship between the concentrations of Klotho protein and NO. Low levels of these parameters in patients with GERD and linked angina reflect endothelial dysfunction and lead to coronary artery spasm mediated by reflux. Conclusions. Linked angina occurs in a quarter of young patients with the thoracalgic phenotype of GERD. The basis of this phenomenon is a decrease in NO synthesis due to endothelial dysfunction, which develops against the background of the Klotho protein deficiency.