Introduction
The use of a multicomponent polychemotherapy program in the treatment often leads to the development of cardiotoxicity, which in turn forces to interrupt a more effective treatment regimen and return to it only after treatment of cardiovascular pathology, and sometimes refuse to continue antitumor therapy. Currently, in clinical cardiology, a serious medical problem is the long QT syndrome, which is a risk factor for cardiac arrhythmias and sudden death. Prolongation of the QT interval often manifests itself in episodes of loss of consciousness and often ends in ventricular fibrillation, which is the immediate cause of sudden death (1).
In clinical practice, congenital and acquired forms of long QT are distinguished (2). This paper presents a description of a clinical case of acquired long QT syndrome, which is caused by the use of an unfavorable combination of drugs. The most common drugs that can prolong the QT interval include antiarrhythmic, class IA III, antibacterial (macrolide and fluoroquinolone groups), several antidepressants, psychotropic, and sedatives, antihistamines, diuretics, and lipid-lowering drugs (3).
The state of the cardiovascular system largely determines the survival rate of patients with oncohematological diseases in critical conditions. Changes in the cardiovascular system in hematological patients in a specialized hospital are detected based on the results of electro-functional research methods (4). In our practice, we have presented a clinical case of a hematological oncological patient with long QT syndrome of non-hereditary, drug-induced genesis. Its identification and description are of great interest in the clinical practice of physicians from the etiology of serious cardiac arrhythmias and conduction disturbances in patients with no history of organic heart disease.