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.