The problem of formation of cardiac arrhythmia such as "torsades de pointes" 
because of prolongation of the QT interval is discussed in this article. It is 
established 2 forms of the long QT syndrome, a congenital and an acquired one. 
The congenital form has seven different known predisposing genes, six of which 
are associated with the myocardial ion channels. The prevalence of the 
congenital form is estimated at less than 1/10000. The molecular basis of 
inherited disorders caused by a mutation in either the gene coding for a 
particular potassium channel called HERG-or another gene, SCN5A, which codes for 
the sodium channel and disruption of which results in a loss of inactivation of 
the Na+ current. Among the congenital forms, particularly interest is focused on 
the potassium channel coded by the HERG gene located on chromosome 7 and with a 
key role in the normal electric cardiac activity. The potassium channel coded by 
the HERG gene is partly responsible for the return of the electric cardiac 
activity to the resting phase before the next myocardial electric activation 
process. Disturbed function will prolong the return to resting phase, which is 
thought to be an essential part of the development mechanism of myocardial 
"torsades de pointes" tachycardia. There may also be correlation between the 
strength of binding of the medicinal substance to the potassium channel coded by 
the HERG gene and prolongation of the QT interval. The investigation revealed 
that different groups of drugs may produce an effect on the QT interval, such as 
some neuroleptics (haloperidol, droperidol, thioridazine) antidepressants 
(paroxetine), narcotic analgesics (methadone), antiarrhythmics (class I), 
antihistamines (H1 receptor blocking agents) and motility stimulants 
(domperidone and cisapride). For the prevention of cardiac arrhythmia such as 
"torsades de pointes".