Ventricular Tachycardia due to Long QT Syndrome Associated to Non-Cardiac Pharmacological Agents

Abstract

EditorialJ Cardiol Curr Res 2016, 5(5): 00176 the declining inflow of sodium and calcium. These ion currents utilize specific channels that are under the influence of multiple factors. The long QT syndrome is characterized by QT interval prolongation and a tendency to develop a potentially lethal ventricular tachycardia [1,2]. Several anti-arrhythmic drugs, as well as some non-cardiac medications, block a specific potassium channel: I Kr . In the case of the anti-arrhythmic drugs, inhibition of I Kr channels is the mechanism for the drug's therapeutic effect. Non-cardiac drugs that cause the long QT syndrome block these channels incidentally.Although, the long QT syndrome was associated with the use of anti-arrhythmic drugs at the beginning, this prolongation may complicate the use of a large group of non-cardiac medications frequently used in internal medicine. Mostly prescribed by general physicians and internists, these non-cardiac drugs are commonly prescribed agents, namely, antibiotics, anti-histamines and anti-psychotic agents. It has been estimated that up to 3% of all drug prescriptions are for medications that may prolong the QT interval [3]. Recognition of the long QT syndrome due to non-cardiac drugs is therefore of great importance. The proarrhythmic potential of non-cardiac medications can be estimated experimentally in cell cultures, in isolated hearts, as well as, in animal models [4][5][6]. For example, drug concentrations at which I Kr channels are blocked can be determined in cell cultures. However, these models only provide rough estimates of a given drug's proarrhythmic potential and have limited clinical implications [4].About five decades ago, Jervell and Lange-Nielsen described the congenital syndrome of deafness, long QT and malignant arrhythmias in infancy [7]. A milder, more common, form of the congenital long QT syndrome was subsequently described by Romano and Ward [8,9]. At that time, the pro-arrhythmic effect of quinidine [10] and some non-cardiac medications [11] were also reported. Although for years the congenital and acquired forms of the long QT syndrome were considered to be two distinct entities [12], it is now clear that all forms of the long QT syndrome are caused by dysfunction of ion channels in the membrane of cardiomyocytes. This ion channel dysfunction may be due to mutations in genes that encode the channel proteins in the congenital syndrome, or may result from the effects of pharmacological agents in the acquired disease [13].Several non-cardiac medications like antibiotics, antihistamines and anti-psychotic drugs, block potassium channels in myocardial cells and may thus prolong the QT interval triggering a life-threatening ventricular arrhythmia known as torsade de pointes [14][15][16]. Most patients with drug induced torsade de pointes have additional clinical risk factors that are readily identifiable such as female gender, organic heart disease, hypokalemia and a history of long QT or drug-induced arrhythmias. For patients without these risk factors it is neit...