Torsade de pointes

Abstract

Torsade de pointes ventricular tachyarrhythmia in the long QT syndrome is a prime example of how molecular biology, ion channel, and cellular and organ physiology, coupled with clinical observations, promise to be the future paradigm for advancement of medical knowledge. Both the congenital and the acquired long QT syndrome are caused by abnormalities (intrinsic, acquired, or both) of the ionic currents underlying ventricular repolarization. In this review, the continually unraveling molecular biology of congenital long QT syndrome is discussed. The various pharmacologic agents associated with the acquired long QT syndrome are listed. Although it is difficult to predict which patients are at risk for torsade de pointes, careful assessment of the risk to benefit ratio is important before prescribing drugs known to cause QT prolongation. The in vivo electrophysiologic mechanism of torsade de pointes in the long QT syndrome is described, using as a paradigm the anthopleurin-A canine model, a surrogate for LQT3. The characteristic association of torsade de pointes with T-wave alternans and short-long cardiac sequences is discussed, with emphasis on electrophysiologic mechanisms. Finally, the expanding knowledge of genetic mutations other than long QT syndrome associated with polymorphic ventricular tachyarrhythmia is emphasized.

The Association between Work-Related Stress and Autonomic Imbalance among Call Center Employees in Japan

“…In this sense, there are few reports using objective outcomes (Collins et al 2005;Otsuka et al 2009;Maeda et al 2015). QT intervals, as well as heart rate variability (HRV) and heart rate, have been considered as an objective marker of the development of ventricular arrhythmia or of the susceptibility to sudden death (El-Sherif and Turitto 2003;Jouven et al 2005), because QT intervals represent the duration between ventricular depolarization and subsequent repolarization (Yun et al 2015) while the corrected QT interval (Bazett 1920), by comparison with QT index (Rautaharju et al 2009), tends to depend on heart rate . In this study, we investigated the impact of work-related stress, as well as home stress, on autonomic nervous function among call center employees undergoing electrocardiography (ECG) at the time of their annual health checkups.…”

Novel sulfonylurea derivatives as H3 receptor antagonists. Preliminary SAR studies

“…[31][32] Drugs that block hERG have been associated with QT interval prolongation as well as serious, and sometimes fatal, cardiac arrhythmias (including torsade de pointes). [33] Blockade of the hERG channel poses a risk of cardiac toxicity and has become a critical issue for regulatory agencies and the pharmaceutical industry. [34] This problem has recently been addressed.…”

The potential contribution of ranolazine to Torsade de Pointe

“…4,5 Both congenital and acquired long QT syndrome are caused by abnormalities of the ionic currents underlying ventricular repolarization. In specific settings, such as bradycardia, these conditions may cause polymorphic ventricular tachycardia.…”

“…However, it may degenerate to ventricular fibrillation if untreated. 4,5 Numerous conditions can cause prolonged QT and induce TdP. These conditions include inherited mutations of ion channels, 6 idiopathic, metabolic abnormalities (hypokalemia, hypocalcemia and hypomagnesemia), and bradyarrhythmias.…”