Polymorphic ventricular tachycardias including torsade de pointes

ESC CardioMed ◽  
2018 ◽  
pp. 2293-2298
Author(s):  
L. Brent Mitchell

Polymorphic ventricular tachycardia (PMVT) is a rapid ventricular tachycardia in which the QRS complexes vary in coupling interval, morphology, and axis on a beat-to-beat basis. PMVT occurs in two distinct forms: PMVT without QT interval prolongation and PMVT with QT interval prolongation. The two types differ in important ways with respect to their differential diagnosis and treatment. PMVT without QT interval prolongation usually emerges in the setting of an unstable structural heart disorder, such as acute ischaemia or decompensated heart failure. Treatment is directed at the underlying heart disorder, correction of acid–base disturbances, hypoxia, and electrolyte abnormalities along with beta-blocking therapy and amiodarone. Invasive antiarrhythmic interventions, such as sympathetic denervation and transcatheter ablation, are occasionally required. Long-term treatment often includes an implantable cardioverter defibrillator. PMVT with QT interval prolongation, known as torsade de pointes VT, occurs when repolarization reserve has been exhausted by either inherited or acquired factors that prolong the QT interval. Classical features of the ‘twisting-of-the-points’ polymorphism and the short–long–short initiation sequence are common but are not universal. Treatment is directed at removal of the cause of the QT interval prolongation, correction of electrolyte disturbances (hypokalaemia and hypomagnesaemia), supplemental magnesium therapy, and treatments to shorten the QT interval such as isoproterenol, pacing, or lidocaine. Long-term treatment is focused on avoidance of QT interval prolonging factors. If the likelihood of subsequent recurrence is not low, consideration is given to placement of a permanent pacemaker or implantable cardioverter defibrillator.

ESC CardioMed ◽  
2018 ◽  
pp. 2293-2298
Author(s):  
L. Brent Mitchell

Polymorphic ventricular tachycardia (PMVT) is a rapid ventricular tachycardia in which the QRS complexes vary in coupling interval, morphology, and axis on a beat-to-beat basis. PMVT occurs in two distinct forms: PMVT without QT interval prolongation and PMVT with QT interval prolongation. The two types differ in important ways with respect to their differential diagnosis and treatment. PMVT without QT interval prolongation usually emerges in the setting of an unstable structural heart disorder, such as acute ischaemia or decompensated heart failure. Treatment is directed at the underlying heart disorder, correction of acid–base disturbances, hypoxia, and electrolyte abnormalities along with beta-blocking therapy and amiodarone. Invasive antiarrhythmic interventions, such as sympathetic denervation and transcatheter ablation, are occasionally required. Long-term treatment often includes an implantable cardioverter defibrillator. PMVT with QT interval prolongation, known as torsade de pointes PMVT, occurs when repolarization reserve has been exhausted by either inherited or acquired factors that prolong the QT interval. Classical features of the ‘twisting-of-the-points’ polymorphism and the short–long–short initiation sequence are common but are not universal. Treatment is directed at removal of the cause of the QT interval prolongation, correction of electrolyte disturbances (hypokalaemia and hypomagnesaemia), supplemental magnesium therapy, and treatments to shorten the QT interval such as isoproterenol, pacing, or lidocaine. Long-term treatment is focused on avoidance of QT interval prolonging factors. If the likelihood of subsequent recurrence is not low, consideration is given to placement of a permanent pacemaker or implantable cardioverter defibrillator.


2012 ◽  
Vol 65 (3) ◽  
pp. 294-296
Author(s):  
Montse Vilaseca-Corbera ◽  
Gabriel Vázquez-Oliva ◽  
Cristina Campoamor-Cela ◽  
Alberto Zamora-Cervantes ◽  
Joan Bassanyanes-Vilarrasa ◽  
...  

2004 ◽  
Vol 39 (6) ◽  
pp. e49-e52 ◽  
Author(s):  
Y. Alkan ◽  
W. E. Haefeli ◽  
J. Burhenne ◽  
J. Stein ◽  
I. Yaniv ◽  
...  

2011 ◽  
Vol 4 (4) ◽  
pp. 223
Author(s):  
Torben K. Becker ◽  
Sai-Ching J. Yeung

Cancer patients are at an increased risk for QT interval prolongation and subsequent potentially fatal Torsade de pointes tachycardia due to the multiple drugs used for treatment of malignancies and the associated symptoms and complications. Based on a systematic review of the literature, this article analyzes the risk for prolongation of the QT interval with antineoplastic agents and commonly used concomitant drugs. This includes anthracyclines, fluorouracil, alkylating agents, and new molecularly targeted therapeutics, such as vascular disruption agents. Medications used in the supportive care can also prolong QT intervals, such as methadone, 5-HT3-antagonists and antihistamines, some antibiotics, antifungals, and antivirals. We describe the presumed mechanism of QT interval prolongation, drug-specific considerations, as well as important clinical interactions. Multiple risk factors and drug–drug interactions increase this risk for dangerous arrhythmias. We propose a systematic approach to evaluate cancer patients for the risk of QT interval prolongation and how to prevent adverse effects.


2008 ◽  
Vol 98 (4) ◽  
pp. 208-212 ◽  
Author(s):  
Konstantinos P. Letsas ◽  
Michalis Efremidis ◽  
Stavros P. Kounas ◽  
Loukas K. Pappas ◽  
Gerasimos Gavrielatos ◽  
...  

2006 ◽  
Vol 44 ◽  
pp. S95
Author(s):  
A. Zambruni ◽  
E. Savelli ◽  
A. Berzigotti ◽  
G. Magini ◽  
E. Mirici Cappa ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document