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Current Opinion in Cardiology Jan 2003Torsade de pointes ventricular tachyarrhythmia in the long QT syndrome is a prime example of how molecular biology, ion channel, and cellular and organ physiology,... (Review)
Review
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.
Topics: Animals; Electrocardiography; Electrophysiologic Techniques, Cardiac; Genetic Predisposition to Disease; Humans; Long QT Syndrome; Polymorphism, Genetic; Torsades de Pointes
PubMed: 12496496
DOI: 10.1097/00001573-200301000-00002 -
Clinical Cardiology Sep 1993The polymorphic ventricular tachycardia torsade de pointes can occur in the congenital long QT syndromes or as a consequence of therapy with QT-prolonging drugs. The... (Review)
Review
The polymorphic ventricular tachycardia torsade de pointes can occur in the congenital long QT syndromes or as a consequence of therapy with QT-prolonging drugs. The latter can include not only antiarrhythmic drugs such as quinidine, but also a number of drugs which are not usually considered to have major cardiovascular effects: these include nonsedating antihistamines, such as terfenadine; antibiotics such as erythromycin; and neuroleptics such as thioridazine. The electrocardiographic hallmark of both the congenital and acquired forms of the long QT syndrome is marked QT(U) lability, particularly as a function of heart rate. The underlying mechanism is thought to be triggered activity arising as a consequence of early afterdepolarizations. An understanding of the basic mechanism has led to an understanding of the effective forms of therapy, which include maneuvers to include the heart rate (pacing, isoproterenol) as well as maneuvers which may not necessarily alter the QT interval but may prevent the arrhythmia (magnesium, beta blockers). Intensive study of the clinical features and basic mechanisms underlying torsade de pointes has led to the definition of a new mechanism for cardiac arrhythmias; understanding such mechanisms may ultimately lead to the development of safer antiarrhythmic therapy.
Topics: Adrenergic beta-Antagonists; Animals; Anti-Arrhythmia Agents; Antipsychotic Agents; Dogs; Electrocardiography; Erythromycin; Heart Rate; Histamine Antagonists; Humans; Long QT Syndrome; Torsades de Pointes
PubMed: 7902224
DOI: 10.1002/clc.4960160910 -
Anesthesia and Analgesia Sep 2013Torsade de pointes is a rare but potentially fatal arrhythmia. More than 40 cases of perioperative torsade de pointes have been reported in the literature; however, the... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Torsade de pointes is a rare but potentially fatal arrhythmia. More than 40 cases of perioperative torsade de pointes have been reported in the literature; however, the current evidence regarding this complication is very limited. To improve our understanding, we performed a systematic review and meta-analysis of all published case reports of perioperative torsade de pointes.
METHODS
MEDLINE was systematically searched for cases of perioperative torsade de pointes. We included patients of all age groups and cases that occurred from the immediate preoperative period to the third postoperative day. Patient and case characteristics as well as QT interval data were extracted.
RESULTS
Forty-six cases of perioperative torsade de pointes were identified; 29 occurred in women (67%), and 2 episodes were fatal (case fatality rate: 4%). Craniotomies and cardiac surgery accounted for 40% of all cases. Preceding events identified by the authors were hypokalemia (12/46, 26%; 99% confidence interval [CI], 9%-43%) and bradycardia (7/46, 15%; 99% CI, 2%-28%). Drugs were implicated in approximately one third of the events (14/46, 30%; 99% CI, 13%-48%). The mean corrected QT (QTc) at baseline was 457 ± 67 milliseconds (minimum 320 milliseconds; maximum 647 milliseconds; data available in 27/46 patients). At the time of the event, the mean QTc increased to 575 ± 77 milliseconds (minimum 413 milliseconds; maximum 766 milliseconds; data available in 33/46 patients). On average, QTc increased by +118 milliseconds (99% CI, 70-166 milliseconds; P < 0.001) between baseline and after the torsade de pointes event. All patients, except for 2, had a substantial prolongation of their QTc interval at the time of the event.
CONCLUSIONS
This systematic review identified several common risk factors for perioperative torsade de pointes. Given the nearly uniform presence of a substantial QTc interval prolongation at the time of a torsade de pointes episode, increased vigilance for perioperative QTc interval prolongation may be warranted.
Topics: Adolescent; Adult; Aged; Child; Data Interpretation, Statistical; Electrocardiography; Female; Humans; Intraoperative Complications; Long QT Syndrome; Male; Middle Aged; Perioperative Care; Postoperative Complications; Predictive Value of Tests; Torsades de Pointes; Young Adult
PubMed: 23744954
DOI: 10.1213/ANE.0b013e318290c380 -
Pacing and Clinical Electrophysiology :... Apr 2018Since its initial description by Jervell and Lange-Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy.... (Review)
Review
Since its initial description by Jervell and Lange-Nielsen in 1957, the congenital long QT syndrome (LQTS) has been the most investigated cardiac ion channelopathy. Although congenital LQTS continues to remain the domain of cardiologists, cardiac electrophysiologists, and specialized centers, the by far more frequent acquired drug-induced LQTS is the domain of all physicians and other members of the health care team who are required to make therapeutic decisions. This report will review the electrophysiological mechanisms of LQTS and torsade de pointes, electrocardiographic characteristics of acquired LQTS, its clinical presentation, management, and future directions in the field.
Topics: Electrocardiography; Humans; Long QT Syndrome; Phenotype; Torsades de Pointes
PubMed: 29405316
DOI: 10.1111/pace.13296 -
Annals of Palliative Medicine May 2020Prolongation of the QT interval by antiarrhythmic drugs is the primary cause of torsade de pointes. Although there are previous reports of drug-induced torsade de...
Prolongation of the QT interval by antiarrhythmic drugs is the primary cause of torsade de pointes. Although there are previous reports of drug-induced torsade de pointes in patients undergoing hemodialysis, torsade de pointes caused by a sudden decrease of potassium levels in patients initiating hemodialysis has not been well described. A 70-year-old woman with recurrent bilateral gluteal abscesses visited the hospital for antibiotic treatment. Twenty-eight days after admission, atrial fibrillation with rapid ventricular rhythm was newly detected and was controlled with intravenous amiodarone treatment. After developing pulmonary edema that did not improve with diuretic treatment, she underwent emergency hemodialysis. During hemodialysis, serum potassium and magnesium levels decreased to 3.1 and 1.7 mg/dL, respectively. The electrocardiogram showed torsade de pointes. Amiodarone treatment was stopped, and magnesium sulfate was infused. A higher concentration of potassium dialysate was used in continuous renal replacement therapy. Torsade de pointes episodes halted, and QT interval prolongation normalized. We describe a case with a rare complication of torsade de pointes upon initiating hemodialysis in a patient with QT prolongation. When initiating hemodialysis, serum potassium levels as well as electrocardiograms should be monitored in patients with a prolonged QT interval.
Topics: Aged; Amiodarone; Anti-Arrhythmia Agents; Female; Humans; Long QT Syndrome; Renal Dialysis; Torsades de Pointes
PubMed: 32389016
DOI: 10.21037/apm.2020.04.29 -
Medicine Jul 2003Numerous medications, including drugs prescribed for noncardiac indications, can lead to QT prolongation and trigger torsade de pointes. Although this complication... (Review)
Review
Numerous medications, including drugs prescribed for noncardiac indications, can lead to QT prolongation and trigger torsade de pointes. Although this complication occurs only rarely, it may have lethal consequences. It is therefore important to know if patients with torsade de pointes associated with noncardiac drugs have risk factors that are easy to identify. We reviewed reports of drug-induced torsade de pointes and analyzed each case of torsade de pointes associated with a noncardiac drug for the presence of risk factors for the long QT syndrome that can be easily identified from the medical history or clinical evaluation (female gender, heart disease, electrolyte disturbances, excessive dosing, drug interactions, and history of familial long QT syndrome). We identified 249 patients with torsade de pointes caused by noncardiac drugs. The most commonly identified risk factor was female gender (71%). Other risk factors were frequently present (18%-41%). Virtually all patients had at least 1 of these risk factors, and 71% of patients had 2 or more risk factors. Our study suggests that almost all patients with torsade de pointes secondary to noncardiac drugs have risk factors that can be easily identified from the medical history before the initiation of therapy with the culprit drug.
Topics: Anti-Bacterial Agents; Antipsychotic Agents; Female; Histamine H1 Antagonists; Humans; Male; Risk Factors; Sex Distribution; Torsades de Pointes
PubMed: 12861106
DOI: 10.1097/01.md.0000085057.63483.9b -
Drugs Jan 1994Torsade de pointes is a polymorphic ventricular tachycardia showing a peculiar electrocardiographic pattern characterised by a continuous twisting in QRS axis around an... (Review)
Review
Torsade de pointes is a polymorphic ventricular tachycardia showing a peculiar electrocardiographic pattern characterised by a continuous twisting in QRS axis around an imaginary baseline. An abnormally prolonged QT interval is actually associated with torsade de pointes and it is constantly observed in the sinus beats preceding the onset of the arrhythmic event. Prolongation of ventricular repolarisation associated with the development of torsade de pointes can be observed in many clinical conditions, commonly referred to as prolonged QT syndromes, which can be divided into two major groups: (a) idiopathic long QT syndrome (LQTS), which include the Jervell-Lange-Nielsen and the Romano-Ward syndromes; and (b) acquired prolonged QT syndromes, which are largely iatrogenic and may follow treatment with antiarrhythmic drugs, tricyclic antidepressants, phenothiazines or macrolide antibiotics, and may be associated with metabolic disturbances (hypokalaemia, hypocalcaemia and hypomagnesaemia). Clinical studies have provided criteria for the definition and guidelines for the management of torsade de pointes, while the electrophysiological mechanisms responsible for its onset are still unclear. Two pathogenetic hypotheses have been proposed to account for the electrophysiological mechanisms underlying the condition: (a) re-entry due to a dispersion of refractory periods; and (b) triggered activity initiated by either early or delayed after-depolarisations. Both mechanisms are supported by clinical and experimental observations but a conclusive answer is not yet available.
Topics: Cardiovascular Agents; Electrocardiography; Humans; Torsades de Pointes
PubMed: 7510621
DOI: 10.2165/00003495-199447010-00004 -
Annals of Noninvasive Electrocardiology... Jan 2022TdP is a form of polymorphic ventricular tachycardia which develops in the setting of a prolonged QT interval. There are limited data describing risk factors, treatment,...
BACKGROUND
TdP is a form of polymorphic ventricular tachycardia which develops in the setting of a prolonged QT interval. There are limited data describing risk factors, treatment, and outcomes of this potentially fatal arrhythmia.
OBJECTIVE
Our goals were as follows: (1) to validate cases presenting with Torsade de Pointes (TdP), (2) to identify modifiable risk factors, and (3) to describe the management strategies used for TdP and its prognosis in a real-world healthcare setting.
METHODS
Case-control study (with 2:1 matching on age, sex, and race/ethnicity) nested within the Genetic Epidemiology Research on Aging (GERA) cohort. Follow-up of the cohort for case ascertainment was between January 01, 2005 and December 31, 2018.
RESULTS
A total of 56 cases of TdP were confirmed (incidence rate = 3.6 per 100,000 persons/years). The average (SD) age of the TdP cases was 74 (13) years, 55 percent were female, and 16 percent were non-white. The independent predictors of TdP were potassium concentration <3.6 mEq/L (OR = 10.6), prior history of atrial fibrillation/flutter (OR = 6.2), QTc >480 ms (OR = 4.4) and prior history of coronary artery disease (OR = 2.6). Exposure to furosemide and amiodarone was significantly greater in cases than in controls. The most common treatment for TdP was IV magnesium (78.6%) and IV potassium repletion (73.2%). The in-hospital and 1-year mortality rates for TdP cases were 10.7% and 25.0% percent, respectively.
CONCLUSIONS
These findings may inform quantitative multivariate risk indices for the prediction of TdP and could guide practitioners on which patients may qualify for continuous ECG monitoring and/or electrolyte replacement therapy.
Topics: Aged; Case-Control Studies; Delivery of Health Care, Integrated; Electrocardiography; Female; Humans; Long QT Syndrome; Torsades de Pointes
PubMed: 34547155
DOI: 10.1111/anec.12888 -
JAMA Cardiology Apr 2023
Topics: Female; Humans; Torsades de Pointes; Long QT Syndrome; Electrocardiography
PubMed: 36652237
DOI: 10.1001/jamacardio.2022.5094 -
Nephrology, Dialysis, Transplantation :... Jun 1996
Review
Topics: Anti-Arrhythmia Agents; Humans; Renal Dialysis; Torsades de Pointes
PubMed: 8671944
DOI: 10.1093/oxfordjournals.ndt.a027507