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At least 19 recordsLinked to original sources
PubMed1993

Experimental models of torsades de pointes.

Torsades de pointes is the most typical ventricular tachycardia involving QT-interval prolongation. It is a rather unusual but potentially lethal ventricular tachycardia with a distinctive morphology favored by bradycardia, antiarrhythmic drugs and hypokalemia and requires specific treatment. Torsades de pointes has been shown to be related to bradycardia-dependent early afterdepolarizations (EAD) and/or increased dispersion of repolarization. However, although EAD can be obtained relatively easily in vitro with quinidine or sotalol, torsades de pointes are very difficult to reproduce in animal models. The models of torsades de pointes which have been proposed can be categorized as morphological, EAD-related or pharmacological models. The purpose of the 'morphological' models was to reproduce the twisting of QRS axis typical of torsades de pointes, with no consideration of other aspects such as long QT or bradycardia. These models were produced by epicardial electrical or chemical (aconitine) stimulation at two distant ventricular sites or by overdosing of quinidine in dogs with acute myocardial infarction. The second type of model focused on the conditions producing EAD in vitro. Ventricular tachycardias were obtained in anesthetized dogs using toxics such as cesium or anthopleurine, both producing EAD in vitro. These ventricular tachycardias were shown to be sensitive to magnesium, heart rate and autonomic tone, but torsades de pointes remained rare, at least after cesium injections. The pharmacological models that could be used to study the QT-dependent proarrhythmic effects of drugs are the anesthetized rabbit with alpha-adrenergic stimulation, and the conscious dog model with chronic AV-block and diuretic-induced hypokalemia. Methoxamine-treated anesthetized rabbits develop ventricular tachycardias during clofilium infusions. These ventricular tachycardias, although appearing at very high heart rates, have typical torsades de pointes aspects and are often associated with giant QT waves. The specificity of the model remains to be tested. In our conscious bradycardic and hypokalemic dogs, quinidine and sotalol but not flecainide, propranolol or lidocaine induced QT-dependent arrhythmogenic effects and torsades de pointes. Efficacy of high rate stimulations and magnesium were repeatedly observed. This demanding model, especially designed for qualitative drug comparisons, is also well suited to studies on the mechanisms of initiation of torsades de pointes. The pertinence of these models for estimating the risk of QT-dependent proarrhythmias associated with non-antiarrhythmic agents remains to be tested.

Animals↗
PubMed1993

Drug therapy for torsade de pointes.

Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life-threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.

Action Potentials↗
PubMed1997

Combined use of astemizole and ketoconazole resulting in torsade de pointes.

Torsade de pointes is a serious ventricular arrhythmia which is usually associated with a long QT interval. It is important to recognize the possible predisposing factors for the management of this arrhythmia. Prolongation of the QT interval and torsade de pointes has been reported in patients with an overdose of astemizole. We report on a 63-year-old woman presenting with torsade de pointes and a long QT interval caused by the combined use of astemizole (at recommended dosage), and ketoconazole. After discontinuation of these drugs and treatment with a temporary pacemaker, magnesium sulfate and lidocaine, the arrhythmia was no longer observed and she was discharged in good condition with a normal electrocardiogram. This case should alert clinicians to the possibility of torsade de pointes with the combined use of astemizole and ketoconazole.

Antifungal Agents↗
PubMed2003

Torsade de pointes.

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.

Animals↗
PubMed1989

Hypocalcemic Torsades de Pointes.

Torsades de pointes is a unique form of ventricular tachycardia that occurs in the presence of prolonged QT interval. Many predisposing factors have been identified. A classical form of torsades de pointes occurring in the presence of hypocalcemia and prolonged QT interval in an elderly woman is reported. In this patient the QT prolongation was markedly rate-dependent. Hypocalcemia was a postoperative complication following removal of parathyroid adenoma, performed earlier for hyperparathyroidism. Torsades de pointes did not recur after normalization of serum calcium. To the authors' knowledge, this is the first electrocardiographic documentation of hypocalcemic torsades de pointes.

Aged↗
PubMed1993

[Torsades de pointes].

Torsades de pointes are defined and characterised by specific, polymorphic but organised ventricular activation on the surface electrocardiogram. They constitute episodes of rapid tachycardia which are usually short lasting and terminate spontaneously. However, they may recur and persist, leading to syncope or sudden death. They occur typically in cases with abnormalities of ventricular repolarisation with prolongation of the QTU interval and variable deformations of the TU waves. The basal abnormalities may be modest or intermittent. A bigeminy with a long coupling interval and alternating long and short cycles often precede the burst of arrhythmia. Abnormalities of ventricular repolarisation and torsades de pointes may be the result of congenital syndromes (catecholamine-dependent torsades) or acquired factors (pause-dependent torsades) such as paroxysmal bradycardia, drugs which prolong the repolarisation and potassium and magnesium deficiencies. The electrophysiological mechanisms comprise reentry and after depolarisation induced activity genetic factors causing abnormalities of the G-proteins, potassium currents or adrenergic receptors may also play a role. Emergency treatment consists of intravenous magnesium salts, sometimes of betablockers or verapamil for maintenance therapy. The association of a potassium-sparing drug may be useful. Cardiac pacing may be necessary. Left sympathetic denervation or implantation of an automatic defibrillator are exceptional therapeutic options in refractory congenital torsades de pointes.

Death, Sudden, Cardiac↗
PubMed2005

Effects of buprenorphine on cardiac repolarization in a patient with methadone-related torsade de pointes.

Torsade de pointes is a rare but potentially fatal ventricular arrhythmia that is often triggered by drugs that prolong the rate-corrected QT (QTc) interval. This arrhythmia has been attributed to levacetylmethadol and methadone, synthetic opioids used to treat heroin addiction. Levacetylmethadol, a derivative of methadone, is being withdrawn from the United States market because its use waned after a black box warning was issued to require electrocardiographic monitoring. Therefore, methadone and buprenorphine are the only opioids available for the treatment of heroin addiction. To our knowledge, the cardiac safety of buprenorphine in patients with methadone-related QTc prolongation has not been described. We report a patient who developed torsade de pointes while receiving high-dose methadone and was successfully inducted onto buprenorphine under close medical supervision. No clinically important QTc prolongation was observed in the acute setting or during follow-up. This observation suggests that buprenorphine may be a safe alternative to oral methadone in patients with opioid addiction who develop torsade de pointes.

Analgesics, Opioid↗
PubMed2004

Hands-on help Torsades de pointes.

Torsades de pointes, a French term that literally means "twisting of the points," is a lethal form of ventricular tachycardia named for its hallmark feature: polymorphic QRS complexes that appear to twist around the isoelectric line. Without treatment, few patients survive Torsades de pointes (TdP) once it develops. The key to preventing sudden cardiac death lies in early detection of warning signs.

Anti-Arrhythmia Agents↗
PubMed1998

Experimental models of torsade de pointes.

Torsade de pointes is a potentially life threatening form of polymorphic ventricular tachycardia typically seen in the setting of congenital and acquired abnormal QT-prolongation. Numerous in vitro studies have investigated basic ionic mechanisms underlying delayed repolarization. The role of different ion channels and the induction of early afterdepolarizations have been studied in various cardiac cells including M cells. In addition, isolated heart models with and without electrical stimulation and/or the use of drugs which prolong repolarization have been developed in recent years. Some of these models have simulated conditions likely to exist in the clinical setting of torsade de pointes, such as bradycardia and hypokalemia. In in vivo canine and rabbit models, torsade-like polymorphic ventricular tachyarrhythmias have been induced by the administration of different agents such as cesium, neurotoxins, e.g., anthopleurin or various class III drugs under conditions designed to mimic the clinical situation. In the context of recent advances in the molecular genetics of long QT syndrome, those models which have used sodium or potassium channel blockers have gained particular interest. Based on all experimental studies it seems probable that the first beats of torsade occur due to early afterdepolarizations and triggered activity. The development of subsequent beats is less clear. Reentry based on inhomogeneity of refractoriness has been suggested as the underlying mechanism.

Animals↗
PubMed1990

Torsades de Pointes.

Torsades de Pointes (T.D.P.) is a ventricular dysrhythmia that is a commonly undiagnosed condition seen within Critical Care areas of most Major Metropolitan Hospitals. It is a condition that requires prompt diagnosis and treatment. Experience has shown a lack of understanding of the clinical features and the treatment of this particular life threatening dysrhythmia. This paper was compiled to increase the awareness of the health professional of Torsades de Pointes, covering areas of physiologic mechanisms, clinical features, causes of the dysrhythmia and most importantly treatment, whether it be mechanical, drug therapy or a combination of both. Controversial issues have been raised and are discussed in this paper including the use of Magnesium Sulphate as first line treatment.

Electrocardiography↗
PubMed1984

Sotalol induced torsade de pointes.

Torsade de pointes is an uncommon ventricular tachyarrhythmia precipitated by a variety of metabolic and pharmacological conditions and requiring unconventional antiarrhythmic therapy. A case is presented demonstrating the occurrence of torsade de pointes following sotalol overdosage and specific features enabling recognition and treatment of this life-threatening arrhythmia are discussed.

Electrocardiography↗
PubMed1989

[Three cases of Torsades de pointes].

Torsades de Pointes is an atypical ventricular tachycardia, a characteristic sinusoidal twisting of QRS complex around the base line, first described by Dessertenne et al in 1966. Since their original description, many literatures including both reviews and case reports have been issued. However, the exact causes, mechanism and its true relation to usual ventricular tachycardia and fibrillation remain to be elucidated. In the present report, three cases of Torsades de Pointes (TDP) were described. All these patients revealed a prolonged QT and QTc interval as has been recognized at the occasion of TDP attacks together with low serum potassium concentration. In addition, one had hypertrophic cardiomyopathy (case 1), cholelithiasis (case 2) and uterus cancer (case 3), respectively. Regarding to the treatment, direct current counter shock was applied to terminate the TDP in all 3 cases, the correction of low serum potassium concentration was also done in each case. Lidocaine was ineffective in case 3 to terminate the TDP, while verapamil was effective in case 3 to convert TDP to normal sinus rhythm. In case 2, no antiarrhythmic drugs were applied, however, cardiac massage and normalization of serum potassium concentration succeeded to recover normal sinus rhythm. The diversity of the causes and treatments of TDP in these three cases was discussed in relation to the genesis of TDP.

Adult↗
PubMed1995

Diuretic-induced hypokalaemia inducing torsades de pointes.

Torsades de pointes (TP), an unique polymorphous type of ventricular tachycardia, is associated with either an acquired or congenitally prolonged QT interval. Several reports have demonstrated TP to follow an acquired prolonged QT interval secondary to chronic hypocalcaemia, hypomagnesaemia, or hypokalaemia. We report a rapid onset, acute extracellular hypokalaemia not associated with other electrolyte disturbances inducing a prolonged QT interval followed by TP. This is the first case report of a rapid onset isolated acute extracellular hypokalaemia inducing TP. Since anaesthetists are involved in therapies that will rapidly reduce extracellular potassium (diuretic, catecholamine, and/or insulin administration, hyperventilation), this cae report serves as a warning that such therapy may have the risk of arrhythmia induction.

Acute Disease↗
PubMed1992

Role of early afterdepolarization in familial long QTU syndrome and torsade de pointes.

Torsade de pointes (TdP) syncopal episodes were almost invariably precipitated by emotional stress or menstruation in a 17-year-old girl. U wave accentuation occurred during sinus rhythm without pauses in periods of heightened sympathetic tone. To examine the role of early afterdepolarization (EAD), monophasic action potentials were recorded during ventricular extrasystoles and TdP occurring spontaneously and induced by ventricular pacing. The effects of lidocaine, verapamil, propranolol, and epinephrine were assessed. Our data show that: (1) EAD plays a significant role in the genesis of familial long QTU syndrome and TdP; (2) rapid ventricular pacing causes postpause-dependent EADs, U waves, and TdP; and (3) EAD is enhanced by epinephrine infusion in the absence of pause, whereas EAD-triggered firing is inhibited by verapamil and propranolol but not by lidocaine.

Action Potentials↗
PubMed1991

Electrophysiologic mechanisms involved in the development of torsades de pointes.

Torsades de pointes (TDP) is a polymorphic ventricular tachycardia with a peculiar electrocardiographic pattern of continuously changing morphology of the QRS complex twisting around an imaginary baseline. The clinical setting under which TDP develops covers many clinico-pathologic conditions, including the long QT syndrome (LQTS). In the present review, we analyze the evolution of the hypotheses for the mechanisms underlying TDP and we discuss some of the experimental models used and their related clinico-pathologic counterparts. Together with the hypothesis that TDP represents a form of reentrant arrhythmia, recent evidence has suggested the possibility that triggered activity may indeed be responsible for TDP. Data collected in vitro are presented that demonstrate a role for catecholamines in the development of afterpotentials in ventricular tissue. Whether adrenergic-mediated afterdepolarizations are the mechanism responsible for TDP in the clinical setting of LQTS has not yet been proven and remains an important area of investigation.

Disease Models, Animal↗
PubMed2003

Assessing predictors of drug-induced torsade de pointes.

Torsades de pointes (TdP) is a malignant polymorphic ventricular tachyarrhythmia that can be caused by drugs that induce electrophysiological changes. Although the number of drugs known to cause TdP has increased in recent years, there is no cell-based assay, in vitro heart preparation or animal model that predicts the potential of a drug to induce TdP in humans. Nevertheless, certain electrophysiological events are known to be associated with the development of TdP. For example, a drug that prolongs action potential duration, induces early afterdepolarizations and ectopic beats, and increases dispersion of ventricular repolarization is likely to cause TdP. By contrast, a drug that does not induce these changes is unlikely to cause TdP. The exact relationship between these electrophysiological events and the development of TdP has not been defined, but the potential of a drug to elicit these events might predict its pro-arrhythmic risk.

Animals↗
PubMed1993

[Torsade de pointes].

Torsade de pointes (TDP) is a polymorphic ventricular tachycardia with a particular electrocardiographic pattern of continuously changing ("twisting") morphology of the QRS complex occurring in the setting of delayed myocardial repolarization (i.e., prolongation of the QT interval). TDP may develop in the setting of an idiopathic disorder (Jervell/Lange-Nielsen syndrome, Romano-Ward syndrome, sporadic long QT syndrome) or may be induced by pharmacologic agents which prolong the QT interval, as well as by other clinical circumstances under which repolarization is delayed (e.g., hypokalemia, hypomagnesemia, bradycardia) (acquired long QT syndrome). Since the treatment of TDP strongly differs from that of conventional ventricular tachycardia, correct diagnosis is critical as it guides the treating physician in selecting the appropriate mode of therapy. In this paper mainly the electrocardiographic criteria presently used for the correct identification of this unusual form of ventricular arrhythmia are presented. Additionally, the potential mechanisms and therapeutic modalities of TDP are discussed.

Anti-Arrhythmia Agents↗
PubMed2005

Cellular mechanisms of Torsade de Pointes.

Torsade de Pointes (TdP) is a life-threatening arrhythmia closely linked to abnormal cardiac repolarization. It has been demonstrated that cardiac ion channel alterations underlying cellular repolarization results in the phenotypic expression of long QT syndrome, which is closely associated with TdP. However, the mechanisms by which prolonged repolarization leads to TdP remain controversial. Prolonged repolarization is associated with triggered activity, and multiple foci of triggered activity can underlie a TdP phenotype. Action potential shortening associated with rapid ventricular rhythms, in theory, removes conditions for triggered activity. Therefore, while triggered activity may initiate TdP, another mechanism may be responsible for the maintenance of TdP. Re-entrant arrhythmias can also give rise to a TdP phenotype. In intact myocardium significant inhomogeneities of repolarization are manifest in the presence of IKr blockade. Large repolarization gradients between subepicardial and midmyocardial cells formed zones of conduction block responsible for sustained reentrant TdP. Gap junction proteins responsible for intercellular coupling between subepicardial and midmyocardial cells are reduced in normal myocardium which may maintain arrhythmogenic gradients of repolarization. Therefore, the mechanism of TdP is multi-factorial and related to triggered activity and spatial inhomogeneities of ion channel expression combined with regional expression patterns of gap junctions.

Cation Transport Proteins↗