Recurrent Torsades De Pointes Research Articles

Left Bundle Branch Pacing in a Child Who Survived Cardiac Arrest with Congenital Complete Heart Block and Recurrent Torsades de Pointes

A 2-year-old girl was referred to the Harapan Kita National Heart Center due to the return of spontaneous circulation after cardiac arrest, bradyarrhythmia and repeated seizures with loss of consciousness. She had been treated with an epilepsy drug for 1 year. Electrocardiography during one epilepsy episode showed complete heart block with junctional escape rhythm and QT interval prolongation, which then progressed to torsades de pointes. Echocardiography revealed left atrium and left ventricle dilatation with reduced ejection fraction. Left bundle branch permanent pacemaker was successfully implanted through left subclavian vein access. During the 3-week follow-up, there were no recurrent seizures and echocardiography revealed improvement of left ventricle ejection fraction.

Rare case of Torsades de Pointes in severe hypothyroidism: literature review and challenges in management

BackgroundHypothyroidism can manifest as several important cardiac abnormalities. There are few reports of ventricular dysrhythmias (VDs) in hypothyroidism. We described a rare case of VDs in severe hypothyroidism and reviewed the literature behind its management.Case presentationA 67-year-old gentleman, with poor compliance to treatment for Hashimoto’s thyroiditis, presented with palpitations to the Emergency Department. He had runs of non-sustained ventricular tachycardia (NSVT). He was treated with intravenous (IV) amiodarone and admitted to the intensive care unit for observation. He then developed recurrent Torsades de Pointes (Tdp) despite treatment with several anti-arhythmics. He required electrical cardioversion and eventual transvenous overdrive pacing (OP). VT recurred while he was on OP. VT resolved and he was weaned off OP only after adequate thyroid hormone replacement.ConclusionsVDs, including NSVT, Tdp, and VT, are rare and potentially lethal in hypothyroidism. Our case demonstrates important challenges in the management of severe hypothyroidism. Here, VDs are often refractory to treatment with drugs and electrical means. The choice(s) of anti-arrhthymics requires careful consideration and can be difficult before thyroid function tests are known. Amiodarone use should be cautioned as it is associated with thyroid dysfunction and QT interval prolongation.There is no literature to guide thyroid hormone replacement in this disease. Aggressive replacement is associated with adverse cardiovascular effects. Our case showed a fine balance between the risk of rapid thyroid hormone replacement and the urgency to terminate VDs. Its administration should be carefully monitored amidst bridging strategies like electrical cardioversion and OP to manage life-threatening VDs.

Extracorporeal treatment for poisoning to beta-adrenergic antagonists: systematic review and recommendations from the EXTRIP workgroup

Backgroundβ-adrenergic antagonists (BAAs) are used to treat cardiovascular disease such as ischemic heart disease, congestive heart failure, dysrhythmias, and hypertension. Poisoning from BAAs can lead to severe morbidity and mortality. We aimed to determine the utility of extracorporeal treatments (ECTRs) in BAAs poisoning.MethodsWe conducted systematic reviews of the literature, screened studies, extracted data, and summarized findings following published EXTRIP methods.ResultsA total of 76 studies (4 in vitro and 2 animal experiments, 1 pharmacokinetic simulation study, 37 pharmacokinetic studies on patients with end-stage kidney disease, and 32 case reports or case series) met inclusion criteria. Toxicokinetic or pharmacokinetic data were available on 334 patients (including 73 for atenolol, 54 for propranolol, and 17 for sotalol). For intermittent hemodialysis, atenolol, nadolol, practolol, and sotalol were assessed as dialyzable; acebutolol, bisoprolol, and metipranolol were assessed as moderately dialyzable; metoprolol and talinolol were considered slightly dialyzable; and betaxolol, carvedilol, labetalol, mepindolol, propranolol, and timolol were considered not dialyzable. Data were available for clinical analysis on 37 BAA poisoned patients (including 9 patients for atenolol, 9 for propranolol, and 9 for sotalol), and no reliable comparison between the ECTR cohort and historical controls treated with standard care alone could be performed. The EXTRIP workgroup recommends against using ECTR for patients severely poisoned with propranolol (strong recommendation, very low quality evidence). The workgroup offered no recommendation for ECTR in patients severely poisoned with atenolol or sotalol because of apparent balance of risks and benefits, except for impaired kidney function in which ECTR is suggested (weak recommendation, very low quality of evidence). Indications for ECTR in patients with impaired kidney function include refractory bradycardia and hypotension for atenolol or sotalol poisoning, and recurrent torsade de pointes for sotalol. Although other BAAs were considered dialyzable, clinical data were too limited to develop recommendations.ConclusionsBAAs have different properties affecting their removal by ECTR. The EXTRIP workgroup assessed propranolol as non-dialyzable. Atenolol and sotalol were assessed as dialyzable in patients with kidney impairment, and the workgroup suggests ECTR in patients severely poisoned with these drugs when aforementioned indications are present.

Chloroquine-induced torsades de pointes in a patient with coronavirus disease 2019

Chloroquine-induced torsades de pointes in a patient with coronavirus disease 2019

Isoproterenol and Lidocaine for Recurrent Torsades de Pointes in a 32-year-old Pregnant Woman

Guidelines recommend magnesium and defibrillation for Torsades de Pointes (TdP) treatment in pregnancy, both of which were unsuccessful at terminating our patient's recurrent ventricular arrhythmias. Both lidocaine and isoproterenol carry potential risks to mother and fetus, but the risk of congenital abnormalities is significantly lower compared to other antiarrhythmics such as amiodarone.

Celiac Disease: aA Rare Cardiac Sequel

We explore the case of a 52-year-old woman who was transferred to our facility with recurrent torsade de pointes requiring repeated defibrillations. She had no previous medical history nor did she report any clear emotional or stressful triggers. In transit there were 14 episodes of polymorphic ventricular tachycardia, 11 of which required defibrillation. Her presenting electrocardiogram showed sinus rhythm with wide spread T-wave inversions and a QTc of 544 ms. In transit she was treated with intravenous potassium and magnesium. On arrival an isoprenaline infusion was commenced, which stabilised the patient. Coronary angiography showed non–obstructive disease with the left ventricular (LV) gram showing mid-wall variant Takotsubo cardiomyopathy. Bedside echocardiography showed low–normal LV systolic function of 55%, with no significant valvulopathy. Cardiac magnetic resonance imaging showed the resolving Takotsubo cardiomyopathy with no evidence of infiltrative disease. Despite clinical improvement, she had persistent hypomagnesaemia. Cardiomyopathy screening and investigations for hypomagnesaemia returned unremarkable with the exception of a strongly positive coeliac serology. With beta blockade, aggressive magnesium replacement, and gluten avoidance her QTc shortened and episodes of polymorphic ventricular tachycardia also settled as a consequence. She was discharged when stable and at the 6-month follow-up she remained asymptomatic with a resolution of her prolonged QT interval. This case identifies coeliac disease as a cause of severe electrolyte disturbances that resulted in recurrent torsade de pointes and Takotsubo cardiomyopathy that was treated conservatively (Figure 1, Figure 2). Figure 2Takotsubo LV gram. View Large Image Figure Viewer Download Hi-res image

Electrophysiological measurements that can explain and guide temporary accelerated pacing to avert (re)occurrence of torsade de pointes arrhythmias in the canine chronic atrioventricular block model

Pacing at higher rates is known to suppress torsade de pointes (TdP) arrhythmias. Nevertheless, exact application and mechanism need further clarification. In the anesthetized canine chronic atrioventricular block model, ventricular remodeling is responsible for a high and reproducible incidence of TdP upon a challenge with dofetilide. We used this model to investigate by what mechanism accelerated pacing averts TdP and what repolarization parameter could be used to guide temporary accelerated pacing (TAP). Ten dogs with repetitive TdP after administration of dofetilide when paced at 60 beats/min were selected. In a serial experiment, TAP was initiated at 100 beats/min after the first ectopic beat. Electrocardiogram and right and left ventricular (LV) monophasic action potential durations (MAPDs) were recorded. In a subset, vertical dispersion was determined with a duodecapolar catheter. Temporal dispersion was quantified as short-term variability (STV). Arrhythmias were quantified with the arrhythmia score. The increase in repolarization parameters observed after administration of dofetilide was counteracted by TAP (eg, LV MAPD from 381 ± 94 ms back to 310 ± 17 ms; P < .05). Temporal dispersion (STVLVMAPD) increased from 0.69 ± 0.37 to 2.59 ± 0.96 ms (P< .05) after administration of dofetilide and back to 1.15±0.54 ms (P < .05) with TAP. This was accompanied by suppression of recurrent TdP in 7 of 10 dogs (P<.05) and a trend toward reduction in vertical (spatial) dispersion from 56 ± 25 to 31 ± 4 ms (P = .06). In those dogs, seconds after capture of TAP, almost all ectopy disappeared, causing a decrease in arrhythmia score from 21 ± 12 to 4 ± 3 (P < .05). TAP is effective in averting TdP by decreasing spatial and temporal measures of repolarization. Increase in temporal dispersion (STV) can guide TAP.

Pharmacological treatment of acquired QT prolongation and torsades de pointes.

Torsades de pointes (TdP) is a characteristic polymorphic ventricular arrhythmia associated with delayed ventricular repolarization as evidenced on the surface electrocardiogram by QT interval prolongation. It typically occurs in self-limiting bursts, causing dizziness and syncope, but may occasionally progress to ventricular fibrillation and sudden death. Acquired long QT syndromes are mainly caused by cardiac disease, electrolyte abnormalities or exposure to drugs that block rectifying potassium channels, especially IKr. Management of TdP or marked QT prolongation includes removal or correction of precipitants, including discontinuation of culprit drugs and institution of cardiac monitoring. Electrolyte abnormalities and hypoxia should be corrected, with potassium concentrations maintained in the high normal range. Immediate treatment of TdP is by intravenous administration of magnesium sulphate, terminating prolonged episodes using electrical cardioversion. In refractory cases of recurrent TdP, the arrhythmia can be suppressed by increasing the underlying heart rate using isoproterenol (isoprenaline) or transvenous pacing. Other interventions are rarely needed, but there are case reports of successful use of lidocaine or phenytoin. Anti-arrhythmic drugs that prolong ventricular repolarization should be avoided. Some episodes of TdP could be avoided by careful prescribing of QT prolonging drugs, including an individualized assessment of risks and benefits before use, performing baseline and periodic electrocardiograms and measurement of electrolytes, especially during acute illnesses, using the lowest effective dose for the shortest possible time and avoiding potential drug interactions. These steps are particularly important in those with underlying repolarization abnormalities and those who have previously experienced drug-induced TdP.

Recurrent Torsades de Pointes Due to Amiodarone Toxicity Treated Successfully with Lidocaine.

The Editor, Sir, Amiodarone is a potent antiarrhythmic agent that is used to treat ventricular arrhythmias and atrial fibrillation. Proarrythmias due to amiodarone therapy is rare. We discuss a case who had amiodarone-induced incessant Torsades de Pointes (TdP), that could only be suppressed by lidocaine.

Drug-induced QT-interval prolongation and recurrent torsade de pointes in a child with heterotaxy syndrome and KCNE1 D85N polymorphism

We present a child case of heterotaxy syndrome (asplenia syndrome) after Fontan procedure that showed extreme prolongation of QT interval and torsade de pointes (TdP) after administration of sodium channel blockers for paroxysmal atrial tachycardia. Despite low serum concentration of the drugs, QT prolongation persisted and TdP attacks with unconsciousness recurred, possibly in association with junctional bradycardia and myocardial damage although he had never experienced QT prolongation during bradycardia before. Temporal cardiac pacing via a venous route to exclude possible implication of bradycardia in induction of TdP was difficult to apply due to total cavopulmonary connection (TCPC) circulation. Continuous intravenous administration of low-dose isoproterenol was started but an appropriate heart rate for prevention of TdP was difficult to obtain. Finally, we were urged to conduct implantation of a DDD pacemaker combined with ICD surgically with epicardial leads, resulting in successful suppression of TdP and syncope. Screening of the genotype disclosed the KCNE1 D85N polymorphism, which is known as one of the typical disease-causing gene variants in long-QT syndrome (LQTS).

Peripartum Cardiomyopathy Presenting with Syncope due to Torsades de Pointes: a Case of Long QT Syndrome with a Novel KCNH2 Mutation

Peripartum cardiomyopathy (PPCM) is a cardiomyopathy of unknown cause that occurs in the peripartum period. We report a case of PPCM presenting with syncope 1 month after an uncomplicated delivery. Electrocardiography showed Torsades de pointes (TdP) and QT interval prolongation. Echocardiography showed left ventricular systolic dysfunction and endomyocardial biopsy showed myocyte degeneration and fibrosis. Administration of magnesium sulfate and temporary pacing eliminated recurrent TdP. Genetic analyses revealed that recurrent TdP occurred via electrolyte disturbance and cardiac failure due to PPCM on the basis of a novel mutation in KCNH2, a gene responsible for inherited type 2 long QT syndrome.

Recurrent Torsade de Pointes During Mild Hypothermia Therapy for a Survivor of Sudden Cardiac Arrest Due to Drug‐induced Long‐QT Syndrome

Recurrent Torsade de Pointes During Mild Hypothermia Therapy for a Survivor of Sudden Cardiac Arrest Due to Drug‐induced Long‐QT Syndrome

Tako-tsubo Cardiomyopathy Complicated by Recurrent Torsade de Pointes in a Patient with Anorexia Nervosa

We report the case of a 57-year-old woman with anorexia nervosa showing evidence of "tako-tsubo" cardiomyopathy complicated by several syncopes due to recurrent episodes of torsades de pointes. Prolongation of QT interval and QT dispersion have been reported both in the "tako-tsubo" cardiomyopathy and in anorexia nervosa. The QT prolongation and the QT dispersion has been linked as risk indicators for sudden cardiac death. The combination of "tako-tsubo" cardiomyopathy with a condition associated with the prolongation of QT and/or with an increase of QT dispersion, such as anorexia nervosa, makes the acute and subacute prognosis of this disease much more severe than usual.

Post Myocardial Ischemia-Associated Torsades De Pointes in a Patient Carrying a KCNQ1 G643S Variant

Polymorphic ventricular tachycardia, which occurs during the subacute phase of myocardial infarction (MI) or ischemia and is not related to ongoing ischemia, has recently been reported. It has characteristics of typical pause-dependent torsades de pointes (TdP) following excessive QT prolongation (post MI/ischemia-associated TdP). We describe a male patient with post MI/ischemia-associated TdP. The patient experienced recurrent TdP with excessive QT prolongation 2 days after transient myocardial ischemia. Genetic screening of the major LQTS-causing genes identified a KCNQ1 G643S variant. This gene variant could be a genetic predisposition to the development of TdP during the subacute phase of MI/ischemia.

Recurrent torsades de pointes in association with a very low calorie diet

The use of very low calorie diets under medical supervision is becoming increasingly popular in the UK, as the incidence of obesity continues to rise. We report the case of torsades de pointes developing during such a diet. Torsades de pointes has been reported in association with very low calorie diets in the past but to our knowledge, this is the first report since the introduction of newer, nutritionally complete versions of the diet. We review the intensive care management of recurrent torsades de pointes resistant to standard therapy and its relationship to dieting and obesity.

QT prolongation and torsade de pointes associated with solifenacin in an 81‐year‐old woman

Solifenacin, an antimuscarinic drug, has been widely used for the treatment of overactive bladder (OAB), but severe cardiac adverse effects have not been reported. An 81-year-old woman was prescribed solifenacin 5 mg day−1 for OAB. Two weeks later she developed the first syncope. Nine days after the first syncope she developed recurrent syncope, and electrocardiogram monitoring showed marked QT prolongation and torsade de pointes (TdP). Concomitant drugs remained unchanged. Serum electrolytes and hepatic function were normal. Calculated creatinine clearance was mildly decreased. We considered that the loss of consciousness was associated with solifenacin. Although intravenous magnesium sulphate could not terminate the recurrence of TdP, increasing the pacing rate prevented further attacks of TdP. Solifenacin might be a possible cause of QT prolongation and TdP. Solifenacin is a newer bladder-selective antimuscarinic drug for the treatment of OAB [1]. Although terodiline, an older antimuscarinic drug for OAB, has been reported to predispose to QT prolongation and TdP and was withdrawn from the market in the early 1990s [2–4], solifenacin has not been reported to have severe cardiac adverse effects [1]. An 81-year-old woman was admitted to the division of orthopaedics with dislocation of hip joint and infection of decubitus. One year before admission she had undergone total hip arthroplasty. Her past medical history included hypertension and pacemaker implantation for sick sinus syndrome. Her medication included amlodipine, but not any over-the-counter drugs or herbals. Electrocardiogram (ECG) on admission showed sinus rhythm with normal QT interval (QT400 ms/QTc360 ms) (Figure 1a). Solifenacin 5 mg day−1 was started for OAB after admission. Her infection was initially treated with intravenous cefazolin, but was changed to intravenous teicoplanin because of methicillin-resistant Staphylococcus aureus infection. Two weeks later she suddenly developed loss of consciousness, but she spontaneously regained full consciousness. Figure 1 ECG monitoring. (a) Sinus rhythm with normal QT interval on admission. (b) Marked QT prolongation after the first syncope. (c) Typical episode of torsade de pointes 9 days after the first syncope Although ECG was not recorded during the episode, ECG monitoring showed QT prolongation (QT600 ms/QTc581 ms) after regaining consciousness (Figure 1b). Nine days after the first syncope she developed recurrent loss of consciousness and ECG monitoring showed TdP (Figure 1c). She was resuscitated with a single DC shock. She was immediately transferred to the division of cardiology. ECG monitoring showed QT prolongation (QT600 ms) and recurrent TdP. Serum electrolytes and hepatic function were normal. Calculated creatinine clearance was 60 ml min−1. We considered that solifenacin was closely related to syncope and TdP. We stopped solifenacin. Intravenous magnesium sulphate could not terminate recurrent episodes of TdP. The pacing rate was increased 60 to 90 beats min−1 to shorten the QT interval, resulting in a QT interval of 600 to 500 ms (QTc 408 ms). There were no further attacks of TdP. Electrocardiographic abnormalities resolved a few days after solifenacin was discontinued. The high bladder selectivity of solifenacin might be expected to reduce adverse effects [1], which include dry mouth, constipation and blurred vision, but severe cardiac adverse effects have not been reported [1]. Known risk factors for drug-induced TdP are female sex, hypokalaemia, hypomagnesaemia, bradycardia, simultaneous administration of inhibitor compounds, and genetic factors [4–6]. Serum electrolytes, especially potassium and magnesium, were normal. Age and mild renal dysfunction had no clinically relevant effects on the pharmacokinetics of solifenacin [1]. The main metabolic pathway of solifenacin is CYP3A4 [1]. Although hepatic dysfunction decreased clearance of solifenacin [1], hepatic function was also normal. Anti-infective agents that were administered intravenously did not include CYP3A4 inhibitors such as erythromycin [4–6]. She had no other structural heart diseases, nor any family history of sudden death. Concomitant drugs remained unchanged. Amlodipine would not have interacted with solifenacin because of little influence of first-pass effect by CYP3A4 at therapeutic dose [7]. Marked QT prolongation and TdP were considered to be related to solifenacin. Intravenous magnesium sulphate, the first-choice treatment of drug-induced TdP [6], was not effective. Recurrence of TdP was prevented after the QT interval was shortened by increasing the pacing rate. We did not investigate her genetic factors and plasma drug concentration. Although the mechanism is not fully understood, the start of solifenacin might have influenced the outcome in our elderly female patient. To our knowledge, this is the first reported case of QT prolongation and TdP associated with solifenacin.

Biventricular Pacing and QT Interval Prolongation

The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB). One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 +/- 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 +/- 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 +/- 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 +/- 9 ms during BiV pacing vs 178 +/- 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 +/- 34 ms with BiV pacing versus 445 +/- 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 +/- 9 ms vs 320 +/- 20 ms, P < 0.0001). During a mean follow-up of 24 +/- 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued. Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.

Torsade de Pointes During Orthotopic Liver Transplantation

Torsade de Pointes During Orthotopic Liver Transplantation

Amiodarone in patients with previous drug-mediated torsade de pointes. Long-term safety and efficacy.

The safety and efficacy of long-term amiodarone therapy were examined in 12 patients who had previously developed torsade de pointes as a complication of previous antiarrhythmic therapy. The QTc intervals were determined at the time of torsade de pointes (570 +/- 40 ms), after 7 days of amiodarone loading (490 +/- 70 ms), and after 3 months of chronic amiodarone administration (580 +/- 80 ms). Compared to a drug-free control period, QTc was significantly prolonged (P less than 0.05) at the time of torsade de pointes, after amiodarone loading, and after 3 months of amiodarone therapy. The QTc intervals at the time of torsade de pointes and after chronic amiodarone treatment were not significantly different. At 16 +/- 7 months of follow-up, all patients remained free of subsequent torsade de pointes, syncope, or sudden death. In addition, 5 of 6 patients with a history of sustained ventricular tachycardia remained free from arrhythmic recurrence despite persistence of inducible ventricular tachycardia during programmed stimulation studies done before discharge. We conclude that amiodarone can often be used safely and effectively in patients who have previously had an episode of drug-mediated torsade de pointes. Amiodarone-induced QTc prolongation, even when marked, does not predict recurrent torsade de pointes. These observations also suggest that the propensity for a drug to produce this arrhythmia is dependent on other electrophysiologic effects in addition to its ability to simply lengthen repolarization.

Magnesium therapy for torsades de pointes

This is the first report of the successful use of magnesium sulfate (MgSO 4) in 3 consecutive patients with torsades de pointes (TdP). In 1 patient, TdP was induced by a combination of quinidine and amiodarone, in the second by procainamide, and in the third by an overdose of imipramine. The QT intervals before TdP were 0.70, 0.64 and 0.56 second, respectively. A bolus of 1.0 to 2.0 g MgSO 4 25% abolished the TdP in all 3 patients; but in the third patient, because of recurrent TdP, a second bolus of 1.0 g and a continuous 24-hour infusion of 1.0 mg/min were administered, preventing TdP. There was no immediate shortening in the QT interval in any patient after MgSO 4. Magnesium can be given safely even in patients with acute myocardial infarction, angina pectoris or systemic hypertension, conditions in which isoproterenol is contraindicated; it can be applied faster than temporary cardiac pacing; and its use for TdP appears worthy of additional trials.