Episodes Of Torsade De Pointes Research Articles

The Incidence of Torsades de Pointes With Perioperative Triple Antiemetic Administration.

The safety of triple antiemetic therapy consisting of ondansetron, haloperidol, and a steroid, to surgical patients is unknown. To determine the incidence of torsade de pointes (TdP) or death following perioperative administration of triple antiemetic therapy. A retrospective cohort study identified 19,874 patients who received 22,202 doses of triple antiemetics during the 2.5-year time frame from March 4, 2020 to September 7, 2022 for surgical nausea prophylaxis or treatment of nausea. These patients above were cross-matched with an electrocardiogram and adverse outcome database; this identified 226 patients with documentation of a QTc > 450 ms, all ventricular tachycardias including TdP within 48 hours of receiving triple antiemetic therapy, or death within 7 days of receiving ondansetron. There were 3 patients who had documented VT (n = 3), but there were no documented incidents of TdP (n = 0). There were 9 codes called on patients within 48 hours of medication administration, and none of them were due to ventricular arrythmias (n = 0). A total of 11 patients died within 7 days of triple antiemetic therapy. Ten of the 11 deaths were determined to not be from the triple antiemetic. One patient died at home within 24 hours of the procedure of an unknown cause (n = 1). No episodes of TdP were identified in patients receiving triple antiemetic therapy perioperatively, though the cause of death in 1 patient could not be determined. This suggest that low-dose triple antiemetic therapy is low risk for the development of TdP.

Correcting the QTc and fixing torsade’s, what can’t steroids do!

Introduction: Long QT syndrome (LQTS) is the congenital or acquired prolongation of the QT interval on an electrocardiogram (ECG). It is well-known that the QT interval is prolonged in adrenal insufficiency (AI) but rarely prolonged enough to cause Torsade de Pointes (TdP). Case Report: Here we report a case of TdP and cardiac arrest in a patient with adrenal insufficiency. The patient had a return of spontaneous circulation after a successful cardiopulmonary resuscitation (CPR). Electrocardiograms persistently showed prolonged QT corrected for heart rate (QTc) prior to and at the time of cardiac arrest, some exceeding 600 milliseconds (ms). The QT interval improved significantly upon administration of steroids and the episodes of TdP resolved. Conclusion: This case highlights the importance of recognizing adrenal insufficiency (AI) as a potentially reversible cause of prolonged QT and TdP.

294 BEYOND BRUGADA SYNDROME: A COMMON ECG PATTERN IN AN UNCOMMON CLINICAL SCENARIO

Abstract Propofol infusion syndrome (PRIS) is a rare but potentially lethal side effect of propofol. In most cases it shows various combinations of signs such as unexplained metabolic acidosis, rhabdomyolysis, hepatomegaly, renal failure, hypertriglyceridemia, malignant arrhythmia and rapidly progressive cardiac failure. The development of coved ST elevation in the right precordial leads of the electrocardiogram (ECG), similar to that seen in the type I Brugada syndrome may be the first sign of cardiac instability. There is no specific treatment for PRIS. Successful management consists of an early recognition of its signs followed by a prompt propofol infusion termination. We present the case of a 35-year-old male affected by mild hypertension. He was found by his wife during a transitory loss of consciousness episode. He had resulted positive to Sars Cov 2 infection a day before and was symptomatic for fever and myalgia. An ambulance was immediately called and the patient was transferred to the emergency department for a suspected out-of-hospital-cardiac arrest. The initial one-lead ECG performed by the emergency physician was unremarkable. On arrival he was in a coma state but with stable hemodynamics. ECG showed only an asymmetric T wave inversion in V4-V6 leads. The cardiac echocardiogram did not show any major alterations. In the meantime, due to worsening of respiratory function, orotracheal intubation was performed and the patient was sedated with propofol, midazolam and fentanyl. Subsequently, an episode of atrial fibrillation was documented. Amiodarone infusion was started and the patient reverted to sinus rhythm after a few hours. The following day two episodes of Torsade de Pointes during prolonged QTc (660 ms) occurred. These arrhythmias were treated successfully with magnesium sulfate infusion. Blood analysis showed severe hypokalemia that was immediately corrected. After the hemodynamic stabilization the ECG showed a pattern highly resembling the Brugada pattern type 1 in the right precordial leads. Moreover CPK, myoglobin, high sensitivity troponin I levels started to rise, along with creatinine, triglycerides and markers of hepatic injury. Propofol had been administered continuously for eight days, so PRIS was suspected as the primum movens of this clinical scenario. Propofol infusion was immediately interrupted. Thereafter, the patient gradually improved and was extubated. As soon as the patient's hemodynamic conditions allowed it, a coronary CT and a cardiac MRI were performed, but were unremarkable. To further evaluate the case, a flecainide challenge test was performed, but no significant ECG change was induced. Nonetheless, given both the history of ventricular arrhythmia, the young age of the patient and the unexplained transitory loss of consciousness a subcutaneous defibrillator was implanted as a form of secondary prevention.

Cardiac Arrest Related to Torsades de Pointes in a Patient Recovering from Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute complication related to severe hyperglycemia. While the mortality rate for DKA is low with appropriate therapy, several complications may lead to deterioration of the clinical course. Here, we report a case of a 23-year-old patient with DKA who suffered from a rare but hemodynamically unstable cardiac arrhythmia, polymorphic ventricular tachycardia with prolonged QT interval, or Torsades de Pointes. During the recovery phase of DKA, three episodes of Torsades de Pointes suddenly occurred, and were recovered by immediate defibrillation. The patient did not have structural heart disease or a genetic predisposition. To the best of our knowledge, this is the first report of an adult with DKA complicated with QT prolongation related to Torsades de Points after correction of ketosis. To manage DKA, more attention may be needed on changes in the QT interval as well as risk factors for Torsades de Points.

Syncope due to non-sustained episodes of Torsade de Pointes associated to androgen-deprivation therapy use: a case presentation

BackgroundAbiraterone is a medication frequently used for metastatic castrate-resistant prostate cancer. We report a case of non-sustained episodes of TdP associated with severe hypokalemia due to androgen-deprivation therapy. Few case presentations describe this association; the novelty lies in the potentially lethal cardiovascular events among cancer patients receiving hormonal therapy.Case presentationA 70-year-old male presented with recurrent syncope without prodrome. ECG revealed frequent ventricular ectopy, non-sustained episodes of TdP, and severe hypomagnesemia and hypokalemia. During potassium and magnesium infusion for repletion, the patient underwent temporary transvenous atrial pacing. As part of the work-up, coronary angiography revealed a mild coronary artery disease, and transthoracic echocardiogram showed a moderately depressed ejection fraction. After electrolyte disturbances were corrected, the QT interval normalized, and transvenous pacing was no longer necessary. Abiraterone was discontinued during the admission, and the patient returned to baseline.ConclusionsCancer treatment is complex and requires a multidisciplinary approach. We presented a case of non-sustained TdP associated with androgen-deprivation therapy in an elderly patient with mild coronary artery disease and moderately reduced ejection fraction. Close follow-up and increased awareness are required in patients with hormonal treatment, especially in the setting of other cardiovascular risk factors.

Propofol abolishes torsade de pointes in different models of acquired long QT syndrome

There is conflicting evidence regarding the impact of propofol on cardiac repolarization and the risk of torsade de pointes (TdP). The purpose of this study was to elucidate the risk of propofol-induced TdP and to investigate the impact of propofol in drug-induced long QT syndrome. 35 rabbit hearts were perfused employing a Langendorff-setup. 10 hearts were perfused with increasing concentrations of propofol (50, 75, 100 µM). Propofol abbreviated action potential duration (APD90) in a concentration-dependent manner without altering spatial dispersion of repolarization (SDR). Consequently, no proarrhythmic effects of propofol were observed. In 12 further hearts, erythromycin was employed to induce prolongation of cardiac repolarization. Erythromycin led to an amplification of SDR and triggered 36 episodes of TdP. Additional infusion of propofol abbreviated repolarization and reduced SDR. No episodes of TdP were observed with propofol. Similarly, ondansetron prolonged cardiac repolarization in another 13 hearts. SDR was increased and 36 episodes of TdP occurred. With additional propofol infusion, repolarization was abbreviated, SDR reduced and triggered activity abolished. In this experimental whole-heart study, propofol abbreviated repolarization without triggering TdP. On the contrary, propofol reversed prolongation of repolarization caused by erythromycin or ondansetron, reduced SDR and thereby eliminated drug-induced TdP.

The Clinical Utility of Continuous QT Interval Monitoring in Patients Admitted With COVID-19 Compared With Standard of Care: A Prospective Cohort Study

BackgroundQT interval monitoring has gained much interest during the COVID-19 pandemic because of the use of QT-prolonging medications and the concern about viral transmission with serial electrocardiograms (ECGs). We hypothesized that continuous telemetry-based QT monitoring is associated with better detection of prolonged QT episodes. MethodsWe introduced continuous cardiac telemetry (CCT) with an algorithm for automated QT interval monitoring to our designated COVID-19 units. The daily maximum automated heart rate-corrected QT (Auto-QTc) measurements were recorded. We compared the proportion of marked QTc prolongation (Long-QTc) episodes, defined as QTc ≥ 500 ms, in patients with suspected or confirmed COVID-19 who were admitted before and after CCT was implemented (control group vs CCT group, respectively). Manual QTc measurement by electrophysiologists was used to verify Auto-QTc. Charts were reviewed to describe the clinical response to Long-QTc episodes. ResultsWe included 33 consecutive patients (total of 451 monitoring days). Long-QTc episodes were detected more frequently in the CCT group (69/206 [34%] vs 26/245 [11%]; P < 0.0001) and ECGs were performed less frequently (32/206 [16%] vs 78/245 [32%]; P < 0.0001). Auto-QTc correlated well with QTc measurement by electrophysiologists with an excellent agreement in detecting Long-QTc (κ = 0.8; P < 0.008). Only 28% of patients with Long-QTc episodes were treated with recommended therapies. There was 1 episode of torsade de pointes in the control group and none in the CCT group. ConclusionsContinuous QT interval monitoring is superior to standard of care in detecting episodes of Long-QTc with minimal need for ECGs. The clinical response to Long-QTc episodes is suboptimal.

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

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

Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia.

Bradycardia-induced torsade de pointes (TdP) tachycardia in patients with spontaneous high-degree atrioventricular block (AVB) is common. The aim of this study was to analyze endocardial recordings during TdP in spontaneous high-degree AVB in humans to better understand the electrophysiological mechanisms underlying this phenomenon. The study group consisted of 5 patients with typical episodes of TdP during spontaneous high-degree AVB. A standard (USCI) temporary bipolar endocardial catheter positioned at the apex of the right ventricle (RV) and bipolar chest leads from two precordial leads V1 and V4 were used to record the tracings during TdP. The presence of a wide spectrum of fragmentations was noted on endocardial electrograms (EGMs), which were invisible on the surface electrocardiogram (ECG) tracing. Endocardial signals indicated that TdP started in the proximity of the RV apex, since the local EGM began prior to the QRS complex on the surface ECG. Early afterdepolarizations (EADs) were observed in 2 out of 5 cases confirming a common opinion about the mechanism of TdP. However, this phenomenon was not observed in 3 other patients suggesting that the arrhythmia was the result of a different mechanism originating in proximity to the RV apex. This work demonstrated early endocardial signals in the RV apex during TdP associated with high-degree AVB in humans, and exhibits a spectrum of fragmented signals in this area occurring on a single or multiple beats. These fragmentations indicate areas of poor conduction and various degrees of intramyocardial block, and therefore a new mechanism of TdP tachycardia in some patients with spontaneous high-degree AVB.

P257 Multiple clinical manifestations of catecholamine secreting paraganglioma

Abstract A 37 years old woman was referred to our hospital due to the onset since the previous day of vertigo associated with nausea and headache. Her previous history revealed an hospitalization ten years before for Tako Tsubo Cardiomyopathy, during which the diagnosis of left temporo-jugular catecholamine secreting paraganglioma was made. Subsequently, there were several hospitalizations for multiple cardiac manifestations, such as acute coronary syndrome during hypertensive crisis, acute pulmonary oedema, one relapse for TakoTsubo syndrome and then an episode of torsade de pointes (TdP) during hypokalemia and elongated QT. The surgical removal of the mass was always rejected by the patient, and therefore, only radiotherapy was performed with significant reduction of the tumour dimensions. Moreover, alpha and beta adrenergic blockers were always administrated. At the admission, she complained neurological symptoms, in particular balance disorder and dysmetria. Brain Computed tomography (CT) was performed and it showed left posterior cerebellar infarction in late acute clinical phase, without haemorrhage. The patient underwent angiography that excluded cerebral artery dissection but showed acute occlusion of posterior internal cerebral artery. Echocardiogram showed moderate left ventricular hypertrophy with normal global and segmental kinetics, left atrial dilatation; besides, left ventricular apical thrombus was excluded. Holter ECG monitoring showed very frequent polymorphic ventricular and supraventricular extrasystolic beats. Urinary metanephrines were markedly increased. In particular urinary normetanephrine was up to 9 times the upper limit of normality (4874 ug/L, normal range 162-527 ug/24 h). Since the surgical intervention was always refused, this case is a rare documentation of the several different cardiovascular clinical manifestation due to catecholamine secretion in a single patient. Paraganglioma could be a catecholamine secreting tumour that arises from cromaffin tissue of the sympathetic nervous system. Clinical manifestations of paraganglioma are extremely variable leading to its designation as "great mimic". Adrenal tumours are associated with several cardiovascular diseases including LV hypertrophy, myocardial infarction, cardiac arrhythmias, heart failure and Tako Tsubo cardiomyopathy. Cerebral accident is a rare manifestation of adrenergic crisis with several possible aetiologies such as vasospasm or cardioembolic events. In our clinical case, considering the type and localization of the cerebral ischemic injury, the stroke is likely to have a cardioembolic etiology. Apical left ventricular trombus and PFO were excluded. Therefore, in view of left atrial enlargement and the frequent supraventricular ectopy, even in the absence of documented arrhythmia, an undiagnosed episode of catecholamines induced atrial fibrillation was suspected, with subsequent cardioembolic event. Abstract P257 Figure.

A rare case of steroid responsive Torsades de pointes

A 37-year-old female with sarcoma on pembrolizumab experienced lightheadedness during hospitalization. Telemetry revealed Torsades de pointes (TdP) that lasted 3.8 seconds (Figure 1). Her potassium, magnesium and troponin were normal. Admission EKG was sinus bradycardic at 44 bpm with a QTc of 478 ms. Cardiac MRI revealed subtle focal myocardial edema in the left ventricular septal wall suspicious for mild myocarditis likely secondary to pembrolizumab. The patient was given 2 grams of intravenous magnesium sulfate and initiated on methylprednisolone 1 mg/kg intravenously daily. She had no further lightheadedness or episodes of TdP. She was discharged on a course of tapering oral prednisone. Patient was also instructed to avoid all QT prolonging medications. Her pembrolizumab was discontinued. The patient was still asymptomatic at follow-up in five weeks and her QTc had decreased to 388 ms.

Late presentation of Torsades de Pointes related to fluoxetine following a multiple drug overdose

BackgroundFluoxetine is a selective serotonin reuptake inhibitor (SSRI) commonly used in the treatment of depression. While most intoxications with SSRI’s have favorable outcomes and do not require interventions other than strict observation of vital signs and heart rhythm, clinicians should be aware of the life-threatening complications that may occur.Case presentationA 61-year-old woman presented to the emergency department after an intentional multiple drug overdose. Upon examination, she was somnolent with stable respiration and hemodynamics. Electrocardiography showed a prolonged QTc interval of 503 ms. The patient was admitted to the ICU for cardiopulmonary monitoring. During admission, the patient remained stable and showed improved neurologic function over time. After 22 h, a second ECG showed normalization of the QTc interval to 458 ms. However, 36 to 40 h after admission, our patient developed recurrent episodes of Torsades de Pointes (TdP) with loss of cardiac output, leading to cardiopulmonary resuscitation. Spontaneous circulation was restored after intravenous administration of magnesium sulphate. Retrospective serum analysis revealed fluoxetine concentrations of 2700 mcg/l.ConclusionMost intoxications with selective serotonin reuptake inhibitors (SSRI) have favorable outcomes and do not require medical interventions other than strict cardiopulmonary observation. However, higher doses have been associated with QTc interval prolongation, TdP, serotonin syndrome, and death. This case illustrates that life-threatening complications may occur late in the course of hospital admission. Even though overdoses with SSRI’s generally result in few fatalities, clinicians should be aware of the life-threatening clinical manifestations that may occur. Despite being an imperfect predictor of imminent TdP, continuous monitoring of cardiac rhythm is strongly recommended when either cardiac or non-cardiac symptoms are present.

Short-Lasting Episodes of Torsade de Pointes in the Chronic Atrioventricular Block Dog Model Have a Focal Mechanism, While Longer-Lasting Episodes AreMaintained by Re-Entry.

This study investigated the arrhythmogenic mechanisms responsible for torsade de pointes (TdP) in the chronic atrioventricular block dog model, known for its high susceptibility for TdP. The mechanism of TdP arrhythmias has been under debate for many years. Focal activity as well as re-entry have both been mentioned in the initiation and the perpetuation of TdP. In 5 TdP-sensitive chronic atrioventricular block dogs, 56 needle electrodes were evenly distributed transmurally to record 240 unipolar local electrograms simultaneously. Nonterminating (NT) episodes were defibrillated after 10 s. Software was developed to automatically detect activation times and to create 3-dimensional visualizations ofthe arrhythmia. For each episode of ectopic activity (ranging from 2 beats to NT episodes), a novel methodology wascreated to construct directed graphs of the wave propagation and detect re-entry loops by using an iterative depth-first-search algorithm. Depending on the TdP definition (number of consecutive ectopic beats), we analyzed 29 to 54 TdP: 29 werelonger than 5 beats. In the total group, 9 were NT and 45 were self-terminating. Initiation and termination were always based on focal activity. Re-entry becomes more important in the longer-lasting episodes (>14 beats), whereas inall NT TdP, re-entry was the last active mechanism. During re-entry, excitation fronts were constantly present in theheart, while during focal TdP, there was always a silent interval between 2 consecutive waves (142 ms) during which excitation fronts were absent. Interbeat intervals were significantly smaller for re-entry episodes-220 versus 310 ms infocal. Electrograms recorded in particular areas during NT TdP episodes had significantly smaller amplitude (0.38) than during focal episodes (0.59). TdP can be driven by focal activity as well as by re-entry depending on the duration of the episode. NTepisodes are always maintained by re-entry, which can be identified in local unipolar electrograms by shorter interbeatintervals and smaller deflection amplitude.

Additive Proarrhythmic Effect of Combined Treatment with QT-Prolonging Agents.

Drug combinations may elevate the risk of proarrhythmia. The aim of the present study was to investigate whether combinations of non-cardiovascular agents induce an additive increase in the proarrhythmic risk. In 12 female rabbit hearts, a drug combination of cotrimoxazole (300µM), ondansetron (5µM) and domperidone (1µM) was infused after obtaining baseline data. In another 13 hearts, a combination of cotrimoxazole (300µM), ondansetron (5µM) and erythromycin (300µM) was infused. Monophasic action potentials and ECG displayed a significant QT prolongation in all groups. This was accompanied by a significant increase in action potential duration. Of note, addition of each drug resulted in a further increase in the QT interval. Furthermore, a significant elevation of spatial dispersion of repolarization was observed. Lowering of potassium concentration in bradycardic AV-blocked hearts provoked early afterdepolarizations and torsade de pointes (TDP) in both study groups. Under baseline conditions, no episodes of TDP recorded. After administration of the first agent, TDP occurred in 5 of 12 hearts (37 episodes) and 5 of 13 hearts (26 episodes), respectively. After additional infusion of the second drug, TDP were recorded in 7 of 12 hearts (55 episodes) and 8 of 13 hearts (111 episodes). After additional infusion of the third drug, TDP occurred in 11 of 12 hearts (118 episodes) and 9 of 13 hearts (88 episodes). Combined treatment with several non-cardiovascular QT-prolonging agents resulted in a remarkable occurrence of proarrhythmia. An additive and significant prolongation of cardiac repolarization combined with an increased spatial dispersion of repolarization represents the underlying electrophysiological mechanism.

179 Phosphodiesterase-5 inhibition with sildenafil suppresses calcium waves by reducing sarcoplasmic reticulum content

Rationale: Occurrence of diastolic Ca2+ waves in cardiac myocytes leads to arrhythmias by inducing delayed after-depolarisations. Waves are initiated when sarcoplasmic reticulum (SR) content reaches a critical threshold level. The...

Abstract 11336: Different Mechanisms of Torsade de Pointes Arrhythmias in the Drug-induced Chronic AV Block Dog

Introduction: The arrhythmia Torsade de Pointes (TdP) is responsible for &gt;5% of all sudden cardiac deaths. However, the mechanism(s) underlying the TdPs is under debate. Clinical and experimental data suggest that TdP may be driven either by focal sources or by moving reentry. One way to study the mechanisms of TdP is to use the electrically remodeled canine heart after chronic AV block (CAVB), which has a high susceptibility for drug-induced TdPs. Methods: Five TdP-sensitive CAVB dogs were studied. In all animals, 66 needle electrodes were evenly distributed transmurally to record 240 unipolar local electrograms simultaneously. If the TdP was non-terminating after 10s, it was defibrillated. Software was developed to automatically detect activation times during the dofetilide-induced TdPs and to create 3D visualisations of the arrhythmia. For each episode of TdP, directed graphs of the wave propagation were created and loops were detected by using an iterative depth first search algorithm(Johnson). Interbeat intervals were computed by taking the average of the time intervals of activation for each electrode. Results: In total we analysed 53 TdPs: from those 9 were non-terminating (&gt; 50 beats) and 44 self terminating. In all non-terminating TdPs reentry loops were identified. In the 44 self terminating TdPs reentry loops were found only in 6 (20±10 beats) cases, while in the 38 (7±4 beats) other cases TdP was driven by focal sources. Secondly, during reentry, excitation fronts were constantly present in the heart, while during ectopic TdP there was always a pause between the end of the previous wave and the beginning of the next wave (121±51 ms) during which excitation fronts were absent. Thirdly, we found that the interbeat intervals were significantly smaller for the cases where reentry loops were detected, then in the cases of the ectopic TdPs (221±21 versus 310±96 ms). Finally, in all cases where reentry loops were detected, the signal of certain electrodes had significantly smaller amplitude than the average amplitude under normal pacing, which via computer simulations could be related to the cores of the reentry loops. Conclusions: In the non-terminating TdPs reentry is always present, while paroxysmal TdP was in most of the cases based on ectopic activity (86%).

In vivo analysis of torsadogenic potential of an antipsychotic drug paliperidone using the acute atrioventricular block rabbit as a proarrhythmia model

We assessed electrophysiological effects of an atypical antipsychotic drug paliperidone in acute atrioventricular block rabbits. Intravenous administration of paliperidone at a clinically relevant dose (0.06 mg/kg) hardly affected the QT interval or monophasic action potential (MAP) duration, and the higher doses (0.6 and 6 mg/kg) prolonged the QT interval and MAP duration. Meanwhile, premature ventricular contractions with R on T phenomenon were observed in 3 out of 6 animals at the middle dose, and torsades de pointes (TdP) episodes were detected in 2 out of 6 animals at the high dose. Intravenous administration of its chemically related compound risperidone at a clinically relevant dose (0.03 mg/kg) hardly affected the electrophysiological parameters, and the higher doses (0.3 and 3 mg/kg) prolonged the QT interval and MAP duration. Meanwhile, the premature ventricular contractions with R on T were observed in 2 out of 6 animals at the middle dose, and TdP episodes were detected in 4 out of 6 animals at the high dose. These results suggest that paliperidone showed torsadogenic potential at supra-therapeutic doses, whose potency can be estimated to be equal or slightly subordinate in comparison with that of risperidone.

Electrocardiographic Parameters Indicating Worse Evolution in Patients with Acquired Long QT Syndrome and Torsades de Pointes.

Acquired long QT syndrome (a-LQTS) is associated with life-threatening ventricular arrhythmias, mainly torsades de pointes (TdP). ECG parameters predicting evolving into ventricular fibrillation (VF) are ill defined. To determine ECG parameters preceding and during TdP associated with higher risk of developing VF. We analyzed 151 episodes of TdP, recorded in 28 patients with a-LQTS (mean QTc 638 ms ± 57). All 28 patients had prolonged QT interval, (mean QTc 638 ms ± 57) ranging from 502 ms to 858 ms correcting by Bazett's formula. The mean TdP heart rate was 218 bpm ± 38 (mean cycle length of TdP 274 ± 47 ms). We classified TdPs episodes into "slower"-TdP (s-TdP) < 220 bpm (range from 145-220 bpm) observed in 81 (53.6%) episodes and "faster"-TdP (f-TdP) ≥ 220 bpm (ranged from 221-281 bpm) observed in 70 (46.4%) episodes. Among 151 episodes of TdP, 21 (13.9%) were unstable (converted into VF). Out of 81 episodes of "slower"-TdP only 2 (2.5%) episodes converted into VF. The mean coupling interval (CI) of the PVC initiating TdP was 510 ms ± 118, the pause-RR interval was 1147 ms ± 335, the prematurity index (PI) of PVC that initiated TdP was 0.45 ± 0.13. The mean cycle length variability of TdP (VRV-TdP) was 30.79 ms ± 19.7. U wave was observed in 86 episodes (56.9%), among that in 69 episodes, the U/T wave ratio was > 1. Macro T wave alternans was observed in 4 patients. The QT interval was not different in patients with VF(+) and VF(-) episodes, 633 ± 60 and 639 ± 57, respectively. Some electrocardiographic parameters can be helpful in determining the risk of TdP evolving into VF. The slower ventricular rate (< 220 bpm), the higher rate instability (VRV > 30 ms) and the short episodes < 20 beats could predict benign evolution.

Torsade de Pointes Triggered by Early Ventricular Escape Beats in a Patient with Complete Atrioventricular Block.

Torsade de pointes is an uncommon and malignant form of polymorphic ventricular tachycardia and associated with a prolonged QT interval, which may be congenital or acquired. Complete atrioventricular block may cause QT interval prolongation and torsade de pointes. In this paper, we present a case with complete atrioventricular block complicated with frequent episodes of torsade de pointes triggered by early premature ventricular contractions despite normal QT intervals.

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.