QTc Prolongation and Torsades de Pointes

Author(s):  
Ankur Srivastava ◽  
James E. Littlejohn

This chapter looks at QTc prolongation and torsades de pointes (Tdp). In cases of recurrent polymorphic ventricular tachycardia, Tdp should be an immediate consideration. Tdp appears like a “twisting of points” of the cardiac axis, which is most often due to acquired QTc prolongation. The QT interval is inversely related to heart rate; therefore, it is corrected (QTc) using formulas such as Bazett's, Fridericia, and Framingham. There are several congenital and acquired causes of QTc prolongation. The congenital long QT syndrome, Romano-Ward syndrome, and Jervell and Lange-Nielsen syndrome are commonly associated with QTc prolongation and Tdp. Drug classes such as anti-arrhythmics, antidepressants, antipsychotics, antibiotics, and antihistamines are the other common cause of acquired QTc prolongation. Primary management of QTc prolongation and Tdp consists of minimizing risk factors like alternative medications and correcting electrolyte abnormalities. In a hemodynamically stable patient with QTc prolongation, treatment should focus on discontinuing the possible offending medications and correcting electrolyte levels. Meanwhile, patients with Tdp and hemodynamic instability require emergent electrical cardioversion in conjunction with preventative measures.

CNS Spectrums ◽  
2017 ◽  
Vol 23 (4) ◽  
pp. 278-283 ◽  
Author(s):  
Anja Elliott ◽  
Thibault Johan Mørk ◽  
Mikkel Højlund ◽  
Thomas Christensen ◽  
Rasmus Jeppesen ◽  
...  

ObjectiveAntipsychotics are associated with a polymorphic ventricular tachycardia, torsades de pointes, which, in the worst case, can lead to sudden cardiac death. The QT interval corrected for heart rate (QTc) is used as a clinical proxy for torsades de pointes. The QTc interval can be prolonged by antipsychotic monotherapy, but it is unknown if the QTc interval is prolonged further with antipsychotic polypharmaceutical treatment. Therefore, this study investigated the associations between QTc interval and antipsychotic monotherapy and antipsychotic polypharmaceutical treatment in schizophrenia, and measured the frequency of QTc prolongation among patients.MethodsWe carried out an observational cohort study of unselected patients with schizophrenia visiting outpatient facilities in the region of Central Jutland, Denmark. Patients were enrolled from January of 2013 to June of 2015, with follow-up until June of 2015. Data were collected from clinical interviews and clinical case records.ResultsElectrocardiograms were available for 65 patients, and 6% had QTc prolongation. We observed no difference in average QTc interval for the whole sample of patients receiving no antipsychotics, antipsychotic monotherapy, or antipsychotic polypharmaceutical treatment (p=0.29). However, women presented with a longer QTc interval when receiving polypharmacy than when receiving monotherapy (p=0.01). A limitation of this study was its small sample size.ConclusionsWe recommend an increased focus on monitoring the QTc interval in women with schizophrenia receiving antipsychotics as polypharmacy.


2011 ◽  
Vol 26 (S2) ◽  
pp. 1295-1295
Author(s):  
P. Wierzbinski ◽  
W. Kryszkowski ◽  
A. Florkowski ◽  
P. Galecki

IntroductionTreatment with antypsychotics is associated with cardiovascular side effects. This results from mechanism of action of antypsychotics. Arrhythmias are the serious side effects. Treatment with antipsychotics may prolong QTc and increase the risk of dangerous supraventricular and ventricular arrhythmias.ObjectivesThe main aims of the research are the following: If Any antypsychotics agents may prolong QT interval? If monotherapy with olanzapine, zyprasidone, arypiprazole and politherapy with perphenazine and olanzapine may induce any arrhythmias?MethodsData for this study were collected from 65 patients hospitalized in the Department of Adult Psychiatry and treated with olanzapine and perphenazine (n = 10) and with olanzapine (n = 20), aripiprazole (n = 20), ziprasidone (n = 15). All patients had 12 leads ECG two times: before admitting the drugs and during the treatment. All ECG were assessed on the presence of any abnormalities and QTc was calculated manually by using Bazzet formula.ResultsAmong treated patients no QTc prolongation was observed. There was no prolonged QTc over 450 ms in Male and 470 ms in female patients treated with antypsychotics in mono and politherapy. Potassium level in all patients was within the norm. Bradykardia (< 50/min) and tachykardia (>100/min) was not observed among participants.ConclusionsAtypical antypsychotics such as olanzapine, arypiprazole, zyiprasidon are cardiovascular safe drugs. They did not induce dangerous for life arrhythmias especially ventricular arrhythmia (known as torsades de pointes), which can progress to ventricular fibrillation and sudden death. Politherapy with olanzapine and first generation agents perphenazine is a safe combination and did not induce any cardiovascular side effects.


2018 ◽  
Vol 7 (2) ◽  
pp. 155-159 ◽  
Author(s):  
Harry W. Daniell, MD

This article reports an elderly female oxycodone consumer who developed Torsades-de-Pointes soon after her opioid-associated rate-corrected QT interval (QTC; a standard measurement on electrocardiograms) prolongation had been augmented by the development of Taku-Tsubo cardiomyopathy (TC), a sequence that followed greatly reduced oxycodone ingestion. Factors that likely contributed to this sequence are discussed, including direct opioid-induced inhibition of human ether-a-go-go-related gene activity and of androgen formation plus QTc prolongation induced by the presence of TC.


2021 ◽  
pp. 266-279
Author(s):  
Jarir At Thobari

Chloroquine (CQ) and Hydroxychloroquine (HCQ) are highly prescribed as medications for COVID-19 infection, although no robust or convincing data has yet been published about the efficacy in COVID-19 patients. Therefore, risk and benefit assessment are necessary for decision to prescribe these drugs in COVID-19 patient in hospitals settings. We systematically searched from MEDLINE Database which investigate the benefits and risks of HCQ and CQ among COVID-19 patients. All records were searched using the search terms Hydroxychloroquine, Chloroquine, COVID-19, and SARS-CoV-2. The selection criteria include all clinical trials and observational studies. We found 11 records about benefit and 7 records about risks on HCQ and CQ in COVID-19 patients after following inclusion and exclusion criteria. From clinical trial and observational studies have showed that HCQ is very limited benefit particularly on reduction of mortality or clinical improvement. Similarly, there were seven observational studies have estimated the cardiac event in use of HCQ or CQ in COVID-19. Even though no increase death, but these studies reported the increase risk of prolong QT-interval in high proportion and other cardiac events such as arrythmia, torsade de pointes and conduction block. We conclude that the benefit effect of HCQ and CQ in COVID-19 remains very limited. However, both medications have independently shown to increase the risk in other populations for QT-interval prolongation, drug-induced torsades de pointes/TDP (a form of polymorphic ventricular tachycardia) and drug-induced other cardiac events. 


2021 ◽  
Vol 16 ◽  
Author(s):  
Erinn Mangona ◽  
Elisa Sandonato ◽  
Todd N. Brothers ◽  
Jayne Pawasauskas

: Drug-induced QTc prolongation is a concerning electrocardiogram (ECG) abnormality. This cardiac disturbance carries a 10% risk of sudden cardiac death due to the malignant arrhythmia, Torsades de Pointes. The Arizona Center for Education and Research on Therapeutics (AzCERT) has classified QTc prolonging therapeutic classes such as antiarrhythmics, antipsychotics, anti-infectives, and others. AzCERT criteria categorizes medications into three risk categories: “known,” “possible,” and “conditional risk” of QTc prolongation and Torsades de Pointes. The list of QTc prolonging medications continues to expand as new drug classes are approved and studied. Risk factors for QTc prolongation can be delineated into modifiable or non-modifiable. A validated risk scoring tool may be utilized to predict the likelihood of prolongation in patients receiving AzCERT classified medication. The resultant risk score may be applied to a clinical decision support system which offers mitigation strategies. Mitigation strategies including discontinuation of possible offending agents with selection of an alternative agent, assessment of potential drug interactions or dose adjustments through pharmacokinetic and pharmacodynamic monitoring, and initiation of both ECG and electrolyte monitoring are essential to prevent a drug-induced arrhythmia. The challenges presented by the COVID-19 pandemic have led to the development of innovative continuous monitoring technology, increasing protection for both patients and healthcare workers. Early intervention strategies may reduce adverse events and improve clinical outcomes in patients identified to be at risk of QTc prolongation.


2018 ◽  
Vol 150 (7) ◽  
pp. 991-1002 ◽  
Author(s):  
Megan Koleske ◽  
Ingrid Bonilla ◽  
Justin Thomas ◽  
Naveed Zaman ◽  
Stephen Baine ◽  
...  

Recent evidence suggests that neuronal Na+ channels (nNavs) contribute to catecholamine-promoted delayed afterdepolarizations (DADs) and catecholaminergic polymorphic ventricular tachycardia (CPVT). The newly identified overlap between CPVT and long QT (LQT) phenotypes has stoked interest in the cross-talk between aberrant Na+ and Ca2+ handling and its contribution to early afterdepolarizations (EADs) and DADs. Here, we used Ca2+ imaging and electrophysiology to investigate the role of Na+ and Ca2+ handling in DADs and EADs in wild-type and cardiac calsequestrin (CASQ2)-null mice. In experiments, repolarization was impaired using 4-aminopyridine (4AP), whereas the L-type Ca2+ and late Na+ currents were augmented using Bay K 8644 (BayK) and anemone toxin II (ATX-II), respectively. The combination of 4AP and isoproterenol prolonged action potential duration (APD) and promoted aberrant Ca2+ release, EADs, and DADs in wild-type cardiomyocytes. Similarly, BayK in the absence of isoproterenol induced the same effects in CASQ2-null cardiomyocytes. In vivo, it prolonged the QT interval and, upon catecholamine challenge, precipitated wide QRS polymorphic ventricular tachycardia that resembled human torsades de pointes. Treatment with ATX-II produced similar effects at both the cellular level and in vivo. Importantly, nNav inhibition with riluzole or 4,9-anhydro-tetrodotoxin reduced the incidence of ATX-II–, BayK-, or 4AP-induced EADs, DADs, aberrant Ca2+ release, and VT despite only modestly mitigating APD prolongation. These data reveal the contribution of nNaVs to triggered arrhythmias in murine models of LQT and CPVT-LQT overlap phenotypes. We also demonstrate the antiarrhythmic impact of nNaV inhibition, independent of action potential and QT interval duration, and provide a basis for a mechanistically driven antiarrhythmic strategy.


2021 ◽  
Vol 96 (5) ◽  
pp. 432-437
Author(s):  
Jinmo Kim ◽  
Ju Yeop Lee ◽  
Won Sang Yoo ◽  
Myung Yong Lee ◽  
Hyun-Kyung Chung

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.


CJEM ◽  
2016 ◽  
Vol 18 (S1) ◽  
pp. S90-S91
Author(s):  
D. Drew ◽  
A. Baranchuk ◽  
R.J. Brison

Introduction: Fever is one of the most common reasons for presentation to the emergency department (ED). Interestingly, a number of small studies suggest that fever may function as a modulator of the QT interval in healthy individuals and an arrhythmogenic trigger in patients with occult congenital QT abnormalities. The objective of this study was to explore whether presence of fever adversely affects the QT interval, and whether medications known to prolong this interval affect any association found. Methods: We performed a retrospective, single center study identifying patients (age > 18 years) presenting to the ED with fever (temperature > 38.0 °C) between January 1st, 2012 and December 31st, 2013 via electronic chart review. The subset for analysis were those who had an ECG both at time of fever and while afebrile (within 30 days of initial ECG). Temperature measurement was within 30 minutes of ECG. Actively paced patients were excluded. Univariate and multiple regression analysis were used to determine risk factors for QT derangement in patients with fever. Results: 2018 febrile visits occurred during the reviewed period, 181 of these patients went on to be included in the study. 54.1% of study subjects were female, and the average age was 68.9 years old. The etiology of fever was predominately infectious (69.6%), with community acquired pneumonia being the most frequent cause (24.3%). We found the median corrected QT interval to be significantly shorter in febrile as compared to afebrile patients [QTc = 388.7ms, (371.5-407.5) vs 406.7, (386.7-434.4); p < 0.001]. This difference was observed in both sexes. Males were found to be more likely to experience medication induced QTc prolongation [OR 5.35, 95% CI = 1.46 - 19.68; P < 0.05]. Two instances of Torsades de pointes were identified in our study, both occurring in males on QT prolonging medications. Conclusion: In an ED patient population, fever generally shortens the QT interval independent of sex. Prolongation of the QT interval during fever should thus increase clinical suspicion of congenital or acquired QT disorders. Additionally, males appear to be more susceptible to medication-induced derangements in the QT interval and may require more vigilant monitoring when treated with multiple QT prolonging medications.


2021 ◽  
pp. 1-3
Author(s):  
Ayşe Ünal Yüksekgönül ◽  
İlker Ertuğrul ◽  
Tevfik Karagöz

Abstract “Torsades de pointes”, a life-threatening rhythm disorder, is a polymorphic ventricular tachycardia that usually develops in association with a prolonged QT interval. Fluconazole, an anti-fungal drug, may also induce QT prolongation, in some cases subsequent torsades de pointes. Herein, we report a 16-year-old female presenting “torsades de pointes” after administration of fluconazole and rapidly improved upon cessation of the drug.


2021 ◽  
Vol 14 (7) ◽  
pp. e243325
Author(s):  
Sameen Iqbal ◽  
Sidra Malik Fayyaz ◽  
Yawer Saeed ◽  
Masooma Aqeel

A young man presented to the emergency department with seizures and recurrent episodes of polymorphic ventricular tachycardia (PMVT)/torsades de pointes (TdP) requiring cardioversion and administration of intravenous magnesium. A battery of tests performed to identify a cause for his arrhythmias and seizures were all normal. A revisit of history with family revealed he had consumed over 100 tablets/day of loperamide for the past 1 year. A prolonged QT interval on his ECG raised concerns for long QT syndrome (LQTS) (congenital or acquired). Our patient was suspected to have loperamide-induced cardiotoxicity. TdP is a specific PMVT that occurs with a prolonged QT interval and is usually drug-induced. Less frequently, congenital LQTS may be implicated. With supportive care, including mechanical ventilation, vasopressors and temporary transvenous overdrive pacing, our patient recovered completely. We describe the importance of a systematic and time-sensitive approach to diagnosing critical illness. Loperamide overdose may cause QT prolongation, life-threatening arrhythmias/cardiogenic shock, or cardiac arrest. Seizures/epilepsy may also be a manifestation in young patients. There is a substantial need to revisit the safety of over-the-counter medications and increasing awareness of manifestations of drug overdose.


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