scholarly journals Sudden cardiac death and antipsychotics. Part 1: Risk factors and mechanisms

2006 ◽  
Vol 12 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Nasser Abdelmawla ◽  
Alex J. Mitchell
Keyword(s):  
Cardiac Disease ◽  
Qt Interval ◽  
Torsade De Pointes ◽  
High Dose ◽  
Qtc Interval ◽  
Clear Explanation ◽  
Increased Risk ◽  
Approximate Relationship ◽  
Mental Health Difficulties ◽  
Therapeutic Doses

Mortality from causes other than suicide is higher than expected in schizophrenia. Cardiovascular causes are most common, accounting for the majority of the 5% of sudden and unexpected deaths. Most cases have no clear explanation on post-mortem examination (‘sudden unexplained deaths’) and are thought to result from fatal arrhythmias. Prospective studies show that people with prolongation of the QT interval beyond 500 ms are at increased risk of serious arrhythmias such as ventricular tachycardia and torsade de pointes. In about 1 in 10 cases, the torsade is fatal. Most antipsychotics prolong the QTc interval in overdose but some prolong it even at therapeutic doses. Droperidol, sertindole and ziprasidone extend the QT interval by an average of 15–35 ms; quetiapine, haloperidol and olanzapine by 5 ms, to 15 ms. There is only an approximate relationship between QT prolongation and risk of sudden death, and the risk related to antipsychotics is thought to increase in people with pre-existing cardiac disease, those taking multiple QT-acting drugs and those taking antipsychotics at high dose for long periods. There is little evidence of an association with route of administration. More data are required to clarify to what extent people with mental health difficulties who die suddenly have pre-existing cardiac disease.

scholarly journals Ciprofloxacin does not Prolong the QTc Interval: A Clinical Study in ICU Patients and Review of the Literature

2017 ◽  
Vol 20 (1) ◽  
pp. 360 ◽  
Author(s):  
Charlotte Heemskerk ◽  
Evelien Woldman ◽  
Marieke Pereboom ◽  
Ruud Van der Hoeven ◽  
Aukje Mantel-Teeuwisse ◽  
...  
Keyword(s):  
Qt Interval ◽  
Torsade De Pointes ◽  
Qtc Interval ◽  
Test Results ◽  
Interval Prolongation ◽  
Icu Patients ◽  
Increased Risk ◽  
Qtc Interval Prolongation ◽  
Student’S T ◽  
Student’S T Test

Purpose. Ciprofloxacin may prolong the QT interval and increase the risk of Torsade de Pointes (TdP). Intravenous administration of ciprofloxacin in patients with additional risks may elevate the risk of QTc interval prolongation. We prospectively assessed whether intravenous ciprofloxacin prolongs the QT interval in patients with additional co-morbidities and risk factors. We also reviewed the literature on the QT prolonging effect or TdP inducing effect of ciprofloxacin. Methods. ICU Patients who were treated with intravenous ciprofloxacin as part of their therapy were recruited. ECG was recorded within 60 min before start and in the last 30 min of 1 h infusion, or within 30 min after the end of ciprofloxacin infusion. QT interval was corrected for the heart rate using both Bazett’s and Fridericia’s formula. The changes were analyzed using the paired Student’s t-test. Results. Ten patients were included in the study (average age 74-y, 6 males). The average baseline QTc interval corrected with Bazett’s formula was 448 ms that was shortened during or after ciprofloxacin infusion by 3 ms and 2 ms based on Bazett’s  (p=0.67) and Fridericia’s (p=0.68) formula, respectively. No observational study  or cohort study thus far has shown that ciprofloxacin has a QT prolonging effect or increases the risk of TdP or (cardiovascular) mortality.  Conclusion. Based on our results and the results of previous studies, it is unlikely that ciprofloxacin has a clinically relevant QT prolonging effect or an increased risk of TdP. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

scholarly journals Drug-induced QT interval prolongation in cancer patients

2011 ◽  
Vol 4 (4) ◽  
pp. 223
Author(s):  
Torben K. Becker ◽  
Sai-Ching J. Yeung
Keyword(s):  
Cancer Patients ◽  
Qt Interval ◽  
Alkylating Agents ◽  
Torsade De Pointes ◽  
Interval Prolongation ◽  
Drug Induced ◽  
Vascular Disruption ◽  
Qt Interval Prolongation ◽  
Increased Risk ◽  
Multiple Drugs

Cancer patients are at an increased risk for QT interval prolongation and subsequent potentially fatal Torsade de pointes tachycardia due to the multiple drugs used for treatment of malignancies and the associated symptoms and complications. Based on a systematic review of the literature, this article analyzes the risk for prolongation of the QT interval with antineoplastic agents and commonly used concomitant drugs. This includes anthracyclines, fluorouracil, alkylating agents, and new molecularly targeted therapeutics, such as vascular disruption agents. Medications used in the supportive care can also prolong QT intervals, such as methadone, 5-HT3-antagonists and antihistamines, some antibiotics, antifungals, and antivirals. We describe the presumed mechanism of QT interval prolongation, drug-specific considerations, as well as important clinical interactions. Multiple risk factors and drug–drug interactions increase this risk for dangerous arrhythmias. We propose a systematic approach to evaluate cancer patients for the risk of QT interval prolongation and how to prevent adverse effects.

Abstract 12640: Energy Drinks Prolong Early Repolarization (J-T Peak ) Phase in a Healthy Population

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Samuel R Kaplan ◽  
Ghufran Syed ◽  
Teri Kozik
Keyword(s):  
Torsade De Pointes ◽  
Energy Drinks ◽  
Energy Drink ◽  
Healthy Population ◽  
Specific Marker ◽  
Qtc Interval ◽  
Qtc Prolongation ◽  
Early Repolarization ◽  
Increased Risk ◽  
Energy Drink Consumption

Introduction: Energy drinks continue to be the fastest growing beverage market with sales expected to reach $60 billion in the next few years, yet have demonstrated adverse cardiovascular effects such as prolongation of the QTc interval on EKG. While QTc prolongation observed with certain drugs has long been used as an indicator of increased risk of torsade de pointes, recent data has identified the early repolarization interval J-T peak (JTp) as a more specific marker for proarrhythmic potential. Drugs that selectively block the human ether-a-go-go related (hERG) potassium ion channel prolong QTc by prolonging both early repolarization (JTp) and late repolarization (T peak -T end [Tpe] interval), and are associated with an increased risk of torsade. In contrast, drugs that additionally block inward late sodium and L-type calcium prolong QTc by prolonging Tpe but not JTp, and have demonstrated reduced risk of torsade. In 2018, the C-Energy-X study demonstrated QTc prolongation in 22 healthy subjects (mean age 28 ± 7yrs) who consumed energy drink while at rest and following short periods of exercise. Our study provides a secondary analysis of this data in terms of its effect on JTp, a potentially more specific marker for torsade risk. Methods: Using H-Scribe software, two evaluators independently measured JTp and RR intervals from C-Energy-X subjects pre- and post-energy drink consumption in the rest and exercise phases. Values were corrected for heart rate using the linear correction formula JTpc=JTp + 0.150(1-RR), where RR is R-to-R interval. Mean JTpc values from each phase were analyzed using a paired sample two-tailed t -test. Results: In the resting phase following energy drink consumption (PCr), there was a statistically significant increase in JTpc intervals for 77% of subjects by a mean of 10.5ms (baseline=234 ± 21.3ms; PCr=245 ± 22.0ms; p =0.015). In the exercise phase following energy drink consumption (PCe), 64% of subjects increased JTpc intervals by a mean of 0.8ms which was not significant (baseline=225 ± 15.7ms; PCe=226 ± 17.9ms; p =0.845). Conclusion: In the resting phase, energy drink consumption was associated with statistically significant prolongation of JTpc, suggesting a theoretical increased risk of torsade de pointes.

scholarly journals Prolonged QT Interval in a Patient With Coronavirus Disease-2019: Beyond Hydroxychloroquine and Azithromycin

2020 ◽  
Vol 8 ◽  
pp. 232470962094840
Author(s):  
B K Anupama ◽  
Soumya Adhikari ◽  
Debanik Chaudhuri
Keyword(s):  
Qt Interval ◽  
Ventricular Arrhythmias ◽  
Torsade De Pointes ◽  
Cardiac Pacing ◽  
Qt Prolongation ◽  
Medication Effects ◽  
Increased Risk ◽  
Repolarization Reserve ◽  
Prolonged Qt Interval ◽  
Prolonged Qt

Recent reports have suggested an increased risk of QT prolongation and subsequent life-threatening ventricular arrhythmias, particularly torsade de pointes, in patients with coronavirus disease-2019 (COVID-19) treated with hydroxychloroquine and azithromycin. In this article, we report the case of a 75-year-old female with a baseline prolonged QT interval in whom the COVID-19 illness resulted in further remarkable QT prolongation (>700 ms), precipitating recurrent self-terminating episodes of torsade de pointes that necessitated temporary cardiac pacing. Despite the correction of hypoxemia and the absence of reversible factors, such as adverse medication effects, electrolyte derangements, and usage of hydroxychloroquine/azithromycin, the QT interval remained persistently prolonged compared with the baseline with subsequent degeneration into ventricular tachycardia and death. Thus, we highlight that COVID-19 illness itself can potentially lead to further prolongation of QT interval and unmask fatal ventricular arrhythmias in patients who have a prolonged QT and low repolarization reserve at baseline.

scholarly journals Effect of Hydroxychloroquine and Azithromycin on QT Interval Prolongation and Other Cardiac Arrhythmias in COVID-19 Confirmed Patients

2021 ◽  
Vol 2021 ◽  
pp. 1-7 ◽  
Author(s):  
Seyed Parsa Eftekhar ◽  
Sohrab Kazemi ◽  
Mohammad Barary ◽  
Mostafa Javanian ◽  
Soheil Ebrahimpour ◽  
...  
Keyword(s):  
High Risk ◽  
Qt Interval ◽  
Therapy Group ◽  
Torsade De Pointes ◽  
Cardiac Monitoring ◽  
Qtc Interval ◽  
Interval Prolongation ◽  
Qt Interval Prolongation ◽  
Significant Difference ◽  
The Mean

Background. Hydroxychloroquine with or without azithromycin was one of the common therapies at the beginning of the COVID-19 pandemic. They can prolong QT interval, cause torsade de pointes, and lead to sudden cardiac death. We aimed to assess QT interval prolongation and its risk factors in patients who received hydroxychloroquine with or without azithromycin. Methods. This study was a retrospective cohort study. One hundred seventy-two confirmed COVID-19 patients were included in this study, hospitalized at Babol University of Medical Sciences hospitals between March 5, 2020, and April 3, 2020. Patients were divided into two groups: hydroxychloroquine alone and hydroxychloroquine with azithromycin. Electrocardiograms were used for outcome assessment. Results. 83.1% of patients received hydroxychloroquine plus azithromycin vs. 16.9% of patients who received only hydroxychloroquine. The mean age of patients was 59.2 ± 15.4 .The mean of posttreatment QTc interval in the monotherapy group was shorter than the mean of posttreatment QTc interval in the combination therapy group, but it had no significant statistical difference ( 462.5 ± 43.1 milliseconds vs. 464.3 ± 59.1 milliseconds; p = 0.488 ). Generally, 22.1% of patients had a prolonged QTc interval after treatment. Male gender, or baseline QTc ≥ 450 milliseconds, or high-risk Tisdale score increased the likelihood of prolonged QTc interval. Due to QTc prolongation, fourteen patients did not continue therapy after four days. Conclusions. Hospitalized patients treated by hydroxychloroquine with or without azithromycin had no significant difference in prolongation of QT interval and outcome. The numbers of patients with prolonged QT intervals in this study emphasize careful cardiac monitoring during therapy, especially in high-risk patients.

Abstract P230: Metabolically Healthy Obesity and QT interval. The Polish Norwegian Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Georgeta Vaidean ◽  
Marta Manczuk ◽  
Jared W Magnani
Keyword(s):  
Qt Interval ◽  
Large Population ◽  
Ventricular Repolarization ◽  
Qtc Interval ◽  
Benign Condition ◽  
Metabolically Healthy Obese ◽  
Increased Risk ◽  
Healthy Obese ◽  
Metabolically Healthy ◽  
Age And Sex

Introduction: Obesity has been linked to increased risk of sudden cardiac death and ventricular arrhythmia. Whether the metabolically healthy obese phenotype is a benign condition, is debatable and few studies examined its ventricular repolarization profile. Purpose: To examine the association of metabolically healthy/unhealthy obesity phenotypes with prolonged corrected QT (QTc) interval in a large population-based study. Methods: Cross-sectional data from an ongoing cohort study in Poland. Data was collected using a standardized protocol. The QT intervals were obtained from digital standard 12-lead resting ECG and were corrected for heart rate by Bazett’s formula. Plasma lipids and glucose were measured in a fasting state. After excluding drugs known to affect the QT interval (antiarrhythmics, digoxin, antipsychotics), the analytic sample size was 11068 participants, ages 45 to 64 years. Based on the presence of obesity (BMI ge 30 kg/ m 2 ) and metabolic syndrome (per the AHA/NHLBI harmonized definition), we defined four phenotypes: metabolically healthy non-obese (MHNO), metabolically unhealthy nonobese (MUNO), metabolically healthy obese (MHO) and metabolically unhealthy obese (MUO). Multivariable linear and logistic regression models were used for analyses. Results: The prevalence of the 4 phenotypes was: MHNO: 51.34%, MUNO: 18.07%, MHO: 10.07%, MUO: 20.52%. The prevalence of an increased QTc interval (greater than >430ms in men/450ms in women) was 14.28%, and the prevalence of a highly prolonged QTc interval (greater than 450ms in men/470ms in women) was 5.2%. The age- and sex-adjusted mean QTc across the 4 phenotypes was: MHNO: 417.05ms (416.39- 417.71; MUNO: 418.82 ms (417.71-419.92); MHO: 420.46 ms (418.99 -421.93); MUO: 422.45 ms (421.41-423.49). The age- and sex adjusted odds (OR, 95% CI) of an increased QTc interval (greater than 430/450ms in men/women) were increased in MUNO (1.11, 0.96-1.29), MHO (1.44, 1.20-1.72) and MUO (1.47, 1.28-1.69), compared to MHNO phenotype. These estimates were minimally attenuated after additional adjustment for prevalent CVD, LVH on ECG, smoking, alcohol intake, physical activity and education: MUNO (1.10, 0.94-1.28), MHO (1.45, 1.21-1.73) and MUO (1.44, 1.26-1.66). We did not detect effect modification by sex. We obtained similar results in subgroup analyses restricted to those without diabetes and after excluding those with third degree atrioventricular blocks or conduction abnormalities with QRS>120ms. Conclusion: Both metabolically healthy- and non-healthy obese phenotypes had a higher likelihood of an increased/borderline QTc interval compared to the MHNO phenotype. Our study furthered our understanding of ventricular repolarization as reflected in the QTc interval, in the setting of different obesity phenotypes.

Abstract P391: The Effects of Obstructive Sleep Apnea on Cardiac Arrhythmia Risk

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Emily Biben ◽  
Lauren Burgess ◽  
Julie Allen ◽  
Noah Jouett ◽  
John Burk ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cardiac Disease ◽  
Qt Interval ◽  
The United States ◽  
Qt Prolongation ◽  
Qtc Interval ◽  
Sleep Study ◽  
Qt Intervals ◽  
Obstructive Sleep

Background: Over 20 million people in the United States suffer from Obstructive Sleep Apnea (OSA). Compared to the general population, OSA patients are 2.6 times more likely to experience sudden cardiac death (SCD), and it is suspected that this is due, in part, to QT prolongation leading to fatal dysrhythmias. OSA events have previously been shown to cause prolonged QT intervals compared to the post-apnea hyperventilation period, and studies have also observed increased QT dispersion in patients without cardiac disease. However, those with cardiac disease may be at the greatest risk for SCD, and it is not known what role QT prolongation plays and what factors influence these responses. Thus, the purpose of this study is to evaluate the factors that affect QT interval during periods of sleep apnea including OSA severity, time of night, and quantity of obstructive apneic events during sleep. Methods: We determined QTc intervals from the electrocardiograms of 36 patients undergoing polysomnography for diagnosis of OSA. Patients that were selected had an apnea hypopnea index >20/Hr and had no prior myocardial infarction or heart failure. Each patient’s ECG during their sleep study was analyzed to assess QT interval throughout the night. Baseline QT intervals were compared to QT intervals during obstructive apneas during the first 2 hours of sleep (Early) and last 2 hours of sleep (Late). In addition, apneas >40 seconds were analyzed in 11 patients for changes in QTc as the apnea progressed. Statistical comparisons were made with paired t tests and a one-way ANOVA analysis with repeated measures. Results: Early analyses of data showed QTc intervals in Early and Late apneas were significantly prolonged compared to awake baseline (p=0.04 and p=0.006 respectively). For patients with apneas >40 seconds, significant differences in QTc interval were observed at increasing time points during the apnea compared to the QTc immediately preceding the apnea (p<0.001). Furthermore, patients with longer apneas tend to have longer baseline QTc (p=0.07). Conclusions: Sleep apneic events are associated with periods of mild QTc prolongation despite some cardiac cycle shortening. The prolongation tends to become enhanced later in the night, implying that there is a cumulative effect of numerous prior apneas. Furthermore, prolongation tends to increase as the apnea duration progresses. Early data analyses also suggest that baseline QTc tends to be longer in patients who have more severe/longer apneic events throughout the night. Future studies will focus on QTc changes in OSA patients with prior heart disease, as these are the patients at greatest risk for serious arrhythmias during the night.

scholarly journals QTc Prolongation in Patients Receiving Triazoles and Amiodarone

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S84-S84 ◽  
Author(s):  
Katherine Cook ◽  
Thitinan Sraubol ◽  
Kristen Bova Campbell ◽  
Ahmad Mourad ◽  
Jonathan Stiber ◽  
...  
Keyword(s):  
Qt Interval ◽  
Ventricular Arrhythmias ◽  
Medical Center ◽  
Torsade De Pointes ◽  
Patient Discharge ◽  
Amiodarone Therapy ◽  
Qtc Interval ◽  
Concomitant Therapy ◽  
Cardiac Events ◽  
Duke University

Abstract Background Prolonged QT interval may lead to ventricular arrhythmias, torsade de pointes and sudden death. Triazole antifungals are often administered to inpatients with cardiac disease and with other QT prolonging drugs. Amiodarone is a commonly used antiarrhythmic that can prolong QT and be proarrhythmic but safety of co-administering these agents in the clinical setting is not known. Methods We conducted a retrospective, observational cohort study of adult inpatients at Duke University Medical Center who received concomitant systemic azoles and amiodarone from 2007 to 2013. Included subjects had ≥1 electrocardiogram (EKG) performed while receiving either agent alone within 1 month of starting concomitant therapy (baseline, BL) and ≥1 follow-up (FU) EKG after ≥2 days of concomitant therapy. A paired t-test was used to assess the maximum change in corrected QT interval (QTc, Bazett’s correction) from BL to FU. Logistic regression was used to evaluate predictors of FU QTc ≥500 ms (age, race, gender, and BL QTc ≥500 ms). Patient discharge diagnoses of ventricular arrhythmias or other cardiac events were reviewed to assess clinical outcome. Results Of 816 subjects identified, 252 had EKG results eligible for analysis. Azoles received were fluconazole (86.5%), voriconazole (11.5%), posaconazole (1.6%) or itraconazole (0.4%). Subjects were a median of 65 (IQR 25–88) years of age, 64.3% male and 78.6% Caucasian. Median duration of concomitant therapy was 7 days (IQR 4–11 days). Mean maximal change in QTc was +32 ms from BL (95% CI 26.2–38.6, P &lt; 0.0001). 25.4 and 48.8% of subjects had a BL and FU QTc ≥500 ms, respectively. BL QTc ≥500 ms but not age, race, or gender was associated with FU QTc ≥500 ms (OR 6.32 95% CI 3.21–12.43). Thirty-day all-cause mortality was 26.2%. No cardiac events were apparent in relation to concomitant azole-amiodarone therapy. Conclusion Prolongation of the QTc interval was frequently observed in this cohort of patients receiving azoles and amiodarone. Clinical impact is challenging to assess in this critically ill, complex patient population but appears to be limited. Additional analyses are needed to further evaluate safety of azoles in the setting of other QTc prolonging agents. Disclosures All authors: No reported disclosures.

scholarly journals The QT long syndrome: clinical and diagnostic aspect

2021 ◽  
Vol 69 (1) ◽  
Author(s):  
Constantin Martiniuc ◽  
◽  
Serghei Pisarenco ◽  
Iurie Simionica ◽  
◽  
...  
Keyword(s):  
Qt Interval ◽  
Torsade De Pointes ◽  
Qt Prolongation ◽  
Current Data ◽  
Polymorphic Ventricular Tachycardia ◽  
Interval Prolongation ◽  
Qt Interval Prolongation ◽  
Increased Risk ◽  
Wide Range ◽  
Life Threatening

QT interval prolongation is a predictor of the life-threatening cardiac arrhythmias — polymorphic ventricular tachycardia (torsade de pointes). Long QT syndrome may be congenital or acquired. It is known that a wide range of both antiarrhythmic and non-cardiac medications might lead to QT interval prolongation. List of drugs that cause QT prolongation is constantly growing and being updated. The review contains current data on the clinical significance of the control of QT interval duration within drug therapy. Clinical conditions associated with an increased risk of QT interval prolongation are described. Drugs that can induce QT prolongation are also discussed.

scholarly journals Assessment of anti-factor Xa activity in critically ill COVID-19 patients receiving three different anticoagulation regimens

2021 ◽  
Vol 9 ◽  
pp. 205031212110499
Author(s):  
Mohammed A Hamad ◽  
Shereen A Dasuqi ◽  
Aamer Aleem ◽  
Rasha A Omran ◽  
Rakan M AlQahtani ◽  
...  
Keyword(s):  
Critically Ill ◽  
Interleukin 6 ◽  
Factor Xa ◽  
Clinical Decision ◽  
Target Range ◽  
High Dose ◽  
Cytokine Storm ◽  
Heparin Infusion ◽  
Increased Risk ◽  
Therapeutic Doses

Introduction: Critically ill COVID-19 patients are at increased risk of thrombosis with an enhanced risk of bleeding. We aimed to explore the role of anti-factor Xa levels in optimizing the high-intensity anticoagulation’s safety and efficacy and finding possible associations between D-dimer levels, cytokine storm markers, and COVID-19-induced coagulopathy or thrombophilia. Methods: Retrospective cohort study conducted on 69 critically ill COVID-19 patients who received three regimens of higher intensity anticoagulation. Results: Seventeen patients (24.6%) received high-dose enoxaparin prophylaxis, 29 patients (42%) received therapeutic doses of enoxaparin, and 23 patients (33.3%) were on therapeutic unfractionated heparin infusion. Fewer than one-third of the whole cohort ( n = 22; 31.8%) achieved the target range of anti-factor Xa. The patients were divided into three subgroups based on anti-factor Xa target status within each anticoagulation regimen; when compared, the only association observed among them was for interleukin-6 levels, which were significantly higher in both the “above the expected range” and “below the expected range” groups compared with the “within the expected range” group ( p = 0.009). Major bleeding episodes occurred in 14 (20.3%) patients and were non-significantly more frequent in the “below the expected anti-factor Xa range group” ( p = 0.415). Seven patients (10.1%) developed thrombosis. The majority of patients had anti-factor Xa levels below the expected ranges (four patients, 57.1%). Conclusion: Conventional anti-factor Xa ranges may not be appropriate as a predictive surrogate for bleeding in critically ill COVID-19. The clinical decision to initiate therapeutic anticoagulation preemptively may be individualized according to thrombosis and bleeding risks. Cytokine storm markers, namely, interleukin-6, may play a role in COVID-19-induced coagulopathy or thrombophilia.

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