Torsades-de-Pointes associated with Taku-Tsubo cardiomyopathy following greatly reduced oxycodone use in an elderly woman

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.

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.


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.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2258-2258
Author(s):  
Robert I. Liem ◽  
Luciana T. Young ◽  
Alexis A. Thompson

Abstract Recent evidence suggests that prolongation in QT interval may be a frequent finding in patients with sickle cell disease (SCD). Few studies, however, have examined the relationship between conduction abnormalities and other cardiac complications, such as left ventricular hypertrophy (LVH) and tricuspid regurgitant jet velocity (TRJV) elevation, in this population. Moreover, long QT may be a marker of increased mortality in conditions, other than SCD, associated with LVH. We therefore sought to evaluate QT interval and its relationship to echocardiographic findings, laboratory parameters and disease severity in a cohort of children and young adults with SCD. Methods We prospectively evaluated the corrected QT interval (QTc) on standard 12-lead ECG in a cross-sectional, convenience sample of 73 subjects (41 males, mean age 14.2±3 years, range 10 to 24) with Hb SS, SC and S-β0 thalassemia undergoing screening for TRJV elevation. Subjects on chronic transfusions were excluded and all studies were performed at baseline on the same day. A review of available medical records was also performed. Results In our cohort, QTc (mean 436±24 ms, range 387 to 531) was prolonged &gt; 440 ms in 30/73 (41%) of subjects at steady state. We also found TRJV elevation ≥ 2.5 m/s in 24/73 (33%) and LVH by ECG or echocardiographic criteria in 32/73 (44%) subjects. Using Pearson’s correlation coefficient, we observed significant correlations between QTc and TRJV (r=0.38, p=0.002), WBC (r=0.37, p=0.001) and several markers of hemolysis, including LDH (r=0.46, p=0001), Hb (r=-0.32, p=0.005), retic (r=0.29, p=0.013), plasma Hb (r=0.27, p=0.03) and AST (r=0.38, p=0.001). Using Student’s t-test for independent samples, only TRJV (2.55±0.33 vs. 2.34±0.26 m/s, p=0.006), LDH (450±166 vs. 329±143 U/L, p=0.001), WBC (10.6±4.7 vs. 8.6±3.3×109/L, p=0.048), retic (14.4±9.2 vs. 10.6±6.1%, p=0.039) and AST (50±22 vs. 38±15 U/L, p=0.009) were significantly higher and Hb (9.1±1.3 vs. 9.9±1.7 g/dL, p=0.04) lower in subjects with QTc &gt; 440 ms compared to those with QTc ≤ 440 ms. We found no significant relationship between QTc and age, LV mass, platelet count or fetal Hb. By χ2 analysis, a larger proportion of subjects with QTc &gt; 440 ms also had a history of acute chest syndrome (p=0.007), gallstones (p=0.047), exchange transfusion (p=0.04) and to a less significant degree, TRJV elevation (p=0.112). Prolonged QTc was not affected by sex, hydroxyurea use or a history of LVH, frequent pain, asthma, splenectomy, priapism and tonsilloadenoidectomy. Given sample size limitations and data reduction methods, we found by logistic regression analysis that the combination of TRJV and history of acute chest syndrome best predicted QTc prolongation, correctly identifying 80% of cases and resulting in positive and negative predictive values of 76% and 81%, respectively. Conclusions We conclude that QTc prolongation is common in a prospectively screened cohort of young sickle cell patients at baseline and is associated with evidence of hemolysis and to a lesser degree, TRJV elevation. Our results contrast with findings in other conditions that link QTc prolongation primarily to LVH. Future studies will be critical to further define QTc variability, pathophysiologic determinants as well as the clinical consequences of conduction abnormalities, which may or may not relate to TRJV elevation, in the sickle cell population.


Author(s):  
John R. Giudicessi ◽  
Matthew Schram ◽  
J. Martijn Bos ◽  
Connor D. Galloway ◽  
Jacqueline B. Shreibati ◽  
...  

Background: Heart rate-corrected QT interval (QTc) prolongation, whether secondary to drugs, genetics including congenital long QT syndrome (LQTS), and/or systemic diseases including SARS-CoV-2-mediated COVID19, can predispose to ventricular arrhythmias and sudden cardiac death. Currently, QTc assessment and monitoring relies largely on 12-lead electrocardiography. As such, we sought to train and validate an artificial intelligence (AI)-enabled 12-lead electrocardiogram (ECG) algorithm to determine the QTc, and then prospectively test this algorithm on tracings acquired from a mobile ECG (mECG) device in a population enriched for repolarization abnormalities. Methods: Using over 1.6 million 12-lead ECGs from 538,200 patients, a deep neural network (DNN) was derived (n = 250,767 patients for training and n = 107,920 patients for testing) and validated (n = 179,513 patients) to predict the QTc using cardiologist over-read QTc values as the gold standard. The ability of this DNN to detect clinically-relevant QTc prolongation (e.g. QTc ≥ 500 ms) was then tested prospectively on 686 genetic heart disease (GHD) patients (50% with LQTS) with QTc values obtained from both a 12-lead ECG and a prototype mECG device equivalent to the commercially-available AliveCor KardiaMobile 6L. Results: In the validation sample, strong agreement was observed between human over-read and DNN-predicted QTc values (-1.76 ± 23.14 ms). Similarly, within the prospective, GHD-enriched dataset, the difference between DNN-predicted QTc values derived from mECG tracings and those annotated from 12-lead ECGs by a QT expert (-0.45 ± 24.73 ms) and a commercial core ECG laboratory [+10.52 ms ± 25.64 ms] was nominal. When applied to mECG tracings, the DNN's ability to detect a QTc value ≥ 500 ms yielded an area under the curve, sensitivity, and specificity of 0.97, 80.0%, and 94.4%, respectively. Conclusions: Using smartphone-enabled electrodes, an AI-DNN can predict accurately the QTc of a standard 12-lead ECG. QTc estimation from an AI-enabled mECG device may provide a cost-effective means of screening for both acquired and congenital LQTS in a variety of clinical settings where standard 12-lead electrocardiography is not accessible or cost-effective.


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.


2018 ◽  
Vol 25 (8) ◽  
pp. 2004-2006 ◽  
Author(s):  
Jessica J Tilton ◽  
Rozhan Sadr ◽  
Vicki L Groo

Prolongation of the corrected QT interval can lead to the deadly arrhythmia torsades de pointes. There are many risk factors for corrected QT prolongation, one being medication. The goal of this case report is to add to the limited literature surrounding the possibility of torsades de pointes when levofloxacin and fluconazole are used concomitantly. Additionally, provide guidance for patient factors that need to be assessed when prescribing the two drugs.


2021 ◽  
Vol 8 (3) ◽  
pp. 369
Author(s):  
Sami M. Alrasheedi ◽  
Bader Alothman ◽  
Ayman Alharbi ◽  
Ahmad Alkhdairi ◽  
Mohammed Zeitouni ◽  
...  

Background: The long QT syndrome is characterized by prolongation of QT interval, which may lead to life-threatening cardiac arrhythmias. Objectives were to assess prevalence, quantity and severity of QTc prolongation with combined drugs (azithromycin and hydroxychloroquine) in adults COVID-19 patients treated on these agents at KFSHRC. And to characterize cardiac complications of QTc prolongation with combined drugs.Methods: A retrospective cohort study at KFSH&RC, in Riyadh, Saudi Arabia. Baseline and daily ECG was done until completion of duration as per KFSH&RC guidelines for management of Covid-19, QTc prolongation>500 or increase of at least 60 ms compared with the pre-drug baseline value, or presence of cardiac conductive complications (torsades de pointes). The QTc prolongation was defined as>470 for male and >480 for female as per American Heart Association. A risk score that has been validated by Tisdale et al, for prediction of QT prolongation drug-related in admitted patients in cardiac care unit. The study duration was specified as one month after study approval by Research Ethics committee.Results: A total of 74 patients were included in the study. The patients were distributed according to their risk score for prediction of QT prolongation as the following: low (67/74), medium (6/74), high (1/74). Two patients with medium risk were started on both azithromycin and hydroxychloroquine. one of them his baseline QT was 490, Azithromycin was stopped as QT reached 502. The second patient has QT baseline 471, after starting treatment; QT range was 472-475, hydroxychloroquine was stopped on day 4. None of them had torsades de pointes. Only one patient with low risk, no baseline QT was recorded, but QT was 499 on day three, so hydroxychloroquine was stopped. Repeated ECG showed: QT decreased to 478, no torsades de pointes.  Conclusions: In this single centered-retrospective cohort, we noticed that a small percentage of patients developed QT prolongation with the use of this combination. With the increasing the risk of developing QT prolongation the number of the patient who developed the condition increased. We used Tisdale score which is a scoring system Identifying hospitalized patients at risk for QT interval prolongation could lead to interventions to reduce the risk of torsades de pointes validated in May 2013.5 None of our population developed significant cardiac complications of QTc prolongation with combined drugs.


2000 ◽  
Vol 136 (3) ◽  
pp. 404-407 ◽  
Author(s):  
Ta Cheng Huang ◽  
Frank C. Cecchin ◽  
Patrick Mahoney ◽  
Michael A. Portman

1993 ◽  
Vol 11 (10) ◽  
pp. 1906-1910 ◽  
Author(s):  
C L Schwartz ◽  
W L Hobbie ◽  
S Truesdell ◽  
L C Constine ◽  
E B Clark

PURPOSE Comprehensive cardiac evaluations are currently recommended for all anthracycline-treated patients to detect subclinical cardiac failure. A screening test is needed that would easily and inexpensively identify patients who are at risk for late cardiac decompensation. METHODS We routinely reviewed the ECG and echocardiogram (ECHO) results of 52 of 56 anthracycline-treated long-term survivors of childhood cancer who had received > or = 100 mg/m2 of ANTH (ANTH = 1 mg/m2 of doxorubicin), and who were not in clinical heart failure. Exercise testing was performed in eight patients with a corrected QT interval (QTc) of > or = 0.43. RESULTS Zero of 15 patients (without chest radiation) who received less than 300 mg/m2 of ANTH versus six of 22 who received > or = 300 mg/m2 of ANTH had a QTc > or = 0.43 (P = .03). Three of 15 patients (with chest radiation) who received less than 300 mg/m2 of ANTH versus 12 of 22 who received > or = 300 mg/m2 of ANTH had a QTc > or = 0.43 (P = .03). For all patients (including those with chest radiotherapy), zero of 19 who received less than 300 mg/m2 of ANTH versus eight of 33 who received > or = 300 mg/m2 of ANTH had a QTc of > or = 0.45 (P = .025). Three of 19 who received less than 300 mg/m2 of ANTH versus 19 of 33 who received > or = 300 mg/m2 of ANTH had a QTc of > or = 0.43 (P = .003). One patient had decreased fractional shortening (FS) and QTc prolongation. Cardiac decompensation (with a FS of 24%) occurred with propranolol in a patient with previously normal FS but prolonged QTc. With exercise, the QTc became further prolonged in all four patients with a QTc of 0.44 to 0.46 and in two of four patients with a QTc of 0.43. CONCLUSION Prolongation of the QTc, a measure of myocardial repolarization, may reflect injury to myocardial cells. QTc prolongation may be predictive of an increased risk of late cardiac decompensation. If the utility of the QTc measure is confirmed, screening for evidence of myocardial damage can be easily and inexpensively performed by oncologists and primary caretakers.


Author(s):  
Archana Ramireddy ◽  
Harpriya Chugh ◽  
Kyndaron Reinier ◽  
Joseph Ebinger ◽  
Eunice Park ◽  
...  

ABSTRACTBackgroundDespite a paucity of clinical evidence, hydroxychloroquine and azithromycin are being administered widely to patients with verified or suspected COVID-19. Both drugs may increase risk of lethal arrhythmias associated with QT interval prolongation.MethodsWe performed a case series of COVID-19 positive/suspected patients admitted between 2/1/2020 and 4/4/2020 who were treated with azithromycin, hydroxychloroquine or a combination. We evaluated baseline and post-medication QT interval (QTc, Bazett’s) using 12-lead ECGs. Critical QTc prolongation was defined as: a) maximum QTc ≥500 ms (if QRS <120 ms) or QTc ≥550 (if QRS ≥120 ms) and b) increased QTc of ≥60 ms. Tisdale score and Elixhauser comorbidity index were calculated.ResultsOf 490 COVID-19 positive/suspected patients, 314 (64%) received either/both drugs, and 98 (73 COVID-19 positive, 25 suspected) met study criteria (age 62±17 yrs, 61% male). Azithromycin was prescribed in 28%, hydroxychloroquine in 10%, and both in 62%. Baseline mean QTc was 448±29 ms and increased to 459±36ms (p=0.005) with medications. Significant prolongation was observed only in men (18±43 ms vs -0.2±28 ms in women, p=0.02). 12% of patients reached critical QTc prolongation. In a multivariable logistic regression, age, sex, Tisdale score, Elixhauser score, and baseline QTc were not associated with critical QTc prolongation (p>0.14). Changes in QTc were highest with the combination compared to either drug, with many-fold greater prolongation with the combination vs. azithromycin alone (17±39 vs. 0.5±40 ms, p=0.07). No patients manifested torsades de pointes.ConclusionsOverall, 12% of patients manifested critical QTc interval prolongation, and traditional risk indices failed to flag these patients. With the drug combination, QTc prolongation was several-fold higher compared to azithromycin alone. The balance between uncertain benefit and potential risk when treating COVID-19 patients with these drugs should be carefully assessed prior to use.


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