Electrocardiographic Abnormalities, Malignant Ventricular Arrhythmias, and Cardiomyopathy Associated With Loperamide Abuse.

A 20-year-old man presented with recurrent syncope and abnormal electrocardiogram (ECG). His evaluation revealed a prolonged QT interval >600 milliseconds, witnessed torsades de pointes (TdP), and dilated cardiomyopathy. At his initial admission, an ICD was implanted and atrial pacing at 80 beats per minute suppressed ventricular arrhythmias. The patient was readmitted with device infection and recurrent TdP leading to intubation. This led to the discovery of a hitherto unrevealed loperamide abuse and his cardiac arrhythmias and LV dysfunction were determined to be related to large doses of loperamide. Following abstinence, his ejection fraction and ECG returned to normal.

Long QT Syndrome With Drugs Used in the Management of Arrhythmias: A Systematic Review.

Long QT syndrome (LQTS) is a severe cardiac disorder characterized by an abnormally prolonged QTc interval on an electrocardiogram (ECG), which can result in life-threatening irregular heart rhythms. The use of certain medications, particularly anti-arrhythmic drugs such as quinidine, sotalol, and amiodarone, can lead to acquired LQTS by prolonging the QT interval through the inhibition of specific ion channels responsible for heart repolarization, which may present symptoms like fainting, seizures, and sudden cardiac arrest. This systematic review, conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines, focused on analyzing the association between Long QT syndrome and drugs utilized for managing arrhythmias, involving a thorough examination of six selected studies from an initial pool of 68 articles. It was found that antiarrhythmic drugs such as amiodarone, sotalol, dofetilide, procainamide, quinidine, and flecainide have the potential to cause QT prolongation as a side effect, which is often influenced by factors including dosage, coexisting medical conditions, electrolyte imbalances, and other risk factors. Prolonged QT interval significantly elevates the risk of a life-threatening arrhythmia called torsade de pointes. The management of this side effect typically involves reducing the medication dosage or discontinuing it altogether and, in some cases, employing selective beta blockers. However, further research is essential to improve the understanding and implementation of strategies to prevent and manage QT prolongation caused by antiarrhythmic drugs. Additional clinical studies are warranted to enhance knowledge and provide comprehensive guidelines to healthcare practitioners regarding the appropriate use of these medications. Close monitoring of the QT interval is recommended for patients receiving anti-arrhythmic therapy, and consideration should be given to patient-specific risk factors for LQTS, including age, sex, and electrolyte imbalances.

QT Prolongation Preceding Ventricular Fibrillation After Amiodarone Administration: A Case Report.

Atrial fibrillation (AF) is the most common long-term arrhythmia in adults. Rhythm control in patients with AF involves efforts to restore and maintain sinus rhythm and is accomplished by medication, catheter ablation, or electrical cardioversion. Amiodarone represents one of the most commonly used antiarrhythmic medications. Prolonged use of amiodarone can lead to many side effects. One of the most severe side effects is drug-induced long QT syndrome (LQTS), which can cause malignant arrhythmias and sudden cardiac death. We presented a case of a 52-year-old male who was admitted to the Coronary Unit due to first diagnosed AF with a rapid ventricular response. After amiodarone infusion was administrated the patient lost consciousness and the monitor displayed torsades de pointes (TdP) ventricular tachycardia with rapid conversion to ventricular fibrillation (VF). Cardiac resuscitation with two direct current (DC) shocks was performed. The patient was stabilized, and restoration of sinus rhythm with significant QT prolongation on the ECG was noted. This is a rare case of short-term amiodarone administration causing LQTS, TdP, and VF. The findings or observations emphasize the significance of diligent ECG monitoring during amiodarone treatment.

High-Degree Atrioventricular Block and Torsades De Pointes in Severe Aortic Stenosis Treated With Transcatheter Aortic Valve Replacement.

Severe aortic stenosis (AS) significantly elevates cardiovascular risk, predisposing patients to high-degree atrioventricular (AV) block and life-threatening tachyarrhythmias, including torsades de pointes (TdP). This case report presents a patient with severe AS who developed high-degree AV block and, subsequently, TdP, highlighting the interplay between bradycardia and mechanisms that trigger ventricular tachycardias. The case underscores the importance of identifying and managing these risk factors to improve patient outcomes.

Development of a pharmaceutical database as an aid to the nonclinical detection of drug-induced cardiac toxicity.

The Health and Environmental Sciences Institute (HESI) Cardiac Safety Committee designed and created a publicly accessible database with an initial set of 128 pharmacologically defined pharmaceutical agents, many with known cardiotoxic properties. The database includes specific information about each compound that could be useful in evaluating hypotheses around mechanisms of drug-induced cardiac toxicity or for development of novel cardiovascular safety assays. Data on each of the compounds was obtained from published literature and online sources (e.g., DrugBank.ca and International Union of Basic and Clinical Pharmacology (IUPHAR) / British Pharmacological Society (BPS) Guide to PHARMACOLOGY) and was curated by 10 subject matter experts. The database includes information such as compound name, pharmacological mode of action, characterized cardiac mode of action, type of cardiac toxicity, known clinical cardiac toxicity profile, animal models used to evaluate the cardiotoxicity profile, routes of administration, and toxicokinetic parameters (i.e., Cmax). Data from both nonclinical and clinical studies are included for each compound. The user-friendly web interface allows for multiple approaches to search the database and is also intended to provide a means for the submission of new data/compounds from relevant users. This will ensure that the database is constantly updated and remains current. Such a data repository will not only aid the HESI working groups in defining drugs for use in any future studies, but safety scientists can also use the database as a vehicle of support for broader cardiovascular safety studies or exploring mechanisms of toxicity associated with certain pharmacological modes of action.

Loperamide-induced cardiogenic syncope: a case report of a life-threatening presentation of an over-the-counter drug.

Background: Loperamide at supratherapeutic doses can cause cardiac toxicity, presenting as cardiogenic shock, prolonged QT, malignant arrhythmias, or in severe cases sudden cardiac death. Surreptitious loperamide use is difficult to diagnose. We present an interesting case of loperamide use presenting with polymorphic ventricular tachycardia, cardiogenic shock. Case summary: A 25-year-old female presented with multiple syncopal episodes for 12 months with an electrocardiogram showing a Brugada-like pattern for which she underwent implantable cardioverter-defibrillator placement. One day following the procedure, she developed cardiogenic shock and was transferred to our tertiary care centre. Extensive workup was unrevealing. She responded well to supportive management, recovering from shock and was transferred to the floor. Unfortunately, she again developed cardiogenic shock, ultimately leading to cardiac arrest. Given the unclear cause for her cardiovascular symptoms, futher medication history was obtained. It was revealed that she was taking 100-150 tablets of loperamide per day. The decision was made to treat with intralipid emulsion therapy empirically given the strong suspicion for loperamide toxicity. The patient recovered well with supportive care. Loperamide levels returned elevated at 190 ng/mL. Repeated studies showed improvement of the conduction block, resolution of arrhythmias, and recovery of right and left ventricular function. Discussion: Acute loperamide toxicity can present as biventricular failure, with difficult-to-control arrhythmias. It requires a high index of suspicion. Treatment for loperamide toxicity is mainly supportive, lipid emulsion therapy can be considered in severe or refractory cases.

A Rare Presentation of Levetiracetam-Induced Torsades De Pointes.

Torsades de pointes occurs in the presence of a prolonged QTc interval, which has many congenital and acquired causes. Levetiracetam is a widely used anti-epileptic medication secondary to its favorable safety profile. We present a rare case of a 59-year-old male who developed torsades de pointes and cardiac arrest after levetiracetam administration. To our knowledge, there is only one other case report documenting torsades de pointes after levetiracetam administration, and our case report will be the first documenting cardiac arrest after levetiracetam administration.

Close Call From a Sweet Twist: A Case of Licorice-Induced Torsades De Pointes.

Torsades de pointes (TdP) is a life-threatening cardiac arrhythmia that can result from QT interval prolongation, sometimes secondary to medication adverse effects and electrolyte derangements. We present a 95-year-old Hispanic male with advanced chronic kidney disease (CKD) that was evaluated for dizziness and progressive weakness. The diagnosis of severe symptomatic hypokalemia and QT prolongation was made, and the patient was admitted for telemetry monitoring and aggressive intravenous electrolyte replacements. While under observation, the patient experienced syncope due to ventricular tachycardia (VT) with episodes of torsades de pointes. Due to refractory potassium depletion and hypertension, workup for hyperaldosteronism revealed renal potassium wasting, inappropriately normal plasma renin levels, and almost undetectable aldosterone levels. Careful analysis revealed the excessive chronic daily ingestion of licorice-containing candy twists and tea, which may cause pseudohyperaldosteronism. Licorice is a commonly used natural product that is available in many forms. It is sometimes used as a natural supplement and as a sweetener that can be widely found in many food products. Excessive ingestion can lead to apparent mineralocorticoid excess, reduced plasma potassium, sodium retention, hypertension, and metabolic alkalosis. Hypokalemia can be severe in some patients and lead to fatal cardiac arrhythmias such as ventricular tachycardia and torsades de pointes. Careful analysis is essential in cases of refractive hypokalemia and renal potassium wasting, especially in elderly patients with underlying renovascular disease.

Heart's Dangerous Symphony: Torsade De Pointes Unleashed by Gitelman Syndrome-Induced Hypomagnesemia.

Gitelman syndrome (GS) is a rare autosomal recessive salt-losing renal tubular disorder associated with a mutation of SLC12A3 or CLCNKB genes which encodes the thiazide-sensitive sodium-chloride co-transporter (NCCT) in the distal renal tubule. It is inherited as an autosomal recessive disorder. Hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and renin-angiotensin-aldosterone system (RAAS) activation are characteristics of GS. GS is often misdiagnosed or underdiagnosed owing to its low incidence and lack of awareness. Its prevalence is estimated to be around 1-10 per 40,000 people. We report a case of cardiac arrest secondary to torsade de pointes (TdP) because of GS-induced hypomagnesemia. Our case highlights the importance of clinicians being aware of the potential electrolyte abnormalities and complications associated with GS, as it can lead to catastrophic consequences if not identified and corrected earlier.

qInward variability-based in-silico proarrhythmic risk assessment of drugs using deep learning model.

Many researchers have suggested evaluation methods and Torsades de Pointes (TdP) metrics to assess the proarrhythmic risk of a drug based on the in silico simulation, as part of the Comprehensive in-vitro Proarrhythmia Assay (CiPA) project. In the previous study, we validated the robustness of 12 in silico features using the ordinal logistic regression (OLR) model by comparing the classification performances of metrics according to the in-vitro experimental datasets used; however, the OLR model using 12 in silico features did not provide desirable results. This study proposed a convolutional neural network (CNN) model using the variability of promising in silico TdP metrics hypothesizing that the variability of in silico features based on beats has more information than the single value of in silico features. We performed the action potential (AP) simulation using a human ventricular myocyte model to calculate seven in silico features representing the electrophysiological cell states of drug effects over 1,000 beats: qNet, qInward, intracellular calcium duration at returning to 50% baseline (CaD50) and 90% baseline (CaD90), AP duration at 50% repolarization (APD50) and 90% repolarization (APD90), and dVm/dtMax_repol. The proposed CNN classifier was trained using 12 train drugs and tested using 16 test drugs among CiPA drugs. The torsadogenic risk of drugs was classified as high, intermediate, and low risks. We determined the CNN classifier by comparing the classification performance according to the variabilities of seven in silico biomarkers computed from the in silico drug simulation using the Chantest dataset. The proposed CNN classifier performed the best when using qInward variability to classify the TdP-risk drugs with 0.94 AUC for high risk and 0.93 AUC for low risk. In addition, the final CNN classifier was validated using the qInward variability obtained after merging three in-vitro datasets, but the model performance decreased to a moderate level of 0.75 and 0.78 AUC. These results suggest the need for the proposed CNN model to be trained and tested using various types of drugs.

The Challenges of Predicting Drug-Induced QTc Prolongation in Humans.

The content of this article derives from a Health and Environmental Sciences Institute (HESI) consortium with a focus to improve cardiac safety during drug development. A detailed literature review was conducted to evaluate the concordance between nonclinical repolarization assays and the clinical thorough QT (TQT) study. Food and Drug Administration and HESI developed a joint database of nonclinical and clinical data, and a retrospective analysis of 150 anonymized drug candidates was reviewed to compare the performance of 3 standard nonclinical assays with clinical TQT study findings as well as investigate mechanism(s) potentially responsible for apparent discrepancies identified. The nonclinical assays were functional (IKr) current block (Human ether-a-go-go related gene), action potential duration, and corrected QT interval in animals (in vivo corrected QT). Although these nonclinical assays demonstrated good specificity for predicting negative clinical QT prolongation, they had relatively poor sensitivity for predicting positive clinical QT prolongation. After review, 28 discordant TQT-positive drugs were identified. This article provides an overview of direct and indirect mechanisms responsible for QT prolongation and theoretical reasons for lack of concordance between clinical TQT studies and nonclinical assays. We examine 6 specific and discordant TQT-positive drugs as case examples. These were derived from the unique HESI/Food and Drug Administration database. We would like to emphasize some reasons for discordant data including, insufficient or inadequate nonclinical data, effects of the drug on other cardiac ion channels, and indirect and/or nonelectrophysiological effects of drugs, including altered heart rate. We also outline best practices that were developed based upon our evaluation.

Frequent torsades de pointes in a child with novel AKAP9 mutation: A case report and literature review.

Introduction: The aim of the present study is to report the diagnosis and treatment of a rare case of frequent torsades de pointes (Tdp) in a child with a novel AKAP9 mutation. A 13-year-old girl suffered from repeated syncope and frequent Tdp. An electrocardiogram (ECG) showed frequent multisource premature ventricular contractions with the R-ON-T phenomenon. The QTc ranged from 410 to 468 ms. The genetic test indicated a heterozygous mutation, namely, c.11714T > C (p.M3905T), in the AKAP9 gene, which is a controversial gene in long QT syndrome. After treatment with propranolol, recurrent syncope occurred, and the patient received an implantable cardioverter defibrillator (ICD). Due to frequent electrical storms at home, the child was additionally treated with propafenone to prevent arrhythmia. The antitachycardia pacing (ATP) function in the ICD was turned off, and the threshold of ventricular tachycardia (VT) assessment was adjusted from 180 beats/min to 200 beats/min. The patient was followed up for 12 months without malignant arrhythmia and electric shock. Conclusion: Genetic testing may be a useful tool to determine the origin of channelopathy, but the results should be interpreted in combination with the actual situation. Rational parameter settings for the ICD and application of antiarrhythmic drugs can reduce the mortality rates of children.

Diagnosing Torsades De Pointes Based on Correlation to QT Interval: A Systematic Review.

Torsades de Pointes (TdP) is a rare form of tachyarrhythmia which can potentially be fatal due to its tendency to degenerate into ventricular fibrillation. It is described as a polymorphic ventricular tachycardia characterized by twisting of the QRS complexes around the electrocardiogram (ECG) baseline in patients with a prolonged QT interval. Prolonged QT interval is known as long QT syndrome. Torsades de Poccurs most commonly in patients with an extended QT interval duration, and even though monitoring an ECG can assist in its prevention, there is no defined duration of a QT interval that can lead to an increased risk of Torsades de Pointes. So, it is hard to determine what QT interval constitutes enough risk for Torsades de Pointes to require intervention. The QT interval duration also depends on other factors, namely heart rate (HR) and other factors such as drugs, congenital diseases, and a combination of both. In this study, we considered various causes of QT prolongation but mainly focused on congenital diseases, drugs, or perioperative risk of QT prolongation and the correlation with the risk of impending TdP. By following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and researching studies on various databases, namely PubMed, Science Direct, Medline, and CiNii we were able to find various systematic reviews and articles showing the association between prolonged QT interval and its degeneration into TdP. This review encourages further research into this topic to understand the implications of QT prolongation and how it can help save the lives of patients with known long QT syndrome, or those on QT prolonging drugs with simple ECG monitoring and treatment for the respective cause.

Torsades de Pointes With a Normal Magnesium Level in the Setting of Short Bowel Syndrome.

Torsades de pointes (TdP) is a potentially fatal arrhythmia, typically presenting with a congenital or acquired etiology. Low serum magnesium level is a known cause leading to this arrhythmia. However, it has been found that even in the setting of a normal serum magnesium level and with no other foreseeable etiology, TdP may still occur, especially in those with chronic electrolyte deficiencies. TdP may be treated in a number of ways, including IV magnesium sulfate or defibrillation if the patient becomes unresponsive and hemodynamically unstable. In some cases, atrial overdrive is required with the use of isoproterenol. A final decision, however, would necessitate asking if the patient can be sent home on medical management to prevent recurrence of the arrhythmia or require placement of a permanent pacemaker. Here, we describe a patient developing recurrent TdP despite normal serum magnesium level in the setting of short bowel syndrome.

Pathogenesis of Ventricular Arrhythmias and Its Effect on Long-Term Prognosis in Patients With Takotsubo Cardiomyopathy.

Takotsubo cardiomyopathy (TTC), also known as broken heart syndrome, stress cardiomyopathy (SCM), or apical ballooning syndrome, is a non-ischemic cardiac disease with an initial clinical presentation that is very similar to acute coronary syndrome (ACS). Ventricular arrhythmias (VAs) contribute significantly to an increase in the rates of death in patients with TTC, especially during the acute phase, in which patients with TTC are more susceptible to develop life-threatening arrhythmias (LTA) such as ventricular tachycardia (VT), ventricular fibrillation (VF), torsades de pointes (TdP), and sudden cardiac death (SCD). However, the pathophysiology of TTC and how VA occurs are still a mystery. We aim to review previous literature and discuss the possible mechanisms of VA in TTC patients. VA usually complicates the acute phase of the disease and worsens the long-term prognosis. Alterations of repolarization (negative T wave, prolonged QTc) indicate a high risk of arrhythmic events (TdP, VT, VF, and SCD). Catecholamine effect on myocardial cells and myocardial edema can create a substrate for the development of VA. Some of the most commonly proposed mechanisms for the development of VA in patients with TTC are coronary vasospasm, myocardial stunning due to catecholamines, re-entry, and triggered activity. Further prospective studies, including a more significant number of patients, are required to understand the disease's pathophysiology better and improve LTA management in patients with TTC.

A Retrospective Analysis of Hospital Electrocardiogram Auto-Populated QT Interval Calculation.

Background The current electrocardiogram (ECG) standard for rate correction of the QT interval (QTc) is a power function known as the Bazett formula (QTcB). QTc formulae are either power functions or linear functions. QTcB is known to lack reliability, as heart rate (HR) rises from or falls below 60 beats per minute (bpm). The American Heart Association (AHA), the American College of Cardiology Foundation (ACCF), and the Heart Rhythm Society (HRS) have recommended using other formulae in place of QTcB since 2009. The Epic Electronic Health Record System (Epic Systems Corporation, Verona, WI) automatically populates the Fridericia formula (QTcFri) on hospital ECG reports without any provider calculation. Methods We aimed to retrospectively investigate the effect of QTcFri on one year of ECGs in the Epic Electronic Health Record (EHR) at a single tertiary care center. Inclusion criteria for ECG reports specified HR 60-120 bpm without QRS duration > 120 ms. Gathered data from Epic EHR ECG reports included patient age, sex, HR, QRS duration (QRSd), QT interval, QTcB, and QTcFri. EHR documented 61,946 ECG reports for the year, with 44,566 meeting criteria for inclusion. General statistical methods included range, median, mean, and standard deviation. Confidence intervals were assessed to maintain the fidelity of analysis. The normality of data distribution was assessed with Kolmogorov-Smirnov testing. The Wilcoxon rank-sum test was then performed to confirm a statistically significant difference between the Bazett and Fridericia formulae. The ∆QTc analysis was conducted on prolonged QTc (males > 450 ms; females > 460 ms) and severely prolonged QTc > 500 ms data subsets. A value of p<0.05 was interpreted as significant. Statistical analysis was performed using SPSS statistical software (IBM Statistics, v. 26; IBM Corp, Armonk, NY). Results The 44,566 ECG reports demonstrated 57% female gender and a mean age of 57 ± 17.5 years. The mean HR was 83 ± 14.7 bpm and the mean ∆QTc was 23 ± 12.9 ms shorter with QTcFri. Mean data showed minimal variation between sexes: age, heart rate, uncorrected QT, QTcB, QTcFri, and ∆QTc varied by less than 2%. Mean QRS varied by 4% between sexes. The Wilcoxon rank-sum test revealed 44,127 ranks with a negative difference, 0 ranks with a positive difference, and 439 ties, p <0.001 (99% CI: 22.5 ms, 23.0 ms). QTcB identified 37.4% (16665/44566) ECGs prolonged. Using QTcFri, 21% (9371/44566) of the total ECGs corrected to normal QTc (<450 ms (men) and 460 ms (women)). QTcFri use reduced the number of ECG reports with QTc > 500 ms by 57.3%. A total of 125 ECG reports, 117 females and eight males, corrected to normal gender-specific QTc with QTcFri. The mean decrease in QTc with the Fridericia formula when QTcB > 500 ms was 31 ± 14.5 ms (99% CI: 30.4 ms, 31.7 ms). Conclusion Our data from the Wilcoxon rank-sum analysis indicated that the EHR QTcFri analysis yields a statistically significant difference (p < 0.001) in QTc calculation of 22 ms over 44,566 ECG reports. The data showed a 21% reduction in inaccurately documented test results. The utilization of this resource will provide the most accurate and clinically relevant data to inform clinical decision-making. Accurate QT interval calculation will better inform downstream clinical decision-making through a wider scope of therapeutic intervention. This analysis is readily available to clinicians without calculation and its awareness will benefit patient care.

Shock From Twisting Peaks: A Rare Case of Recurrent Torsades de Pointes Secondary to Leuprolide-Induced Prolonged QT.

Leuprolide acetate is a synthetic nonpeptide analog that is a potent gonadotropin-releasing hormone receptor agonist. It is used in diverse clinical applications, including treatment for prostate cancer, endometriosis, and uterine fibroids as well as the in vitro fertilization technique. Prolonged QT interval leading to torsades de pointes (TdP) is one of the very rare side effects of leuprolide therapy. Herein, we report a 68-year-old male patient with a history of prostate cancer post-radiation and on androgen suppression therapy with leuprolide who suffered from out-of-hospital cardiac arrest. After initial resuscitation, the patient's electrocardiogram (ECG) showed a prolonged corrected QT interval (QTc), which subsequently progressed into a TdP rhythm, requiring lidocaine drip initially. The patient's symptoms improved, and his ECG rhythm was resolved after initiating mexiletine and propranolol treatment with no recurrent TdP episodes after discontinuation of leuprolide.

Electrophysiological characterization of drug response in hSC-derived cardiomyocytes using voltage-sensitive optical platforms.

INTRODUCTION: Voltage-sensitive optical (VSO) sensors offer a minimally invasive method to study the time course of repolarization of the cardiac action potential (AP). This Comprehensive in vitro Proarrhythmia Assay (CiPA) cross-platform study investigates protocol design and measurement variability of VSO sensors for preclinical cardiac electrophysiology assays. METHODS: Three commercial and one academic laboratory completed a limited study of the effects of 8 blinded compounds on the electrophysiology of 2 commercial lines of human induced pluripotent stem-cell derived cardiomyocytes (hSC-CMs). Acquisition technologies included CMOS camera and photometry; fluorescent voltage sensors included di-4-ANEPPS, FluoVolt and genetically encoded QuasAr2. The experimental protocol was standardized with respect to cell lines, plating and maintenance media, blinded compounds, and action potential parameters measured. Serum-free media was used to study the action of drugs, but the exact composition and the protocols for cell preparation and drug additions varied among sites. RESULTS: Baseline AP waveforms differed across platforms and between cell types. Despite these differences, the relative responses to four selective ion channel blockers (E-4031, nifedipine, mexiletine, and JNJ 303 blocking IKr, ICaL, INa, and IKs, respectively) were similar across all platforms and cell lines although the absolute changes differed. Similarly, four mixed ion channel blockers (flecainide, moxifloxacin, quinidine, and ranolazine) had comparable effects in all platforms. Differences in repolarisation time course and response to drugs could be attributed to cell type and experimental method differences such as composition of the assay media, stimulated versus spontaneous activity, and single versus cumulative compound addition. DISCUSSION: In conclusion, VSOs represent a powerful and appropriate method to assess the electrophysiological effects of drugs on iPSC-CMs for the evaluation of proarrhythmic risk. Protocol considerations and recommendations are provided toward standardizing conditions to reduce variability of baseline AP waveform characteristics and drug responses.

The Identification of Torsades de Pointes via CEEG: A Case Report on a Patient with Physiologically Provoked Nonepileptic Events.

Continuous electroencephalography (CEEG) is chiefly performed at The Medical University of South Carolina (MUSC) for identifying seizures, including its refined use within the epilepsy monitoring unit (EMU) as a differentiator between epileptic and psychogenic etiologies. CEEG also provides critical data that carry implications outside the bounds of both epilepsy and psychogenic events, such as the characterization of unorthodox clinical phenomena that are of physiological (though nonepileptic) origins. Although nonepileptic events (NEEs) are primarily linked with psychogenic phenomena (conversion disorder, malingering) that can mimic epileptic activity, they, like seizures, have diverse semiologies and etiologies. Although it is reasonable for seasoned neurodiagnostics professionals to develop an expectation that NEEs are of psychogenic origin, it is essential to acknowledge that they include etiologies that lay beyond those of psychiatric influence. Such a case is presented in which a 74-year-old female patient who, though initially suspected of having either psychogenic or epileptic seizures, was found to be having frequent episodes of the life-threatening cardiac convulsive syncope torsades de pointes (TdP). The patient had several known risk factors for TdP, including a prolonged QT complex, female gender, advancing age, active medications known to provoke TdP, and electrolyte imbalances (low magnesium and potassium) (Trinkley et al. 2013). TdP was first suspected through the CEEG by a combination of remarkable EEG background changes, recorded video evidence of clinical features, and accompanying single-lead electrocardiogram (ECG) data captured during the events. Upon proper diagnosis, the patient was urgently treated with restorative measures, including electrolyte replenishment, pacemaker implantation, and cessation of provocative medications.