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A 93-year-old man was admitted to our hospital with complaints of pain and coldness in both lower legs. He was diagnosed with arterial occlusive disease of the lower extremities. There were no obvious stenosis or occlusion of lower extremity arteries, which would be indications for surgery, and drug therapy was started. On the 8th day of hospitalization, after complaining of feeling unwell, polymorphic ventricular tachycardia appeared in a few seconds and the electrocardiogram (ECG) showed shark fin like ST-segment elevation in the leads V1–6. Echocardiography demonstrated akinesis in the anterior septum and akinesis from middle to apical anterior left ventricular wall, which suggested acute coronary syndrome. Emergency coronary angiography was performed and no obvious severe stenosis, thrombus, or dissection was observed on intravascular ultrasonography and changes due to ischemic heart disease were judged to be negative. Left ventricular angiography confirmed decreased wall motion throughout the apex, and the patient was considered to have takotsubo syndrome. Echocardiography on the 20th day of hospitalization showed that the wall motion abnormality had improved except the apex, and the ECG showed negative T wave conversion. The patient was discharged on the 33rd day of hospitalization. This case highlights the diverse electrocardiographic manifestations of takotsubo syndrome (TTS). In particular, rare electrocardiographic changes were observed in an elderly male patient with TTS. [ABSTRACT FROM AUTHOR]

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

Abstract Background Takotsubo cardiomyopathy is a novel form of rapidly reversible heart failure occurring secondary to a stressor that mimics an acute coronary event. The underlying etiology of the stressor is highly variable and can include medical procedures. Pacemaker insertion is an infrequent cause of Takotsubo cardiomyopathy. Case presentation An 86-year-old Caucasian woman underwent an uncomplicated pacemaker insertion for symptomatic complete heart block in the background of slow atrial fibrillation. A transient episode of polymorphic ventricular tachycardia was noted on day 1 following the procedure; however, her pacemaker was checked and, as she remained stable, she was discharged home. She presented again 5 days later with symptomatic heart failure. Chest X-ray confirmed pulmonary edema. Echocardiography confirmed new onset severe left ventricle dysfunction. Pacemaker checks were normal and lead placement was confirmed. Though her troponin I was elevated, her coronary angiogram was normal. Contrast enhanced echocardiography suggested apical ballooning favoring Takotsubo cardiomyopathy. She was treated for heart failure and made a good recovery. Her follow-up echocardiography a month later showed significant improvement in left ventricle function. Conclusions Takotsubo cardiomyopathy is mediated by a neuro-cardiogenic mechanism due to hypothalamic–pituitary–adrenal axis activation. It generally has a good prognosis. Complications though uncommon, can occur and include arrhythmias. Pacemaker insertion as a precipitant stressor is an infrequent cause of Takotsubo cardiomyopathy. As pacemaker insertions are more frequent in the elderly age group, this phenomenon should be recognized as a potential complication.

Hypothyroidism can have a significant impact on cardiac contractility, vascular resistance, blood pressure, and cardiac rhythm. Ventricular arrhythmias induced by hypothyroidism are infrequently reported, especially in pediatric cases. A 15-year-old girl with autoimmune hypothyroidism experienced pulseless ventricular arrhythmias on 2 separate occasions because of nonadherence to levothyroxine medication. Subsequent investigations revealed an SCN5A mutation associated with Brugada syndrome. A loop recorder captured polymorphic ventricular tachycardia (PMVT), specifically Torsades de Pointes during her second event. Both arrhythmias were addressed only after stabilizing her thyroid hormone levels with replacement therapy. Although rare, patients with uncontrolled hypothyroidism may present with ventricular arrhythmias, particularly PMVT. The cornerstone of treatment for hypothyroidism-induced ventricular arrhythmia is thyroid replacement therapy. The identification of an SCN5A mutation unmasked by overt hypothyroidism emphasizes the need for a comprehensive cardiac evaluation in patients with hypothyroidism being assessed for PMVT. [ABSTRACT FROM AUTHOR]

Background: Takotsubo cardiomyopathy is a novel form of rapidly reversible heart failure occurring secondary to a stressor that mimics an acute coronary event. The underlying etiology of the stressor is highly variable and can include medical procedures. Pacemaker insertion is an infrequent cause of Takotsubo cardiomyopathy. Case presentation: An 86-year-old Caucasian woman underwent an uncomplicated pacemaker insertion for symptomatic complete heart block in the background of slow atrial fibrillation. A transient episode of polymorphic ventricular tachycardia was noted on day 1 following the procedure; however, her pacemaker was checked and, as she remained stable, she was discharged home. She presented again 5 days later with symptomatic heart failure. Chest X-ray confirmed pulmonary edema. Echocardiography confirmed new onset severe left ventricle dysfunction. Pacemaker checks were normal and lead placement was confirmed. Though her troponin I was elevated, her coronary angiogram was normal. Contrast enhanced echocardiography suggested apical ballooning favoring Takotsubo cardiomyopathy. She was treated for heart failure and made a good recovery. Her follow-up echocardiography a month later showed significant improvement in left ventricle function. Conclusions: Takotsubo cardiomyopathy is mediated by a neuro-cardiogenic mechanism due to hypothalamic–pituitary–adrenal axis activation. It generally has a good prognosis. Complications though uncommon, can occur and include arrhythmias. Pacemaker insertion as a precipitant stressor is an infrequent cause of Takotsubo cardiomyopathy. As pacemaker insertions are more frequent in the elderly age group, this phenomenon should be recognized as a potential complication. [ABSTRACT FROM AUTHOR]

Telemedicine and remote monitoring devices, including implantable loop recorders (ILR), are increasingly adopted in the cardiologic setting. These are valuable tools in the arrhythmic stratification of patients at risk of sudden cardiac death, providing a tailored therapeutic management to prevent lethal arrhythmias. We report a case of an asymptomatic 18-year-old boy with a family history of syncope and cardiac arrest, who had a diagnosis of Brugada syndrome with an inducible type 1 pattern and carrier of a missense mutation of the SCN5A gene. In light of the risk factors, although not recommended by current guidelines, we decided to proceed with the implantation of an ILR with remote monitoring service. A few months later, an episode of asymptomatic sustained polymorphic ventricular tachycardia was promptly observed by the remote monitoring, leading to a timely implantation of a subcutaneous cardiac implantable defibrillator. [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation is the most prevalent cardiac arrhythmia, presenting symptomatic patients with diminished quality of life and worsening of heart failure. Dofetilide, a class 3 antiarrhythmic agent, is a proven and safe rhythm control medication. Initial risk of QT prolongation leading to torsade de pointes (TdP) necessitates a standard protocol mandating hospitalization for three days for initiation. Objectives: To assess safety when adhering to initiation protocol and identify traits for susceptibility to TdP in elective dofetilide admissions. Methods: We conducted a retrospective study involving patients admitted to Mayo Clinic sites across four states for elective inpatient initiation of dofetilide between 2003 and 2022. Patients’ charts underwent review, focusing on dofetilide-related TdP occurrences, baseline characteristics including QT intervals, laboratory values, comorbidities, and concomitant medications. Patients who experienced TdP were subjected to further evaluation to identify potential risk factors. Results: Of 2036 patients identified, mean age 66.4 ± 11.4 years, and 67.2 % male, 16 experienced dofetilide-related TdP (incidence rate 0.79%). Notably, 81% (13/16) of TdP cases occurred in patients who deviated from the FDA/manufacturer algorithm protocol. The concomitant use of active intravenous diuretic therapy, digoxin, and QT-prolonging drugs emerged as identifiable risk factors. Additionally, females exhibited a higher incidence of TdP (1.5%) than males (0.44%) {odd ratio [OR] 3.46; P = 0.017}. Conclusion: Overall incidence of TdP related to dofetilide initiation was low (0.79%). Adherence to protocol during elective hospital admissions appears extraordinarily safe. Patients who did not require concurrent use of intravenous diuretics, digoxin, or QT prolonging drugs exhibited lower risk of TdP.

Abstract Capecitabine, a pro-drug of 5-fluorouracil, is commonly used in the treatment of breast and colorectal cancer. Its side effects, including nausea, vomiting, diarrhea, fatigue, loss of appetite, and bone marrow suppression, are well recognized. However, coronary vasospasm represents a less commonly recognized but significant complication of fluoropyrimidine-based therapies such as capecitabine. Proposed mechanisms for this adverse effect complication include direct endothelium-independent vasoconstriction, activation of protein kinase C, and activation of the cyclooxygenase pathway. In this report, we present a case of capecitabine-induced coronary vasospasm leading to progressive, focal ST-elevations, myocardial ischemia, and subsequently polymorphic ventricular tachycardia. These events were captured on telemetry, in a male in his early 40s, diagnosed with stage IIIB sigmoid colon cancer. Notably, the patient had no pre-existing coronary artery disease or other cardiovascular risk factors. Upon diagnosis, the patient was initiated on a calcium channel blocker, verapamil, to mitigate further coronary vasospasm events. After thorough discussions that prioritized the patient’s input and values, an implantable cardioverter-defibrillator was placed subcutaneously. Following discharge, the patient restarted capecitabine therapy along with verapamil prophylaxis and did not experience any subsequent shocks from his ICD as assessed during his outpatient follow-up visits. This case emphasizes the need to involve patients in decision-making processes, especially when managing unexpected and serious complications, to ensure treatments align with their quality of life and personal preferences.

A 32-year-old female with no cardiac risk factors was admitted for treatment of a perianal abscess. During her hospital stay, she had a pulseless electrical activity arrest with a return of spontaneous circulation after one round of cardiopulmonary resuscitation (CPR). After transfer to the Intensive Care Unit (ICU), the patient had polymorphic ventricular tachycardia (PVT) requiring defibrillation shock. Her PVT was resistant to medical interventions. She was shocked a total of 33 times before her arrhythmia was terminated by passing a temporary transvenous pacemaker with overdrive pacing. After an extensive review of her history and presentation, no clear cause of her resistant arrhythmia was identified, however, she was found to have recently started taking over-the-counter weight loss supplements containing raspberry ketones which is a potentially cardiotoxic ingredient.

Background Catheter ablation of premature ventricular contractions (PVCs) that trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation has been reported as a novel therapy to reduce the syncope events in patients with catecholaminergic PVT, whereas the long‐term ablation outcome and its value in improving exercise‐induced ventricular arrhythmias remain unclear. Methods and Results Fourteen consecutive selected patients with catecholaminergic PVT (mean±SD age, 16±6 years; 43% male patients) treated with maximum β‐blockers with no possibility of adding flecainide were prospectively enrolled for catheter ablation. The primary end point was syncope recurrence, and the secondary end point was the reduction of the ventricular arrhythmia score during exercise testing. Twenty‐six PVT/ventricular fibrillation–triggering PVCs were identified for ablation. The trigger beats arose from the left ventricle in 50% of the cases and from both ventricles in 36% of the cases. Purkinje potentials were observed at 27% of the targets. After a mean follow‐up of 49 months after ablation, 8 (57%) patients were free from syncope recurrence. Ablation of trigger beat significantly reduced the syncope frequency (mean±SD, 4.3±1.6 to 0.5±0.8 events per year; P

Familial ST-depression syndrome represents a novel inherited disease characterized by nonischemic ST-segment depressions in multiple leads. The ECG phenotype appears to debut around puberty, while the typical onset of arrhythmias occurs around 50 years of age. Clinical manifestations include supraventricular arrhythmias, fast polymorphic ventricular tachycardia, sudden cardiac death, and left ventricular systolic dysfunction. The optimal treatment is unknown but asymptomatic individuals without red flags may not need treatment. In contrast, ICD implantation should be considered in patients with probable arrhythmic syncope and in those fulfilling general criteria for ICD treatment. Future research should focus on establishing the disease prevalence, optimizing risk stratification and treatment, and elucidating the underlying genetic etiology. [ABSTRACT FROM AUTHOR]

Polymorphic ventricular tachycardia (PMVT) is a highly lethal arrhythmia which is commonly caused by acute myocardial ischaemia. PMVT mediated by short-coupled ventricular ectopy patients with ischaemic heart disease but in the absence of acute ischaemia may relate to transient peri-infarct Purkinje fibre irritability and has been termed 'Angry Purkinje Syndrome'. We present a case series of three patients with PMVT storm 3–5 days following coronary artery bypass graft surgery (CABG). In all three cases, recurrent episodes of PMVT were initiated by monomorphic ventricular ectopy with a short coupling interval. Acute coronary ischaemia was excluded in all three patients with a coronary angiogram and graft study. Two out of three of the patients commenced oral quinidine sulphate with subsequent rapid suppression of arrhythmia. Implantable cardiac defibrillators were implanted in all three patients and revealed no recurrence of PMVT following hospital discharge. The Angry Purkinje Syndrome is a rare but important cause of ventricular tachycardia storm after CABG surgery and is mediated by short-coupled ventricular ectopy in the absence of acute myocardial ischaemia. This arrhythmia may be highly responsive to quinidine. [ABSTRACT FROM AUTHOR]

We illustrate use of induced pluripotent stem cells (iPSCs) as platforms for investigating cardiomyocyte phenotypes in a human family pedigree exemplified by novel heterozygous RYR2-A1855D and SCN10A-Q1362H variants occurring alone and in combination. The proband, a four-month-old boy, presented with polymorphic ventricular tachycardia. Genetic tests revealed double novel heterozygous RYR2-A1855D and SCN10A-Q1362H variants inherited from his father (F) and mother (M), respectively. His father showed ventricular premature beats; his mother was asymptomatic. Molecular biological characterizations demonstrated greater TNNT2 messenger RNA (mRNA) expression in the iPSCs-induced cardiomyocytes (iPS-CMs) than in the iPSCs. Cardiac troponin Ts became progressively organized but cytoplasmic RYR2 and SCN10A aggregations occurred in the iPS-CMs. Proband-specific iPS-CMs showed decreased RYR2 and SCN10A mRNA expression. The RYR2-A1855D variant resulted in premature spontaneous sarcoplasmic reticular Ca2+ transients, Ca2+ oscillations and increased action potential durations. SCN10A-Q1362H did not confer any specific phenotype. However, the combined heterozygous RYR2-A1855D and SCN10A-Q1362H variants in the proband iPS-CMs resulted in accentuated Ca2+ homeostasis disorders, action potential prolongation and susceptibility to early afterdepolarizations at high stimulus frequencies. These findings attribute the clinical phenotype in the proband to effects of the heterozygous RYR2 variant exacerbated by heterozygous SCN10A modification. This article is part of the theme issue 'The heartbeat: its molecular basis and physiological mechanisms'. [ABSTRACT FROM AUTHOR]

Myotonic Dystrophy (DM) is the most common form of muscular dystrophy with onset in adults. Cardiac manifestations are common in DM, but ventricular arrhythmias are uncommon and torsades de pointes is rarely described. Here we describe a patient with primary presentation of syncope, with recurrent polymorphic ventricular tachycardias and with torsades de pointes configuration.

Objectives. To elaborate a risk assessment model for the development of polymorphic ventricular tachycardia (PVT) in patients with drug-induced long QT syndrome (LQTS) caused by class III antiarrhythmic drugs. Material and methods. The study included 64 patients with drug-induced LQTS, 37 (57.8%) out of them were women and 27 (42.2%) men, their mean age made up 57.2±9.4 years. All patients underwent clinical, laboratory and instrumental studies, including 12-lead ECG recording, 24-hour Holter ECG monitoring while receiving antiarrhythmic therapy. Depending on the presence or absence of unsustainable PVT according to Holter monitoring, the patients were divided into 2 groups: “PVT” (n=17) and “Without PVT” (n=47). Based on the obtained data, a logistic regression equation with a binary response and a logit link function was constructed to predict the development of PVT. Results. A logistic regression model has been elaborated, which includes the following indicators: patients’ gender, serum magnesium level, QT interval dispersion, and index of cardioelectrophysiological balance (QT/QRS). With a calculated threshold probability value of ≥0.599, the resultant model can identify patients at high risk of PVT development with drug-induced LQTS while taking class III antiarrhythmic drugs with a sensitivity of 88.24%, specificity of 90.00% and total accuracy of 89.55%. Conclusions. The developed model will make it possible to predict the risk of ventricular arrhythmias in the sick with drug-induced LQTS, which will lead to a decrease in the number of cardiovascular complications and sudden cardiac death cases in this category of patients.

Tachycardiomyopathies due to their pathophysiology of loss of myocardial coupling, provide the adequate substrate for ventricular dysfunction that leads to lethal ventricular arrhythmias. The following is the case of a 75-year-old female patient, with no known history, who presented with symptoms of advanced heart failure and atrial fibrillation, who later developed non-sustained polimorphic ventricular tachycardia during her hospital stay for which it was necessary to perform resuscitation maneuvers with electrical cardioversion on two separate occasions and the restoration of sinus rhythm with drugs to improve left ventricular function. [ABSTRACT FROM AUTHOR]

Introduction: Torsades de Pointes (TdP) is a potentially lethal polymorphic ventricular tachydysrhythmia associated with and caused by prolonged myocardial repolarization. However, prediction of TdP is challenging. We sought to determine if electrocardiographic myocardial repolarization heterogeneity is necessary and predictive of TdP. Methods: We performed a case control study of TdP at a large urban hospital. We identified cases based on a hospital center electrocardiogram (ECG) database search for tracings from 1/2005 to 6/2019 with heart rate corrected QT (QTc) > 500, QRS < 120, and heart rate (HR) < 60, and a subsequent natural language search of electronic health records for the terms: TdP, polymorphic ventricular tachycardia, sudden cardiac death, and relevant variants. Controls were drawn in a 2:1 ratio to cases from a similar pool of ECGs, and matching for QTc, heart rate, sex, and age. We abstracted historical, laboratory, and ECG data using detailed written instructions and an electronic database. We included a second blinded data abstractor to test data abstraction and manual ECG measurement reliability. We used General Electric (GE) QT Guard software for automated repolarization measurements. We compared groups using unpaired statistics. Results: We included 75 cases and 150 controls. The number of current QTc prolonging medications and serum electrolytes were substantially the same between the two groups. We found no significant difference in measures of QT or T wave repolarization heterogeneity. Conclusion: Electrocardiographic repolarization heterogeneity is not greater in otherwise unselected patients with QTc prolongation who suffer TdP and does not appear predictive of TdP. However, previous observations suggest specific repolarization characteristics may be useful for defined patient subgroups at risk for TdP. [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation is the most prevalent cardiac arrhythmia, presenting symptomatic patients with diminished quality of life and worsening of heart failure. Dofetilide, a class 3 antiarrhythmic agent, is a proven and safe rhythm control medication. Initial risk of QT prolongation leading to torsade de pointes (TdP) necessitates a standard protocol mandating hospitalization for three days for initiation., Objectives: To assess safety when adhering to initiation protocol and identify traits for susceptibility to TdP in elective dofetilide admissions., Methods: We conducted a retrospective study involving patients admitted to Mayo Clinic sites across four states for elective inpatient initiation of dofetilide between 2003 and 2022. Patients' charts underwent review, focusing on dofetilide-related TdP occurrences, baseline characteristics including QT intervals, laboratory values, comorbidities, and concomitant medications. Patients who experienced TdP were subjected to further evaluation to identify potential risk factors., Results: Of 2036 patients identified, mean age 66.4 ± 11.4 years, and 67.2 % male, 16 experienced dofetilide-related TdP (incidence rate 0.79%). Notably, 81% (13/16) of TdP cases occurred in patients who deviated from the FDA/manufacturer algorithm protocol. The concomitant use of active intravenous diuretic therapy, digoxin, and QT-prolonging drugs emerged as identifiable risk factors. Additionally, females exhibited a higher incidence of TdP (1.5%) than males (0.44%) {odd ratio [OR] 3.46; P = 0.017}., Conclusion: Overall incidence of TdP related to dofetilide initiation was low (0.79%). Adherence to protocol during elective hospital admissions appears extraordinarily safe. Patients who did not require concurrent use of intravenous diuretics, digoxin, or QT prolonging drugs exhibited lower risk of TdP., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors.)

Background: There is limited information on the mode of arrhythmia initiation in idiopathic ventricular fibrillation (IVF). A non-pause-dependent mechanism has been suggested to be the rule., Objectives: The aim of this study was to assess the mode and characteristics of initiation of polymorphic ventricular tachycardia (PVT) in patients with short or long-coupled PVT/IVF included in THESIS (THerapy Efficacy in Short or long-coupled idiopathic ventricular fibrillation: an International Survey), a multicenter study involving 287 IVF patients treated with drugs or radiofrequency ablation., Methods: We reviewed the initiation of 410 episodes of ≥1 PVT triplet in 180 patients (58.3% females; age 39.6 ± 13.6 years) with IVF. The incidence of pause-dependency arrhythmia initiation (prolongation by >20 ms of the preceding cycle length) was assessed., Results: Most arrhythmias (n = 295; 72%) occurred during baseline supraventricular rhythm without ambient premature ventricular complexes (PVCs), whereas 106 (25.9%) occurred during baseline rhythm including PVCs. Nine (2.2%) arrhythmias occurred during atrial/ventricular pacing and were excluded from further analysis. Mode of PVT initiation was pause-dependent in 45 (15.6%) and 64 (60.4%) of instances in the first and second settings, respectively, for a total of 109 of 401 (27.2%). More than one type of pause-dependent and/or non-pause-dependent initiation (mean: 2.6) occurred in 94.4% of patients with ≥4 events. Coupling intervals of initiating PVCs were <350 ms, 350-500 ms, and >500 ms in 76.6%, 20.72%, and 2.7% of arrhythmia initiations, respectively., Conclusions: Pause-dependent initiation occurred in more than a quarter of arrhythmic episodes in IVF patients. PVCs having long (between 350 and 500 ms) and very long (>500 ms) coupling intervals were observed at the initiation of nearly a quarter of PVT episodes., Competing Interests: Funding Support and Author Disclosures The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Lyme disease is commonly encountered in endemic areas of the United States harboring the causal organism Borrelia burgdorferi. Lyme carditis can manifest in early disseminated infections, usually as atrioventricular nodal blockade. Timely antibiotic therapy typically suppresses myocardial inflammation and reverses cardiac conduction disturbances. We present a case of a previously healthy male who presented to the emergency department with non-prodromal syncope, multifocal annular rashes, and antecedent inflammatory knee pain and effusion, found to have positive 2-tier Lyme testing and pause-dependent polymorphic ventricular tachycardia leading to cardiac arrest. Lyme carditis occurs in early disseminated infections but rarely leads to cardiac arrest. Acute management is entrained in well-established guidelines for therapy, and together with risk stratification scoring can be considered by emergency care physicians in the workup of undifferentiated syncope with concern for Lyme disease with cardiac involvement. [ABSTRACT FROM AUTHOR]

Polymorphic ventricular tachycardia (PVT) is a lethal cardiac arrhythmia. It requires medical intervention, including defibrillation, or imminent death may result. A 26-year-old male patient presented to the emergency department with complaints of syncope while working on the farm; later diagnostic testing indicated PVT. As cardiovascular disorders are becoming increasingly prevalent in urban as well as rural areas, it is a need of time to make our facilities well equipped for resuscitation measures by implementing advanced cardiac life support.

Bidirectional ventricular tachycardia (BVT) is part of the spectrum of polymorphic ventricular tachycardia (VT). This is a case report of a 59-year-old male with stable coronary artery disease and baseline normal left ventricular ejection fraction (LVEF) who was followed for high burden symptomatic monomorphic premature ventricular complexes (PVC). He was admitted for syncope. The ECG showed recurrent non-sustained alternating morphology and double cycle length VT runs associated with deterioration in LVEF but without coronary artery disease progression. The patient had a successful catheter ablation of two distinct left ventricular PVC focus. This is a rare ECG pattern of alternating morphology VT similar to a bidirectional VT. [ABSTRACT FROM AUTHOR]

Abstract Providers should be aware of the possibility of cardiac resynchronization therapy‐related proarrhythmia which could be life‐threatening. His‐bundle pacing may serve as an alternative, more physiological, option in the management as it preserves the normal sequence of depolarization from the septum to the lateral wall, and from endocardium to epicardium.

In 1992, the Brugada brothers published a patient series of aborted sudden death, who were successfully resuscitated from ventricular fibrillation (VF). These patients had a characteristic coved ST-segment elevation in the right precordial leads on their 12-lead electrocardiogram with no apparent structural heart abnormality. This disease was referred to as “right bundle branch block, persistent ST-segment elevation, and sudden death syndrome.” The term Brugada syndrome (BrS) was first coined for this new arrhythmogenic entity in 1996. BrS is more prevalent in Southeast Asian ethnic groups and was considered a familial disease due to the presence of syncope and/or sudden deaths in several members of the same family, however, the genetic alteration was only noted in 1998. The genetic characterization of BrS has proven to be challenging. The most common and well-established BrS genotype involves loss-of-function mutations in the SCN5A gene, but only represents between 15% and 30% of the diagnosed patients. Patients with BrS can present with a range of symptoms which can include syncope, seizures, and nocturnal agonal breathing due to polymorphic ventricular tachycardia or VF. If these arrhythmias are sustained, sudden cardiac death may result. Despite the significant progress on the understanding of BrS over the last two decades, there remain a number of uncertainties and challenges; we present an update review on the subject.

Polymorphic ventricular tachycardia (PVT) and ventricular fibrillation (VF) are life-threatening complications of takotsubo syndrome (TTS). Data regarding risk factors for PVT/VF based on the TTS variant are lacking. This study aimed to identify demographic and clinical factors associated with PVT and VF in patients with TTS. Patients meeting the InterTak criteria for TTS between 2010 and 2022 were retrospectively identified. The occurrence of PVT/VF with each risk factor was analyzed using logistic regression. Sensitivity analysis was performed to assess the interaction between risk factors. PVT/VF occurred in 27 of 296 patients with TTS (9.1%). Patients with PVT/VF were younger (52 vs 62 years, p = 0.019) and more frequently used stimulants in the 4 weeks before admission (22.2% vs 8.2%, odds ratio [OR] 3.20, p = 0.023). All PVT/VF occurred within 24 hours of hospitalization. An initial QTc threshold of 490 ms had the highest sensitivity and specificity for the occurrence of PVT/VF (area under the curve = 0.687). Patients with PVT/VF were more likely to have a QTc >490 ms on admission (55.6% vs 18.7%, OR 5.45, p <0.01), apical variant TTS (78% vs 56%, OR 2.69, p = 0.038), and an admission ejection fraction <30% (63% vs 41.5%, OR 2.39, p = 0.032); each factor was independently associated with PVT/VF irrespective of QTc duration on sensitivity analysis. In conclusion, nearly 1 in 10 patients with TTS had PVT/VF. A QTc >490 ms, recent stimulant use, apical variant TTS, and severe left ventricular systolic dysfunction on admission are associated with higher PVT/VF risk, with the first 24 hours being a high-risk period., Competing Interests: Declaration of competing interest The authors have no competing interests to declare., (Copyright © 2024. Published by Elsevier Inc.)

Opioid dependence is a common problem, and therapeutic alternatives are scarce and ineffective. Ibogaine, illegal in several countries, has been reported as a possible therapy in alternative clinics and it is also used as a recreational drug, despite its cardiotoxic potential, including QT prolongation. We report a case of long QT leading to multiple episodes of cardiac arrest after a single dose of ibogaine (200mg, 2.6mg/Kg) in a patient without structural heart disease. This case highlights the fact that even low doses of ibogaine can be lethal and warns us about the consequences of its use., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Mestre et al.)

Aims Distinctive types of polymorphic ventricular tachycardia (VT) respond differently to different forms of therapy. We therefore performed the present study to define the electrocardiographic characteristics of different forms of polymorphic VT. Methods and results We studied 190 patients for whom the onset of 305 polymorphic VT events was available. The study group included 87 patients with coronary artery disease who had spontaneous polymorphic VT triggered by short-coupled extrasystoles in the absence of myocardial ischaemia. This group included 32 patients who had a long QT interval but nevertheless had their polymorphic VT triggered by ectopic beats with short coupling interval, a subcategory termed 'pseudo-torsade de pointes] (TdP). For comparison, we included 50 patients who had ventricular fibrillation (VF) during acute myocardial infarction ('ischaemic VF' group) and 53 patients with drug-induced TdP ('true TdP' group). The QT of patients with pseudo-TdP was (by definition) longer than that of patients with polymorphic VT and normal QT (QTc 491.4 ± 25.2 ms vs. 447.3 ± 55.6 ms, P  < 0.001). However, their QT was significantly shorter than that of patients with true TdP (QTc 564.6 ± 75.6 ms, P  < 0.001). Importantly, the coupling interval of the ectopic beat triggering the arrhythmia was just as short during pseudo-TdP as during polymorphic VT with normal QT (359.1 ± 38.1 ms vs. 356.6 ± 39.4 ms, P  = 0.467) but was much shorter than during true TdP (581.2 ± 95.3 ms, P  < 0.001). Conclusions The coupling interval helps discriminate between polymorphic VT that occurs despite a long QT interval (pseudo-TdP) and polymorphic arrhythmias striking because of a long QT (true TdP). [ABSTRACT FROM AUTHOR]

Background: Loperamide, commonly sold under the brand name Imodium® (Johnson & Johnson, Fort Washington, PA), is a widely available, over-the-counter antidiarrheal medication that possesses µ-opioid agonist properties and can have catastrophic cardiac events when misused or abused. Since the start of the opioid epidemic in the United States, there has been an increasing number of case reports and deaths linking loperamide abuse with cardiac events such as torsades de pointes (TdP) and Brugada syndrome.Case Report: This case report presents a 22-year-old man who presented in cardiac arrest from polymorphic ventricular tachycardia consistent with TdP and a Type 1 Brugada pattern after intentional loperamide abuse. We discuss this patient's management and the proposed pathophysiology of these two cardiotoxicities, of which, to our knowledge, no previously published case report has displayed both in the same patient after a supratherapeutic loperamide ingestion. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: As the prevalence of opioid dependency and misuse has increased, so, too, has the misuse of un-scheduled medications such as loperamide to achieve central nervous system opioid effects. It is important for the emergency physician to know about and understand loperamide-associated cardiotoxicities such as prolongation of the QRS, unmasking of Brugada patterns, QT prolongation, or ventricular dysrhythmias such as TdP to be able to recognize and treat it. [ABSTRACT FROM AUTHOR]

BACKGROUND: Long QT syndrome type 1 (LQT1) is a congenital disease arising from a loss of function in the slowly activating delayed potassium current IKs, which causes early afterdepolarizations (EADs) and polymorphic ventricular tachycardia (pVT). OBJECTIVE: The purpose of this study was to investigate the mechanisms underlying pVT using a transgenic rabbit model of LQT1. METHODS: Hearts were perfused retrogradely, and action potentials were recorded using a voltage-sensitive dye and CMOS cameras. RESULTS: Bolus injection of isoproterenol (140 nM) induced pVT initiated by focal excitations from the right ventricle (RV; n = 16 of 18 pVTs). After the pVT was initiated, complex focal excitations occurred in both the RV and the left ventricle, which caused oscillations of the QRS complexes on ECG, consistent with the recent proposal of multiple shifting foci caused by EAD chaos. Moreover, the action potential upstroke in pVT showed a bimodal distribution, demonstrating the coexistence of 2 types of excitation that interacted to produce complex pVT: Na(+) current (INa)-mediated fast conduction and L-type Ca(2+) current (ICa)-mediated slow conduction coexist, manifesting as pVT. Addition of 2 μM tetrodotoxin to reduce INa converted pVT into monomorphic VT. Reducing late INa in computer simulation converted pVT into a single dominant reentry, agreeing with experimental results. CONCLUSION: Our study demonstrates that pVT in LQT1 rabbits is initiated by focal excitations from the RV and is maintained by multiple shifting foci in both ventricles. Moreover, wave conduction in pVT exhibits bi-excitability, that is, fast wavefronts driven by INa and slow wavefronts driven by ICa co-exist during pVT.

Purpose of review: Catheter ablation of ventricular fibrillation (VF) is challenging due to the difficulty in interpreting fibrillatory electrograms and the complete hemodynamic collapse with VF precluding detailed mapping. Successful ablation can be performed by eliminating triggers of VF. We review the contemporary advances in VF ablation, especially targeting the substrate for VF. Recent findings: Strategies to map and eliminate the substrate for VF can be applied generally, even in the absence of a reliable trigger. VF substrate can be mapped during sinus rhythm with signature low-voltage, fractionated, and late electrograms. Such substrate can be harbored within regions of scar in structural heart disease, or localized as epicardial microstructural abnormality in Brugada syndrome, inferolateral J-wave syndrome, and unexplained VF. Ablation of such substrate is an effective antiarrhythmic strategy. Furthermore, innovations in expeditious panoramic mapping techniques have generated interest in directly mapping and ablating drivers that sustain VF. Summary: Advances in understanding of ablation targets and innovations in mapping techniques are enabling successful ablation of VF in the electrophysiology laboratory. Beyond ablation of VF triggers in a subset of patients, progress is being made in ablating the substrate for VF in patients afflicted by this lethal arrhythmia. [ABSTRACT FROM AUTHOR]

We present a unique case of an 80-year-old male who presented to our emergency department following cardiac defibrillation when he was found to be in polymorphic ventricular tachycardia (VT) after a syncopal event while at cardiac rehabilitation. He had known coronary artery disease and had a four-vessel coronary artery bypass graft (CABG) 20 years prior to presentation. He underwent left heart catheterization (LHC) two months prior to the syncopal event for worsening shortness of breath and the decision at that time was to proceed with medical management and intervene with redo-CABG if shortness of breath did not improve or progressively worsened. While admitted under our care after the polymorphic VT event, we faced the dilemma of whether to proceed with redo-CABG first since cardiac ischemia is a common cause of polymorphic VT or whether to insert an implantable cardioverter-defibrillator (ICD) before proceeding with redo-CABG. We present the current literature that addresses ICD implantation for secondary prevention and our approach to this complicated case., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Singu et al.)

Objective: Our objective was to know the percent mortality of ventricular arrhythmia (VA) storm, its major leading factor and the predictors of inhospital mortality of VA storm in our population. Methodology: In this retrospective observational study conducted at The Aga Khan University Hospital Karachi, all patients with age =16, with VA storm were included. Baseline demographic, clinical characteristics, laboratory parameters and management interventions were recorded in pre prepared questionnaire. The data was analyzed using SPSS version 21. Results: Of the total 74 patients, 86.5% were male, 77% were having monomorphic VT and 60.8% were in pulmonary edema. Hypertension (73%), IHD (63.5%), DM (48.6%) MR (56.8%) TR (50%) and LV dysfunctions were the commonest risk factors of VA storm. The mean hospital stay was 5.64 ± 5.63 and 59.5% patients were discharged home in stable condition. On bivariate analysis female gender, polymorphic VT, pulmonary edema, intubation, baseline hemoglobin levels, and baseline WBC counts were predictors of in-hospital mortality of VA storm with hazard ratios (HR) of 2.22 [0.95-5.18], 2.44 [1.18-5.08], 13.49 [1.82-99.85], 17.54 [2.38-129.44], 1.25 [1.05-1.47], and 1.06 [1.01-1.11] respectively. On multivariate analysis, female gender, intubation, and baseline hemoglobin level were independent predictors of in-hospital mortality of VA storm with adjusted HRs of 3.88 [1.02-14.77], 9.9 [0.95-103.25], and 1.47 [1.2-1.79] respectively. Conclusion: VA storm mortality for conservative management in our region is comparable to the international figures. Also we have similar risk factors for VA storm like low EF, structural heart disease and similar predictors of in-hospital mortality for VA storm. [ABSTRACT FROM AUTHOR]

Providers should be aware of the possibility of cardiac resynchronization therapy‐related proarrhythmia which could be life‐threatening. His‐bundle pacing may serve as an alternative, more physiological, option in the management as it preserves the normal sequence of depolarization from the septum to the lateral wall, and from endocardium to epicardium. [ABSTRACT FROM AUTHOR]

A 79-year-old woman with a history of atrial fibrillation (AF) ablation was referred to our hospital for ventricular fibrillation, which was terminated by an automated external defibrillator. The heart rate corrected QT interval was 489 ms. The electrocardiogram monitoring recorded a polymorphic ventricular tachycardia (VT) reproducibly induced by a single morphology premature ventricular contraction (PVC). Therefore, we performed a trigger PVC ablation and implanted an implantable cardioverter defibrillator. No VT events were observed for at least one year after the ablation. A prolonged QT interval after the AF ablation should be carefully noted because it could introduce fatal complications. < Learning objective: A rare late fatal complication of ventricular tachycardia (VT) after atrial fibrillation (AF) ablation can occur even more than one month after the AF ablation. The AF ablation might have an adverse effect on the masked prolonged QT interval. A trigger ablation of the polymorphic VT was helpful to control lethal VTs.> [ABSTRACT FROM AUTHOR]

In 1992, the Brugada brothers published a patient series of aborted sudden death, who were successfully resuscitated from ventricular fibrillation (VF). These patients had a characteristic coved ST‑segment elevation in the right precordial leads on their 12‑lead electrocardiogram with no apparent structural heart abnormality. This disease was referred to as "right bundle branch block, persistent ST‑segment elevation, and sudden death syndrome." The term Brugada syndrome (BrS) was first coined for this new arrhythmogenic entity in 1996. BrS is more prevalent in Southeast Asian ethnic groups and was considered a familial disease due to the presence of syncope and/or sudden deaths in several members of the same family, however, the genetic alteration was only noted in 1998. The genetic characterization of BrS has proven to be challenging. The most common and well‑established BrS genotype involves loss‑of‑function mutations in the SCN5A gene, but only represents between 15% and 30% of the diagnosed patients. Patients with BrS can present with a range of symptoms which can include syncope, seizures, and nocturnal agonal breathing due to polymorphic ventricular tachycardia or VF. If these arrhythmias are sustained, sudden cardiac death may result. Despite the significant progress on the understanding of BrS over the last two decades, there remain a number of uncertainties and challenges; we present an update review on the subject. [ABSTRACT FROM AUTHOR]

Background: Autonomic modulation is finding an increasing role in the treatment of ventricular arrhythmias. Renal denervation (RDN) has been described as a treatment modality for refractory ventricular tachycardia (VT) in case series.Objective: The purpose of this study was to evaluate RDN as an adjunctive therapy to cardiac sympathetic denervation (CSD) for ablation refractory VT.Methods: Patients who underwent RDN after radiofrequency ablation and CSD procedures at our center from 2012 to 2019 were evaluated.Results: Ten patients underwent RDN after CSD (9 bilateral and 1 left-sided only) with a median follow-up of 23 months. The mean age was 59.9 ± 10.4 years, and 9/10 (90%) were men. All had cardiomyopathy with a mean ejection fraction of 33% ± 11% (20% ischemic). Four (40%) underwent CSD during the same hospitalization as that for RDN. Patients who underwent RDN as adjunctive therapy to CSD had a decrease in all implantable cardioverter-defibrillator therapies (shocks + antitachycardia pacing [ATP]) from 29.5 ± 25.2 to 7.1 ± 10.1 comparing 6 months pre-RDN to 6 months post-RDN (P = .028). Implantable cardioverter-defibrillator shocks were significantly decreased from 7.0 ± 6.1 to 1.7 ± 2.5 comparing 6 months pre-RDN to 6 months post-RDN (P = .026). This benefit was driven by a decrease in therapies for 6 patients who had a staged procedure, not performed during the same hospitalization (28.5 ± 24.3 to 1.0 ± 1.2; P = .043).Conclusion: RDN demonstrates the potential benefit when VT recurs after radiofrequency ablation and CSD. The benefit is seen in patients who undergo a staged procedure. The need for acute RDN after CSD portends a poor prognosis. [ABSTRACT FROM AUTHOR]

Aims: We recently reported that patients with coronary artery disease (CAD) who develop polymorphic ventricular tachycardia (VT) during the healing phase of an acute coronary event, generally fail to respond to revascularization or standard antiarrhythmic therapy but respond immediately to quinidine therapy. Here, we describe that CAD patients presenting with out-of-hospital polymorphic VT without a recent coronary event or an obvious precipitating factor, also respond uniquely to quinidine therapy.Methods and Results: Retrospective study of patients with unheralded, mainly out-of-hospital, polymorphic VT related to CAD but without evidence of acute myocardial ischaemia. We identified 20 patients who developed polymorphic VT without precipitating factors. The polymorphic VT events were triggered by extrasystoles with short (376 ± 49 ms) coupling interval. Arrhythmic storms occurred in 70% patients. These arrhythmic storms were generally refractory to conventional antiarrhythmic therapy but invariably responded to quinidine therapy. Revascularization was antiarrhythmic in 3 patients despite the absent clinical or ECG signs of ischaemia. During long-term follow-up (range 2 months to 11 years), 3 (15%) of patients not receiving quinidine developed recurrent polymorphic VT. There were no recurrent arrhythmias during long-term quinidine therapy.Conclusions: Patients with CAD may develop polymorphic VT in the absence of obvious acute ischaemia or apparent precipitating factors, presenting as out-of-hospital polymorphic VT with high risk of arrhythmic storms that respond uniquely to quinidine therapy. [ABSTRACT FROM AUTHOR]

Catecholaminergic Polymorphic Ventricular Tachycardia is a rare but often lethal genetic disorder that affects approximately 1 in 10,000 people. It often first manifests as stress or exercise-related syncope or sudden unexplained cardiac death, primarily in the pediatric and young adult population. We present a case of a 6-year-old male who had a sudden unexplained prehospital cardiac arrest after being scared by a domestic animal and who presented in ventricular fibrillation. The patient was subsequently defibrillated with a return of spontaneous circulation. During the course of care, medications with beta-1 and -2 agonist properties were administered, followed by multiple further episodes of polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF). Once these medications were discontinued and beta blockers were administered, the patient had no further episodes of PVT/VF and was subsequently discharged from hospital 7 days later, completely neurologically intact. This case suggests the need for caution when considering administering beta agonists in a pediatric cardiac arrest patient with no known history of heart disease who presents in VF or PVT after an incident of extreme stress or strenuous physical activity. [ABSTRACT FROM AUTHOR]

A 52-year-old man complaining of persistent recurring chest pain at night underwent coronary angiogram at another institution. Normal coronaries were observed and he was discharged with muscle spasmolytic prescription. Since symptoms had continued, 24-hour Holter monitoring was ordered at our facility and results revealed huge ST elevation and polymorphic ventricular tachycardia. Cold pressor test performed in catheterization laboratory also resulted in ventricular tachycardia. Nifedipine was prescribed and follow-up Holter monitoring revealed no further vasospastic episodes. Utility of 24-hour Holter rhythm monitoring and cold pressor test in patients with recurrent chest pain at night is demonstrated in this report.