ABSTRACT
Coronavirus disease 2019 (COVID-19) is associated with cardiovascular complications; however, Takotsubo cardiomyopathy (TCM) with QT prolongation and Torsade de pointes has been reported only rarely. We present a case of TCM after QT prolongation and Torsade de pointes. A 58-year-old woman was admitted because of COVID-19-related pneumonia. Seven days after admission, she developed sudden loss of consciousness without any indication of cardiovascular disease. A monitoring electrocardiogram indicated Torsade de pointes and a prolonged QT interval. Emergency cardiac catheterization revealed TCM. She was treated with favipiravir and steroids, followed by rehabilitation, and her condition improved. To detect asymptomatic TCM, routine electrocardiography screening should be considered for patients with COVID-19.
Subject(s)
COVID-19 , Long QT Syndrome , Takotsubo Cardiomyopathy , Torsades de Pointes , Humans , Female , Middle Aged , Torsades de Pointes/diagnosis , Torsades de Pointes/etiology , Torsades de Pointes/therapy , Takotsubo Cardiomyopathy/complications , Takotsubo Cardiomyopathy/diagnosis , COVID-19/complications , Long QT Syndrome/complications , Long QT Syndrome/diagnosis , ElectrocardiographySubject(s)
Leukemia , Long QT Syndrome , Torsades de Pointes , Humans , Arsenic Trioxide/adverse effects , Torsades de Pointes/chemically induced , Torsades de Pointes/diagnosis , Torsades de Pointes/therapy , Arrhythmias, Cardiac , Long QT Syndrome/chemically induced , Long QT Syndrome/diagnosis , ElectrocardiographyABSTRACT
The obesity pandemic is becoming one of the most prevalent diseases nowadays. There is a wide spectrum of treatment, ranging from hygienic-dietary measures to bariatric surgery. Endoscopic intragastric balloon placement is becoming increasingly more frequent, due to its technical simplicity, safety and short-term success(1). Although complications are rare some can be severe, so pre-endoscopic evaluation must be carried out carefully. A 43-year-old woman with a history of grade I obesity (BMI 32.7) had an Orbera® intragastric balloon implanted successfully. After the procedure she presented frequent nausea and vomiting, partially controlled with antiemetics. She attended the Emergency Department(ED) with a persistent emetic syndrome - oral intolerance and short-term loss of consciousness(syncope), for which she was admitted. Lab tests showed metabolic alkalosis with severe hypokalemia(K+ 1.8mmol/L), so fluid therapy was initiated for hydroelectrolytic replacement. During the patient's stay in the ED, two episodes of polymorphic ventricular tachychardia "Torsades de Pointes" (PVT-TDP) occurred, leading to cardiac arrest and requiring electrical cardioversion to restore sinus rhythm, in addition to a temporary pacemaker placement. Telemetry showed a corrected QT interval of >500ms, compatible with Long QT Syndrome(LQTS). Once the patient was hemodynamically stabilized a gastroscopy was performed. The intragastric balloon located in the fundus was removed using an extraction kit, puncturing and aspirating 500ml of saline solution, and extracting the collapsed balloon without any complications. The patient achieved an adequate oral intake afterwards, and no recurrence of emetic episodes were noticed. Previous ECGs revealed a prolonged QT interval and a genetic study confirmed a congenital type 1 LQTS. Treatment was initiated with beta-blockers and a bicameral automatic defibrillator was implanted in order to prevent recurrences. Intragastric balloon placement is generally a safe procedure, serious complications present in 0.70% of cases(2). It is essential to have a proper pre-endoscopic evaluation, including patient's medical history and comorbidities. Episodes of PVT-TDP may present precipitated by certain medications (eg. metoclopramide) or hydroelectrolytic imbalances (eg, hypokalemia)(3). A standardized evaluation of ECG before intragastric balloon placement may be useful to prevent these rare but serious complications.
Subject(s)
Gastric Balloon , Hypokalemia , Long QT Syndrome , Torsades de Pointes , Female , Humans , Adult , Torsades de Pointes/etiology , Torsades de Pointes/therapy , Gastric Balloon/adverse effects , Emetics , Hypokalemia/complications , Long QT Syndrome/therapy , Long QT Syndrome/complications , Obesity/complications , DNA-Binding ProteinsABSTRACT
Összefoglaló. A szerzok egy 44 éves, autoimmun betegségben szenvedo nobeteg kórlefolyását ismertetik. A váratlan kórházi kamrafibrillációt követo sikeres resuscitatio után a beteg comatosus állapotban maradt, ezért terápiás hypothermiában részesült. A hypothermiás kezelés hatására jelentos QT-megnyúlás és "torsade de pointes" kamrai tachycardia lépett fel. A hypothermia okozta szívritmuszavar oka a homérséklet-csökkenés kiváltotta QT-megnyúlás és korai utódepolarizációs mechanizmusú triggerelt aktivitás. A szerzok felhívják a figyelmet arra, hogy jelen tudásunk szerint enyhe hypothermiát javasolt alkalmazni az ajánlásban szereplo hypothermiás tartományon belül. Orv Hetil. 2022; 163(13): 523-526. Summary. The authors describe the course of disease in a 44-year-old female patient with autoimmune disease. After successful resuscitation following unexpected hospital ventricular fibrillation, the patient remained in a comatose state and therefore received therapeutic hypothermia. Hypothermic treatment resulted in significant QT prolongation and "torsade de pointes" ventricular tachycardia. The probable cause of arrhythmia is the QT prolongation caused by the hypothermia and the consequential early afterdepolarization and triggered activity. The authors draw attention to the fact that - to the best of our knowledge - milder hypothermia is recommended within the preset hypothermic range. Orv Hetil. 2022; 163(13): 523-526.
Subject(s)
Hypothermia, Induced , Long QT Syndrome , Torsades de Pointes , Adult , Arrhythmias, Cardiac , Electrocardiography , Female , Humans , Long QT Syndrome/complications , Long QT Syndrome/therapy , Torsades de Pointes/chemically induced , Torsades de Pointes/therapyABSTRACT
Drug-induced QT prolongation, primarily antiarrhythmic drugs, is a common cause of torsade de pointes (TdP). Although there have been previous reports of drug-induced TdP in patients, it has not been well documented when caused by citalopram during the pacemaker battery-depletion phase. To improve delirium recognition, we report a case of citalopram-induced TdP during the pacemaker battery-depletion phase. An 84-year-old Chinese female was brought to the hospital presenting recurrent syncope. She lost consciousness and was admitted after her syncope TdP was documented. Her pacemaker was inspected and found to be operating in an extremely ineffective manner. Although she had prolonged QT interval after the pacemaker was replaced, she did not suffer another syncope attack, and ECG monitoring revealed no cardiac arrhythmia or TdP. During her admission, she was treated with citalopram for depression. Citalopram was discontinued when the QT interval shortened progressively. In this study, we described a case of citalopram-induced TdP during the depletion phase of a pacemaker battery. This case should serve as a cautionary lesson to clinicians to avoid using citalopram during the pacemaker battery-depletion phase.
Subject(s)
Long QT Syndrome , Pacemaker, Artificial , Torsades de Pointes , Aged, 80 and over , Citalopram/adverse effects , DNA-Binding Proteins , Electrocardiography , Female , Humans , Long QT Syndrome/complications , Pacemaker, Artificial/adverse effects , Syncope/chemically induced , Syncope/therapy , Torsades de Pointes/chemically induced , Torsades de Pointes/diagnosis , Torsades de Pointes/therapyABSTRACT
BACKGROUND: This case demonstrates the severe electrolyte derangements that may present after a common therapy such as a bowel preparation for an outpatient procedure and the rare yet potential detrimental outcomes of those abnormalities. It also highlights the implications of long QT syndrome regarding pharmacology and treatment. CASE PRESENTATION: We present a case of 48 year-old female with severe electrolyte derangements and long QT syndrome (LQTS) leading to Torsades de Pointes (TdP), pulseless ventricular fibrillation, and unsynchronized defibrillation in the post anesthesia care unit (PACU) after uneventful upper and lower endoscopy. This led to an unanticipated intensive care unit admission for aggressive electrolyte repletion, cardiology consultation, and implantable cardioverter defibrillator (ICD) placement. CONCLUSIONS: This is a rare presentation after an outpatient procedure that would have had a detrimental outcome if not promptly diagnosed and treated appropriately. Therefore, we aim to provide further insight into the diagnosis and treatment of severe hypokalemia and long QT syndrome resulting in Torsades de Pointes and ventricular fibrillation.
Subject(s)
Anesthesia Recovery Period , Endoscopy/methods , Outpatients , Torsades de Pointes/physiopathology , Torsades de Pointes/therapy , Water-Electrolyte Balance/physiology , Defibrillators, Implantable , Female , Humans , Middle AgedABSTRACT
Dofetilide, a class III antiarrhythmic, is widely used in the treatment of cardiac arrhythmias. Antiarrhythmic drugs can have a long duration of action that prolongs the QT interval. This causes bradycardia that predisposes to R-on-T phenomenon subsequently leading to torsades de pointes (TdP). This necessitates constant monitoring to prevent or treat ventricular arrhythmias or bradycardia associated with cardiac medications. Although extremely rare, dofetilide overdose has been described in the literature. However, no evidence found in the current literature required prolonged intervention after the initial acute stabilization, leading to scarcity of data for treatment of ongoing dofetilide overdose. We present the case of an intentional dofetilide overdose in a 61-year-old Caucasian woman with a history of congestive heart failure, atrial fibrillation, stage IIIb chronic kidney disease, diabetes mellitus type II, hypothyroidism, morbid obesity, and hypertension that required extensive interventions for refractory TdP that lasted 4 days. Therapeutic as well as excess dosage of dofetilide can lead to TdP, which is usually controlled by decreasing the dose or terminating drug administration. If the arrhythmia is not resolved, guidelines recommend management with activated charcoal if ingestion is within 15 minutes, followed by administration of 2 g IV (intravenous) magnesium and addressing the electrolyte imbalance. However, if the arrhythmia is persistent due to ongoing dofetilide toxicity, isoproterenol is given as a bridge to overdrive pacing and dopamine is used as an alternative to isoproterenol.
Subject(s)
Torsades de Pointes , Female , Humans , Middle Aged , Phenethylamines , Sulfonamides/adverse effects , Torsades de Pointes/chemically induced , Torsades de Pointes/therapySubject(s)
Electrocardiography , Long QT Syndrome/diagnostic imaging , Torsades de Pointes/diagnostic imaging , Adrenergic beta-Antagonists/therapeutic use , Defibrillators, Implantable , Diagnosis, Differential , Female , Humans , Long QT Syndrome/therapy , Middle Aged , Torsades de Pointes/therapyABSTRACT
Human-induced pluripotent stem cell (iPSC) technology paves the way for next-generation drug-safety assessment. In particular, human iPSC-derived cardiomyocytes, which exhibit electrical activity, are useful as a human cell model for assessing QT-interval prolongation and the risk of the lethal arrhythmia Torsade de Pointes (TdP). In addition to proarrhythmia assay, contractile behavior has received increased attention in drug development. In this study, we developed a novel high-throughput in vitro assay system using motion vectors to evaluate the contractile activity of iPSC-derived cardiomyocytes as a physiologically relevant human platform. The methods presented here highlight the use of commercially available iPSC-derived cardiomyocytes, iCell cardiomyocytes, for contractility evaluation recorded by the motion vector system.
Subject(s)
Biological Assay/methods , Induced Pluripotent Stem Cells/cytology , Myocytes, Cardiac/cytology , Arrhythmias, Cardiac/therapy , Cells, Cultured , Humans , Long QT Syndrome/therapy , Torsades de Pointes/therapyABSTRACT
An 82-year-old woman was admitted to our hospital because of dyspnea and bradycardia during exertion. Electrocardiography revealed complete atrioventricular block. During pacemaker implantation, a small dose (12.5 mg) of hydroxyzine was injected for sedation, and torsade de pointes (Tdp) occurred. The QT interval was prolonged after administration of hydroxyzine, and Tdp was observed after the R on T phenomenon occurred, indicating that hydroxyzine was capable of prolonging the QT interval and causing Tdp. Therefore, we must be cautious when administering hydroxyzine for sedation during surgery, especially in patients with bradycardia.
Subject(s)
Atrioventricular Block , Pacemaker, Artificial , Torsades de Pointes , Aged, 80 and over , Atrioventricular Block/chemically induced , Atrioventricular Block/diagnosis , Electrocardiography , Female , Humans , Hydroxyzine/adverse effects , Torsades de Pointes/chemically induced , Torsades de Pointes/diagnosis , Torsades de Pointes/therapyABSTRACT
BACKGROUND: Abiraterone is a medication frequently used for metastatic castrate-resistant prostate cancer. We report a case of non-sustained episodes of TdP associated with severe hypokalemia due to androgen-deprivation therapy. Few case presentations describe this association; the novelty lies in the potentially lethal cardiovascular events among cancer patients receiving hormonal therapy. CASE PRESENTATION: A 70-year-old male presented with recurrent syncope without prodrome. ECG revealed frequent ventricular ectopy, non-sustained episodes of TdP, and severe hypomagnesemia and hypokalemia. During potassium and magnesium infusion for repletion, the patient underwent temporary transvenous atrial pacing. As part of the work-up, coronary angiography revealed a mild coronary artery disease, and transthoracic echocardiogram showed a moderately depressed ejection fraction. After electrolyte disturbances were corrected, the QT interval normalized, and transvenous pacing was no longer necessary. Abiraterone was discontinued during the admission, and the patient returned to baseline. CONCLUSIONS: Cancer treatment is complex and requires a multidisciplinary approach. We presented a case of non-sustained TdP associated with androgen-deprivation therapy in an elderly patient with mild coronary artery disease and moderately reduced ejection fraction. Close follow-up and increased awareness are required in patients with hormonal treatment, especially in the setting of other cardiovascular risk factors.
Subject(s)
Abiraterone Acetate/adverse effects , Antineoplastic Agents/adverse effects , Heart Rate/drug effects , Long QT Syndrome/chemically induced , Prostatic Neoplasms, Castration-Resistant/drug therapy , Steroid Synthesis Inhibitors/adverse effects , Syncope/chemically induced , Torsades de Pointes/chemically induced , Aged , Cardiac Pacing, Artificial , Fluid Therapy , Humans , Long QT Syndrome/diagnostic imaging , Long QT Syndrome/physiopathology , Long QT Syndrome/therapy , Male , Syncope/diagnosis , Syncope/physiopathology , Syncope/therapy , Torsades de Pointes/diagnosis , Torsades de Pointes/physiopathology , Torsades de Pointes/therapy , Treatment OutcomeABSTRACT
BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has affected millions of people worldwide resulting in significant morbidity and mortality. Arrhythmias are prevalent and reportedly, the second most common complication. Several mechanistic pathways are proposed to explain the pro-arrhythmic effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. A number of treatment approaches have been trialled, each with its inherent unique challenges. This rapid systematic review aimed to examine the current incidence and available treatment of arrhythmias in COVID-19, as well as barriers to implementation. METHODS: Our search of scientific databases identified relevant published studies from 1 January 2000 until 1 June 2020. We also searched Google Scholar for grey literature. We identified 1729 publications of which 1704 were excluded. RESULTS: The incidence and nature of arrhythmias in the setting of COVID-19 were poorly documented across studies. The cumulative incidence of arrhythmia across studies of hospitalised patients was 6.9%. Drug-induced long QT syndrome secondary to antimalarial and antimicrobial therapy was a significant contributor to arrhythmia formation, with an incidence of 14.15%. Torsades de pointes (TdP) and sudden cardiac death (SCD) were reported. Treatment strategies aim to minimise this through risk stratification and regular monitoring of corrected QT interval (QTc). CONCLUSION: Patients with SARS-CoV-2 are at an increased risk of arrhythmias. Drug therapy is pro-arrhythmogenic and may result in TdP and SCD in these patients. Risk assessment and regular QTc monitoring are imperative for safety during the treatment course. Further studies are needed to guide future decision-making.
Subject(s)
Arrhythmias, Cardiac/etiology , COVID-19/complications , Long QT Syndrome/chemically induced , Anti-Arrhythmia Agents/therapeutic use , Anti-Bacterial Agents/adverse effects , Antimalarials/adverse effects , Arrhythmias, Cardiac/epidemiology , Arrhythmias, Cardiac/therapy , Atrial Fibrillation/epidemiology , Atrial Fibrillation/etiology , Atrial Fibrillation/therapy , Atrial Flutter/epidemiology , Atrial Flutter/etiology , Atrial Flutter/therapy , Azithromycin/adverse effects , Bradycardia/epidemiology , Bradycardia/etiology , Bradycardia/therapy , Cardiac Pacing, Artificial/methods , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/etiology , Electric Countershock/methods , Hospitalization , Humans , Hydroxychloroquine/adverse effects , Incidence , Long QT Syndrome/epidemiology , Long QT Syndrome/therapy , SARS-CoV-2 , Tachycardia, Ventricular/epidemiology , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/therapy , Torsades de Pointes/epidemiology , Torsades de Pointes/etiology , Torsades de Pointes/therapy , Ventricular Fibrillation/epidemiology , Ventricular Fibrillation/etiology , Ventricular Fibrillation/therapy , COVID-19 Drug TreatmentABSTRACT
BACKGROUND: The clinical symptoms and adverse events caused by pacemaker battery depletion are not uncommon, but it is easy to miss or misdiagnose them clinically. To raise the level of awareness towards this clinical situation, we report two cases. CASE PRESENTATION: We described two cases of pacemaker battery depletion. Case 1 was an 83-year-old male manifesting chest pain and dyspnea. Automatic reprogramming after pacemaker battery depletion resulted in pacemaker syndrome. While case 2 was an 80-year-old female with complete atrioventricular heart block and torsade de pointes, due to complete depletion of pacemaker battery. In addition, we introduce a method that can easily identify the depletion of the pacemaker battery, which has clinical promotion value of a certain degree. CONCLUSIONS: Those cases emphasize that serious morbidity can arise from pacemaker battery depletion, even in the early stages. Therefore, early detection and diagnosis is especially important.
Subject(s)
Atrioventricular Block/etiology , Chest Pain/etiology , Dyspnea/etiology , Electric Power Supplies/adverse effects , Equipment Failure , Pacemaker, Artificial/adverse effects , Torsades de Pointes/etiology , Aged, 80 and over , Atrioventricular Block/diagnosis , Atrioventricular Block/therapy , Chest Pain/diagnosis , Chest Pain/therapy , Device Removal , Dyspnea/diagnosis , Dyspnea/therapy , Fatal Outcome , Female , Humans , Male , Torsades de Pointes/diagnosis , Torsades de Pointes/therapy , Treatment OutcomeABSTRACT
As the coronavirus disease 19 (COVID-19) global pandemic rages across the globe, the race to prevent and treat this deadly disease has led to the "off-label" repurposing of drugs such as hydroxychloroquine and lopinavir/ritonavir, which have the potential for unwanted QT-interval prolongation and a risk of drug-induced sudden cardiac death. With the possibility that a considerable proportion of the world's population soon could receive COVID-19 pharmacotherapies with torsadogenic potential for therapy or postexposure prophylaxis, this document serves to help health care professionals mitigate the risk of drug-induced ventricular arrhythmias while minimizing risk of COVID-19 exposure to personnel and conserving the limited supply of personal protective equipment.
Subject(s)
Death, Sudden, Cardiac , Hydroxychloroquine , Long QT Syndrome , Lopinavir , Risk Adjustment/methods , Ritonavir , Torsades de Pointes , Anti-Infective Agents/administration & dosage , Anti-Infective Agents/adverse effects , Betacoronavirus/drug effects , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Drug Combinations , Drug Monitoring/methods , Drug Repositioning/ethics , Drug Repositioning/methods , Electrocardiography/methods , Humans , Hydroxychloroquine/administration & dosage , Hydroxychloroquine/adverse effects , Long QT Syndrome/chemically induced , Long QT Syndrome/mortality , Long QT Syndrome/therapy , Lopinavir/administration & dosage , Lopinavir/adverse effects , Pandemics , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Ritonavir/administration & dosage , Ritonavir/adverse effects , SARS-CoV-2 , Torsades de Pointes/chemically induced , Torsades de Pointes/mortality , Torsades de Pointes/therapySubject(s)
Fever/complications , Syncope/etiology , Ventricular Fibrillation/etiology , Ventricular Premature Complexes/complications , Amiodarone/therapeutic use , Coronary Angiography , Drug Therapy, Combination , Electric Countershock , Electrocardiography , Female , Humans , Lidocaine/therapeutic use , Middle Aged , Pharyngitis/complications , Purkinje Fibers/physiopathology , Recurrence , Streptococcal Infections/complications , Tonsillitis/complications , Torsades de Pointes/etiology , Torsades de Pointes/physiopathology , Torsades de Pointes/therapy , Ventricular Fibrillation/drug therapy , Ventricular Fibrillation/physiopathology , Ventricular Fibrillation/therapy , Ventricular Premature Complexes/physiopathologyABSTRACT
This is an article in the Journal of Clinical Pharmacology's Core Entrustable Professional Activities in Clinical Pharmacology series that discusses drug-induced proarrhythmia and is offered as a teaching aid for medical students and residents. Drugs from diverse pharmacological classes can lead to multiple types of arrhythmias including the polymorphic ventricular tachycardia torsades de pointes (TdP). Although typically occurring in self-limiting bursts with or without associated symptoms, which can range from mild lightheadedness and palpitations to syncope and seizures, TdP can also occasionally progress to ventricular fibrillation and sudden cardiac death. To provide patients with the optimal therapeutic benefits of potentially proarrhythmic drugs, prescribers are responsible for obtaining a good understanding of the compound's benefit-risk properties and perform a judicious assessment of the patient's clinical characteristics and individual risk factors. Dose adjustments and/or additional monitoring of electrocardiograms and electrolyte balances may be appropriate in some cases. This article explains the pharmacological mechanism of action of drug-induced proarrhythmia associated with compounds that prolong the repolarization period, illustrates how this liability is conveyed in a drug's prescribing information (label), details the clinical characteristics of patients most susceptible to this type of proarrhythmia, and describes interventions that can be made if TdP occurs. Three clinical vignettes are provided at the end of the article to highlight the relevance of the preceding discussions.
Subject(s)
Arrhythmias, Cardiac/chemically induced , Drug Prescriptions , Arrhythmias, Cardiac/therapy , Drug Labeling , Drug Monitoring , Drug-Related Side Effects and Adverse Reactions/epidemiology , Drug-Related Side Effects and Adverse Reactions/therapy , Education, Medical , Electrocardiography , Humans , Long QT Syndrome/chemically induced , Long QT Syndrome/therapy , Patient Education as Topic , Risk Assessment , Torsades de Pointes/chemically induced , Torsades de Pointes/therapyABSTRACT
One of the more challenging aspects of ECG interpretation is measurement and interpretation of the QT interval. This interval represents the time taken for the ventricles to completely repolarise after activation. Abnormal prolongation of the QT interval can lead to torsades de pointes, a form of potentially life-threatening polymorphic ventricular tachycardia (VT). Detection of a prolonged QT interval is essential as this can be a reversible problem, particularly in the context of the use of a variety of commonly prescribed medications in the hospital setting. Automated ECG printouts cannot be relied upon to diagnose QT interval prolongation; thus, the onus is on the clinician to identify it. This is a difficult task, as the normal QT interval is typically measured relative to the heart rate. Therefore, the QT interval often requires "correction" for the current heart rate, in order to correctly stratify the risk of torsades de pointes. A wealth of correctional formulae have been derived, but none has proven superior. We present an approach to the ECG in this context, and a step-by-step guide to manually measuring and correcting the QT interval, and an approach to management in common hospital-based clinical scenarios.
Subject(s)
Long QT Syndrome , Physicians , Torsades de Pointes , Electrocardiography , Humans , Long QT Syndrome/chemically induced , Long QT Syndrome/diagnosis , Long QT Syndrome/therapy , Torsades de Pointes/chemically induced , Torsades de Pointes/diagnosis , Torsades de Pointes/therapyABSTRACT
Stroke involving some areas of the cerebral hemisphere, such as insula, amygdala, and lateral hypothalamus, may cause changes in autonomic control of cardiac function. A 58-year-old woman presented to the emergency department for acute onset of left facial-brachial-crural hemiparesis and dysarthria. A brain CT scan showed subacute ischemic lesion with hemorrhagic infarction in right insular-rolandic cortex. Over the next few days ECG showed severe bradycardia with elongation of QTc, significative pauses (5 seconds), runs of nonsustained ventricular tachycardia and torsades de pointes. Drug induced and other several possible causes of elongation of QT and bradycardia such as hypokalemia, a history of heart failure, and structural heart disease were ruled out. The case confirms that insular cortex plays a major role in stroke-induced cardiovascular changes.
Subject(s)
Cerebral Cortex/blood supply , Heart Conduction System/physiopathology , Heart Rate , Long QT Syndrome/etiology , Stroke/complications , Torsades de Pointes/etiology , Action Potentials , Bradycardia/etiology , Bradycardia/physiopathology , Cardiac Pacing, Artificial , Cerebral Cortex/diagnostic imaging , Female , Humans , Long QT Syndrome/diagnosis , Long QT Syndrome/physiopathology , Long QT Syndrome/therapy , Middle Aged , Pacemaker, Artificial , Stroke/diagnostic imaging , Stroke/physiopathology , Stroke/therapy , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/physiopathology , Torsades de Pointes/diagnosis , Torsades de Pointes/physiopathology , Torsades de Pointes/therapy , Treatment OutcomeABSTRACT
BACKGROUND: The standard approach for urgent trans-venous temporary cardiac pacemaker (TVTP) implantation is fluoroscopy guidance. The delay in activation of the fluoroscopy-room and the transfer of unstable patients may be life-threatening. Echocardiography-guided TP implantation may increase the safety of the patients by obviating the need for in-hospital transfer. We examined the feasibility and safety of echocardiography-guided vs. fluoroscopy-guided TVTP implantation. METHODS: From January 2015 to September 2017 data for consecutive patients who needed emergent TVTP implantation were retrospectively reviewed. Ultrasound-guided TVTP protocol that was introduced in our center in January 2015 involved ultrasound guidance for both central venous access and pacing lead positioning. Access sites included femoral, subclavian, or jugular veins. Electrodes were placed in the right ventricular apex by means of echocardiographic monitoring in intensive care unit or by fluoroscopic guidance. Endpoints were achievement of successful ventricular pacing and procedural complications. RESULTS: Sixty-six patients (17 echocardiography-guided and 49 fluoroscopy-guided) were included. There were no differences in pacing threshold between the echocardiography-guided group and the fluoroscopy-guided group (0.75 ± 0.58 mA vs. 0.57 ± 0.35 mA, p = 0.24). The access site for implantation was femoral vein in 27% for the fluoroscopy-guided vs. none for the echocardiography-guided approach (p = 0.015). One hematoma and one related infection occurred in the fluoroscopy-guided group. The need for electrode repositioning was observed in 1 patient in each group. There were no procedural-related deaths in either group. CONCLUSIONS: Echocardiography-guided temporary cardiac pacing is a feasible and safe alternative to fluoroscopy-guided approach and significantly lowers the need for in-hospital transfer.
Subject(s)
Arrhythmias, Cardiac/therapy , Cardiac Catheterization/methods , Echocardiography/methods , Pacemaker, Artificial , Prosthesis Implantation/methods , Aged , Aged, 80 and over , Atrioventricular Block/therapy , Case-Control Studies , Emergencies , Feasibility Studies , Female , Fluoroscopy/methods , Heart Arrest/therapy , Humans , Male , Middle Aged , Point-of-Care Systems , Retrospective Studies , Sick Sinus Syndrome/therapy , Surgery, Computer-Assisted , Tachycardia, Ventricular/therapy , Torsades de Pointes/therapyABSTRACT
Se estableció los efectos de la claritromicina sobre el intervalo QT corregido (iQTc) en pacientes gerontes, que requirieron hospitalización por infección respiratoria, mediante registro electrocardiográfico al inicio y al final del tratamiento. Se observó en 61% de los casos un aumento del iQTC (0,04 seg en promedio). No obstante las comorbilidades asociadas, ningún caso evolucionó a taquicardia ventricular polimórfica
The effects of clarithromycin on the corrected QT interval (iQTc) in elderly patients, who required hospitalization due to respiratory infection, were established by electrocardiographic recording at the beginning and at the end of the treatment. An increase in iQTC was observed in all cases (0.04 sec on average). Despite the associated comorbidities, no case evolved to polymorphic ventricular tachycardia