Electrical Storm Secondary to Amiodarone-Related Torsades de Pointes Following PCI for Acute Myocardial Infarction: A Case Report

Electrical Storm Secondary to Amiodarone-Related Torsades de Pointes Following PCI for Acute Myocardial Infarction: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Electrical Storm Secondary to Amiodarone-Related Torsades de Pointes Following PCI for Acute Myocardial Infarction: A Case Report Rong Chen, Tudi Li, Jiaying Zhang, Shiyang Zhang, Zhihuan Zeng, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8539511/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: Electrical storm (ES) is a life-threatening complication of acute myocardial infarction (AMI) post-percutaneous coronary intervention (PCI), characterized by recurrent malignant ventricular arrhythmias. Amiodarone, a widely used class Ⅲ antiarrhythmic drug, may induce QT interval prolongation and torsades de pointes (TdP), especially in the presence of electrolyte disturbances and reduced myocardial repolarization reserve. Case presentation: A 78-year-old female with a 20-year history of uncontrolled hypertension was admitted to the emergency department with "chest tightness and retrosternal pain for 5 days, acute exacerbation for 4 hours". Clinical evaluation confirmed acute non-ST-segment elevation myocardial infarction and acute decompensated heart failure. Emergency PCI was performed 6 hours after admission, with successful stenting of the left anterior descending artery (LAD). Amiodarone was administered for new-onset atrial fibrillation, which was followed by progressive QT interval prolongation and hypokalemia. On day 5 of hospitalization, the patient developed TdP-related ES, which was successfully managed with electrical defibrillation, immediate amiodarone withdrawal, electrolyte supplementation, and isoproterenol infusion. Conclusion: For AMI patients receiving amiodarone post-PCI, close monitoring of QT interval (corrected QT, QTc) and electrolyte levels is essential. Timely identification and intervention of modifiable risk factors can effectively improve outcomes of ES caused by amiodarone-related TdP. Electrical storm Amiodarone Torsades de pointes Percutaneous coronary intervention Acute myocardial infarction Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Background Electrical storm (ES) is defined as three or more episodes of ventricular fibrillation (VF) or hemodynamically unstable ventricular tachycardia (VT) within 24 hours, requiring electrical defibrillation or cardioversion [ 1 ]. It is a rare but fatal complication of AMI, with high short-term mortality [ 2 ]. Amiodarone exerts broad-spectrum antiarrhythmic effects by blocking potassium channels, but its side effect of QT interval prolongation may precipitate TdP [ 3 ]. TdP is a polymorphic VT characterized by twisting QRS complex morphology around the isoelectric line, closely associated with QTc prolongation (QTc > 500 ms in both genders) or a significant increase from baseline (> 60 ms) [ 4 ]. Hospitalized AMI patients often have multiple TdP risk factors, including advanced age, female gender, and electrolyte disorders, which further increase the proarrhythmic risk of amiodarone by reducing myocardial repolarization reserve [ 4 , 5 ]. Herein, we report a case of ES caused by amiodarone-related TdP on day 5 post-PCI for AMI, aiming to provide clinical insights for the prevention and management of such complications. Case presentation An 78-year-old female was admitted to the emergency department complaining of chest tightness and retrosternal dull pain for 5 days, with acute exacerbation over the past 4 hours. The pain was non-exertional, unrelieved by rest, and non-radiating. She had a 20-year history of hypertension, with irregular oral administration of nifedipine controlled-release tablets and no regular blood pressure monitoring. She denied a history of diabetes mellitus, hyperlipidemia, smoking, alcohol consumption, as well as a family history of cardiovascular diseases or sudden cardiac death. Vital signs on admission were as follows: temperature 36.4℃, heart rate 86 beats per minute (bpm), respiratory rate 22 breaths per minute, blood pressure 139/88 mmHg, oxygen saturation 92% (on room air); height 155 cm, weight 58 kg, and body mass index 24.0 kg/m². Physical examination findings: the patient was alert with clear consciousness; no cyanosis or jaundice was observed on the skin and mucous membranes; bilateral superficial lymph nodes were non-palpable and non-enlarged; breath sounds were clear bilaterally, with fine moist rales auscultated at the bases of both lungs; heart rate was 86 bpm, rhythm regular, heart sounds of normal intensity, and no pathological murmurs were detected; the abdomen was soft, without tenderness or rebound tenderness; the liver and spleen were not palpable below the costal margin; no lower extremity edema was noted; and neurological examination revealed no abnormalities. Auxiliary examinations were performed upon admission. Electrocardiogram (ECG) demonstrated sinus rhythm and ST-segment depression in leads Ⅱ, Ⅲ, aVF, and V4-V6 ( Fig. 1 ) , with a QT interval of 378 ms. The detailed results of admission laboratory tests are summarized in Table 1 . Transthoracic echocardiography (TTE) showed a left ventricular ejection fraction (LVEF) of 49%, left ventricular end-diastolic diameter of 53 mm, hypokinesis of the anterior and lateral walls of the left ventricle, and no significant valvular lesions. Based on the above findings, the patient was diagnosed with acute non-ST-segment elevation myocardial infarction (Killip class II) and acute decompensated heart failure. Standard anti-ischemic therapy was initiated immediately after admission: aspirin 300 mg, ticagrelor 180 mg, and intravenous nitroglycerin infusion. Shortly thereafter, the patient developed atrial fibrillation with a ventricular rate of 120–130 bpm ( Fig. 2 A ) . Metoprolol administration failed to control the ventricular rate; therefore, intravenous amiodarone was administered at a dose of 150 mg infused over 10 minutes, followed by a continuous infusion at 1 mg/min for 24 hours. Sinus rhythm was restored within 2 hours of amiodarone initiation ( Fig. 2 B ) , and the patient was subsequently switched to oral amiodarone 200 mg three times daily for maintenance therapy. Emergency coronary angiography (CAG) was performed 6 hours after admission ( Fig. 3 ) . The angiographic findings were as follows: the coronary circulation was right-dominant; the left main coronary artery was normal; the proximal segment of the left circumflex artery (LCX) was chronically occluded with a Thrombolysis in Myocardial Infarction (TIMI) flow grade of 0, with collateral circulation supplied by the first diagonal branch; the left anterior descending artery (LAD) had mild proximal calcification and an acute occlusion in the mid-segment (TIMI 0); the proximal segment of the right coronary artery (RCA) was diffusely chronically occluded (TIMI 0) with minimal collateral circulation. Intra-aortic balloon pump (IABP) support (2:1 counterpulsation) was implemented prior to the interventional procedure. A 2.75×23 mm drug-eluting stent (Abbott Xience Alpine) was successfully implanted at the occluded segment of the LAD, resulting in the restoration of TIMI flow grade 3 in the target vessel. Two hours postoperatively, the patient's hemodynamic status improved (blood pressure 125/75 mmHg), lung rales resolved, and the IABP was removed. Elective revascularization of the LCX and RCA was planned for a later stage. During hospital days 2–4, the patient's hemodynamic status remained stable; however, serial ECGs showed progressive prolongation of the corrected QT interval (QTc): 435 ms on day 2, 472 ms on day 3, and 498 ms on day 4 ( Fig. 2 C ) . Electrolyte analysis on day 4 revealed hypokalemia (serum potassium: 3.07 mmol/L) and hypomagnesemia (serum magnesium: 0.85 mmol/L). Intravenous potassium supplementation was initiated immediately, with 15 mL of 10% potassium chloride diluted in 500 mL of 5% glucose solution infused at a rate of 20 drops/min, targeting a serum potassium level of 4.0–4.5 mmol/L. On hospital day 5, ECG monitoring revealed torsades de pointes (TdP) ( Fig. 4 ) , accompanied by syncope and convulsions. Immediate asynchronous electrical defibrillation with a biphasic shock of 200 J was performed. Subsequent interventions included: immediate discontinuation of both oral and intravenous amiodarone; intravenous injection of 2 g 25% magnesium sulfate (diluted in 20 mL of 5% glucose solution); and continuous intravenous infusion of isoproterenol at an initial dose of 1 µg/min, with titration to maintain the ventricular rate at 90–100 bpm. Within 2 hours of the initial TdP episode, four recurrent episodes occurred, all of which were successfully converted to sinus rhythm by electrical defibrillation ( Fig. 5 ) . After 24 hours of continuous isoproterenol infusion, the patient's sinus rhythm stabilized without further arrhythmic events. Re-examination showed a QTc interval of 425 ms and a serum potassium level of 3.8 mmol/L. The isoproterenol infusion was then gradually tapered and eventually discontinued. The patient was discharged on hospital day 10. Discharge evaluations showed: LVEF 52% (by TTE), troponin I < 0.04 ng/mL, and N-terminal pro-brain natriuretic peptide 2150 pg/mL. The discharge medication regimen was as follows: spironolactone 20 mg once daily, rivaroxaban 15 mg once daily, clopidogrel 75 mg once daily, atorvastatin 20 mg once nightly, dapagliflozin 10 mg once daily, potassium magnesium aspartate 1 tablet three times daily, and sacubitril/valsartan 50 mg twice daily. During the 6-month follow-up period, the patient remained asymptomatic with stable vital signs and good medication adherence. Repeat ECGs showed no QT interval prolongation or arrhythmias. Repeat TTE demonstrated an improved LVEF of 55%. The patient declined the planned elective PCI for revascularization of the LCX and RCA. Discussion and conclusions This case describes an elderly female with AMI who developed ES due to amiodarone-related TdP post-PCI. Key clinical features include multiple TdP risk factors (advanced age, female gender, AMI, hypokalemia), progressive QTc prolongation after amiodarone administration, and successful rescue with targeted interventions. Amiodarone blocks the rapid component of the delayed rectifier potassium current (IKr), prolonging ventricular repolarization and QT interval [ 6 ]. Unlike high-risk QT-prolonging drugs, amiodarone usually uniformly prolongs repolarization across all myocardial layers, resulting in a low intrinsic TdP risk. However, in patients with reduced repolarization reserve (e.g., AMI, electrolyte disturbances), the proarrhythmic risk increases significantly [ 7 ]. This patient had AMI-induced myocardial ischemia and hypokalemia (3.07 mmol/L), which further impaired repolarization reserve by inhibiting IKr and increasing myocardial repolarization heterogeneity [ 8 ]. The combination led to progressive QTc prolongation (from 392 ms to 498 ms) and finally triggered TdP. ES development was attributed to persistent arrhythmic triggers: delayed amiodarone withdrawal during QTc prolongation and incomplete correction of hypokalemia [ 9 ]. Recurrent TdP further activated the sympathetic nervous system, forming a vicious cycle of "arrhythmia → sympathetic activation → further arrhythmia", consistent with ES pathophysiology described in the literature [ 10 ]. The diagnosis of TdP mainly relies on ECG features and clinical context. TdP is characterized by polymorphic VT with twisting QRS morphology, accompanied by QTc > 500 ms or ≥ 60 ms increase from baseline [ 11 ]. Although the maximum QTc of this patient was 498 ms (not exceeding 500 ms), it increased by 106 ms from the baseline, combined with typical TdP morphology and hypokalemia, so the diagnosis was clear. Differential diagnosis is crucial to avoid mismanagement. Idiopathic ventricular fibrillation was excluded due to the presence of structural heart disease (AMI) and QT prolongation [ 12 ]. Congenital long QT syndrome was ruled out by normal baseline QTc and negative family history [ 13 ]. Ischemia-induced polymorphic VT was excluded by the absence of new coronary stenosis [ 14 ]. These differentiations are based on literature-described disease characteristics, enhancing diagnostic accuracy . The treatment of TdP-related ES should focus on trigger removal, substrate correction, and arrhythmia suppression. The treatment strategy in this case aligned with guidelines and literature recommendations[ 3 , 15 ]: Discontinuing QT-prolonging drugs is a Class I recommendation for drug-induced long QT syndrome. Amiodarone was immediately withdrawn after TdP diagnosis, eliminating the direct cause of QT prolongation. Magnesium sulfate (2 g intravenous) is first-line therapy for TdP regardless of serum magnesium level. Potassium supplementation targeted 4.0-4.5 mmol/L to improve repolarization reserve. Isoproterenol infusion (maintaining ventricular rate at 90–100 beats/min) shortened QT interval and reduced repolarization heterogeneity. This is consistent with literature showing that increasing heart rate can effectively suppress TdP. Immediate defibrillation for hemodynamically unstable TdP is mandatory, which maintained hemodynamic stability during recurrent episodes. This case highlights key considerations for AMI patients post-PCI: First, AMI patients receiving amiodarone require QTc monitoring every 8–12 hours and electrolyte surveillance. Timely intervention for QTc prolongation (e.g., QTc > 500 ms or ≥ 60 ms increase from baseline) or electrolyte disorders reduces TdP risk. Second, AMI patients should maintain potassium levels at 4.0-4.5 mmol/L. Even mild hypokalemia synergistically increases proarrhythmic risk with QT-prolonging drugs. Third, for drug-related TdP-induced ES, prioritize trigger removal over aggressive antiarrhythmic therapy. Beta-blockers may be used for sympathetic activation, while isoproterenol or overdrive pacing is effective for recurrent TdP [ 16 ]. In conclusion, amiodarone-related TdP is a rare but severe complication post-PCI for AMI. Comprehensive risk assessment, close monitoring of QTc and electrolytes, and evidence-based interventions improve patient outcomes. This case provides valuable insights for managing similar complications. Abbreviations ES: Electrical storm; AMI: Acute myocardial infarction; PCI: Percutaneous coronary intervention; TdP: Torsades de pointes; VT: Ventricular tachycardia; VF: Ventricular fibrillation; NSTEMI: Non-ST-segment elevation myocardial infarction; ECG: Electrocardiogram; QTc: Corrected QT interval; CAG: Coronary angiography; TIMI: Thrombolysis in myocardial infarction; LAD: Left anterior descending artery; LCX: Left circumflex artery; RCA: Right coronary artery; IABP: Intra-aortic balloon pump; LVEF: Left ventricular ejection fraction; IKr: Rapid component of the delayed rectifier potassium current. Declarations Ethics approval and consent to participate This study was conducted in strict accordance with the ethical principles of medical research and the Helsinki Declaration. Consent for publication We confirm that informed consent was obtained from the participants for the use of clinical information within the scope that does not compromise their anonymity. Availability of data and materials The datasets analyzed during the current study are available from the corresponding author upon request. Competing interests The authors declare that they have no competing interests. Funding Guangzhou Science and Technology Plan Project (No. 2025A03J3718),Medical Research Fund of Guangdong Province (No. B2024095), Teaching Reform Project of the First Affiliated Hospital (Clinical Medical School) of Guangdong Pharmaceutical University (No. 2024JX09),which has played a pivotal role in making this project possible. Author Contributions Rong Chen: Writing–original draft; Tudi Li: Data curation; Jiaying Zhang: Data curation; Shiyang Zhang: Writing–review & editing; Zhihuan Zeng, Xiuhong Weng: Supervision, Writing–review & editing, Funding acquisition. All authors read and approved the final manuscript. Acknowledgements Not applicable. References Credner SC, Klingenheben T, Mauss O, et al. Electrical storm in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications. J Am Coll Cardiol. 1998;32(7):1909-1915. doi:10.1016/s0735-1097(98)00495-1 Liu B, Xie B, Chen X, et al. A successful case of electrical storm rescue after acute myocardial infarction. BMC Cardiovasc Disord. 2022;22(1):537. Published 2022 Dec 9. doi:10.1186/s12872-022-02982-2 Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997-4126. doi:10.1093/eurheartj/ehac262 Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047-1060. doi:10.1161/CIRCULATIONAHA.109.192704 Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022. doi:10.1056/NEJMra032426 Khan SA, Emmanuel S, Shantha Kumar V, et al. Long QT Syndrome With Drugs Used in the Management of Arrhythmias: A Systematic Review. Cureus. 2024;16(7):e65857. Published 2024 Jul 31. doi:10.7759/cureus.65857 Friedman A, Miles J, Liebelt J, et al. QT Dispersion and Drug-Induced Torsade de Pointes. Cureus. 2021;13(1):e12895. Published 2021 Jan 25. doi:10.7759/cureus.12895 Grune J, Lewis AJM, Yamazoe M, et al. Neutrophils incite and macrophages avert electrical storm after myocardial infarction. Nat Cardiovasc Res. 2022;1(7):649-664. doi:10.1038/s44161-022-00094-w Han C, Qiu R, Li L, et al. Electrical storm refractory multiple antiarrhythmic medications was stopped by interatrial shunting procedure-A case report. Front Cardiovasc Med. 2022;9:1012916. Published 2022 Nov 17. doi:10.3389/fcvm.2022.1012916 Elsokkari I, Tsuji Y, Sapp JL, Nattel S. Recent Insights Into Mechanisms and Clinical Approaches to Electrical Storm. Can J Cardiol. 2022;38(4):439-453. doi:10.1016/j.cjca.2021.12.015 El-Sherif N, Turitto G, Boutjdir M. Acquired long QT syndrome and torsade de pointes. Pacing Clin Electrophysiol. 2018;41(4):414-421. doi:10.1111/pace.13296 Belhassen B. Idiopathic ventricular fibrillation. Heart Rhythm. 2024;21(4):509-511. doi:10.1016/j.hrthm.2024.01.012 Kaufman ES, Eckhardt LL, Ackerman MJ, et al. Management of Congenital Long-QT Syndrome: Commentary From the Experts. Circ Arrhythm Electrophysiol. 2021;14(7):e009726. doi:10.1161/CIRCEP.120.009726 Kuroda S, Mizukami A, Hayashi T, Yoshioka K, Suzuki M, Matsumura A. Verapamil-sensitive ventricular tachycardia demonstrating multiform QRS morphology in a patient with ischemic cardiomyopathy. HeartRhythm Case Rep. 2019;5(12):573-577. Published 2019 Sep 6. doi:10.1016/j.hrcr.2019.08.013 Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2018;15(10):e73-e189. doi:10.1016/j.hrthm.2017.10.036 Thomas SH, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes. Br J Clin Pharmacol. 2016;81(3):420-427. doi:10.1111/bcp.12726 Table Table1 Summary of Laboratory Findings on Admission Parameter Adult Reference Range Admission Value White blood cell count (×10⁹/L) 3.5-9.5 11.62 Neutrophil proportion 0.40-9.5 0.771 Hemoglobin (g/L) 115-150 116 Cardiac troponin I (ng/mL) ＜0.01 11.27 Creatine kinase-MB (ng/mL) ＜5.00 69.64 Myoglobin (ng/mL) ＜70 ＞600 D-dimer (mg/L) ＜0.5 1.45 NTpro-BNP（ng/ml） ＜300 5052 Creatinine (μmol/L) 41-81 89 Potassium (mmol/L) 3.5-5.3 3.07 AST（U/L） 7-40 15 ALT（U/L） 13-35 75 Total cholesterol (mmol/L) 3.6-5.69 8.61 Triglycerides (mmol/L) 0.33-1.7 1.42 High-density lipoprotein (mmol/L) 0.91-1.95 1.29 Low-density lipoprotein (mmol/L) - 5.43 Fasting blood glucose (mmol/L) 3.9-6.1 10.32 2-hour postprandial blood glucose (mmol/L) 3.89-7.8 12.09 Glycated hemoglobin (%) 4.2-6.2 7.7 Arterial blood gas analysis PH 7.25-7.45 7.505 PCO2(mmHg) 32-45 29.3 PO2（mmHg） 80-100 58.1 Additional Declarations No competing interests reported. Supplementary Files Table1.docx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8539511","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":583530835,"identity":"59f35e44-5b3c-40fb-8bb6-ac97be856557","order_by":0,"name":"Rong Chen","email":"","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":false,"prefix":"","firstName":"Rong","middleName":"","lastName":"Chen","suffix":""},{"id":583530836,"identity":"be79e603-dca0-4af9-ad6a-140cdcaea58c","order_by":1,"name":"Tudi Li","email":"","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":false,"prefix":"","firstName":"Tudi","middleName":"","lastName":"Li","suffix":""},{"id":583530837,"identity":"fbe926ac-a929-428e-99b5-5d7cfd267f8c","order_by":2,"name":"Jiaying Zhang","email":"","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":false,"prefix":"","firstName":"Jiaying","middleName":"","lastName":"Zhang","suffix":""},{"id":583530838,"identity":"82387961-8998-4105-8107-6e23682bf7f1","order_by":3,"name":"Shiyang Zhang","email":"","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":false,"prefix":"","firstName":"Shiyang","middleName":"","lastName":"Zhang","suffix":""},{"id":583530839,"identity":"81a93a2b-2431-481c-b8a1-f90596b6aedc","order_by":4,"name":"Zhihuan Zeng","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAnklEQVRIiWNgGAWjYHACNoYPBjZ2pGlhnFGQlkyaFmaeD4cYG4hWL+9//NljG4MDzAzsh49uIEqL4YED6cY5Bnf4GHjS0m4Qp6Wx4Zh0jsEzZgYJHjMitTQztklbGBxmbCBaizwbM5s0A0laDHjY2CR7DNKS2Yj2i3z/8WcSP/7Y2PGzHz5GpC0HoAw2opSDbWkgWukoGAWjYBSMWAAAsCQqJOnoIBgAAAAASUVORK5CYII=","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":true,"prefix":"","firstName":"Zhihuan","middleName":"","lastName":"Zeng","suffix":""},{"id":583530840,"identity":"2581df54-99ef-4536-bd16-d144144c4338","order_by":5,"name":"Xiuhong Weng","email":"","orcid":"","institution":"First Affiliated Hospital of Guangdong Pharmaceutical University","correspondingAuthor":false,"prefix":"","firstName":"Xiuhong","middleName":"","lastName":"Weng","suffix":""}],"badges":[],"createdAt":"2026-01-07 09:38:42","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8539511/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8539511/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":101826808,"identity":"087de38f-f4ba-48b9-8543-e940891762bb","added_by":"auto","created_at":"2026-02-04 05:18:37","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":280183,"visible":true,"origin":"","legend":"\u003cp\u003eSerial coronary angiography and PCI images. (A) Coronary angiography showing CTO of the LCX.(B) Coronary angiography demonstrating diffuse CTO in the proximal segment of the RCA. (C) Coronary angiography revealing acute occlusion in the mid-segment of the LAD. (D) PCI angiography of the LAD, confirming TIMI 3 coronary flow restoration.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/4eaccc769990d757eeec1922.png"},{"id":101826811,"identity":"a4a39ad5-3054-4908-ac67-0bcad0243332","added_by":"auto","created_at":"2026-02-04 05:18:37","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":941868,"visible":true,"origin":"","legend":"\u003cp\u003eElectrocardiogram on admission\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/e7f63cab28b08e1b8483afeb.png"},{"id":101880798,"identity":"c8c237f8-19a7-483e-bcf7-b4c45630248b","added_by":"auto","created_at":"2026-02-04 15:06:23","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":667587,"visible":true,"origin":"","legend":"\u003cp\u003e(A) Sudden Atrial Fibrillation after admission(B) Sinus rhythm restored with amiodarone at 2 h after admission(C) Marked QT interval prolongation on the 4th hospital day\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/63744ef77f51030d494d153f.png"},{"id":101826810,"identity":"5b3753b5-c97d-4d64-9a51-e93f91a9749a","added_by":"auto","created_at":"2026-02-04 05:18:37","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":743697,"visible":true,"origin":"","legend":"\u003cp\u003eSudden torsades de pointes was noted on continuous electrocardiographic monitoring\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/3511c5ec0371614480a9516f.png"},{"id":101826813,"identity":"16838509-cc52-40c6-a700-9fd2a3d58a36","added_by":"auto","created_at":"2026-02-04 05:18:37","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":1207627,"visible":true,"origin":"","legend":"\u003cp\u003eElectrocardiogram of defibrillation during electrical storm onset\u003c/p\u003e","description":"","filename":"5.png","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/82772f13f241a59412a88d44.png"},{"id":104423507,"identity":"f78c120a-9671-4182-9dee-0ef5a63cc3a4","added_by":"auto","created_at":"2026-03-11 14:13:14","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":4144799,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/c1255574-974d-4969-b59e-d9b1be4aec9f.pdf"},{"id":101881167,"identity":"520871f4-0795-4707-9333-1ac93df961cd","added_by":"auto","created_at":"2026-02-04 15:10:22","extension":"docx","order_by":0,"title":"","display":"","copyAsset":false,"role":"supplement","size":13883,"visible":true,"origin":"","legend":"","description":"","filename":"Table1.docx","url":"https://assets-eu.researchsquare.com/files/rs-8539511/v1/15cbf9d635e8afc33f4a8d45.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":"Electrical Storm Secondary to Amiodarone-Related Torsades de Pointes Following PCI for Acute Myocardial Infarction: A Case Report","fulltext":[{"header":"Background","content":"\u003cp\u003eElectrical storm (ES) is defined as three or more episodes of ventricular fibrillation (VF) or hemodynamically unstable ventricular tachycardia (VT) within 24 hours, requiring electrical defibrillation or cardioversion [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. It is a rare but fatal complication of AMI, with high short-term mortality [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Amiodarone exerts broad-spectrum antiarrhythmic effects by blocking potassium channels, but its side effect of QT interval prolongation may precipitate TdP [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. TdP is a polymorphic VT characterized by twisting QRS complex morphology around the isoelectric line, closely associated with QTc prolongation (QTc\u0026thinsp;\u0026gt;\u0026thinsp;500 ms in both genders) or a significant increase from baseline (\u0026gt;\u0026thinsp;60 ms) [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Hospitalized AMI patients often have multiple TdP risk factors, including advanced age, female gender, and electrolyte disorders, which further increase the proarrhythmic risk of amiodarone by reducing myocardial repolarization reserve [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Herein, we report a case of ES caused by amiodarone-related TdP on day 5 post-PCI for AMI, aiming to provide clinical insights for the prevention and management of such complications.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eAn 78-year-old female was admitted to the emergency department complaining of chest tightness and retrosternal dull pain for 5 days, with acute exacerbation over the past 4 hours. The pain was non-exertional, unrelieved by rest, and non-radiating. She had a 20-year history of hypertension, with irregular oral administration of nifedipine controlled-release tablets and no regular blood pressure monitoring. She denied a history of diabetes mellitus, hyperlipidemia, smoking, alcohol consumption, as well as a family history of cardiovascular diseases or sudden cardiac death.\u003c/p\u003e\n\u003cp\u003eVital signs on admission were as follows: temperature 36.4℃, heart rate 86 beats per minute (bpm), respiratory rate 22 breaths per minute, blood pressure 139/88 mmHg, oxygen saturation 92% (on room air); height 155 cm, weight 58 kg, and body mass index 24.0 kg/m². Physical examination findings: the patient was alert with clear consciousness; no cyanosis or jaundice was observed on the skin and mucous membranes; bilateral superficial lymph nodes were non-palpable and non-enlarged; breath sounds were clear bilaterally, with fine moist rales auscultated at the bases of both lungs; heart rate was 86 bpm, rhythm regular, heart sounds of normal intensity, and no pathological murmurs were detected; the abdomen was soft, without tenderness or rebound tenderness; the liver and spleen were not palpable below the costal margin; no lower extremity edema was noted; and neurological examination revealed no abnormalities.\u003c/p\u003e\n\u003cp\u003eAuxiliary examinations were performed upon admission. Electrocardiogram (ECG) demonstrated sinus rhythm and ST-segment depression in leads Ⅱ, Ⅲ, aVF, and V4-V6 \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e1\u003c/span\u003e\u003cstrong\u003e)\u003c/strong\u003e, with a QT interval of 378 ms. The detailed results of admission laboratory tests are summarized in Table \u003cspan\u003e1\u003c/span\u003e. Transthoracic echocardiography (TTE) showed a left ventricular ejection fraction (LVEF) of 49%, left ventricular end-diastolic diameter of 53 mm, hypokinesis of the anterior and lateral walls of the left ventricle, and no significant valvular lesions.\u003c/p\u003e\n\u003cp\u003eBased on the above findings, the patient was diagnosed with acute non-ST-segment elevation myocardial infarction (Killip class II) and acute decompensated heart failure. Standard anti-ischemic therapy was initiated immediately after admission: aspirin 300 mg, ticagrelor 180 mg, and intravenous nitroglycerin infusion. Shortly thereafter, the patient developed atrial fibrillation with a ventricular rate of 120–130 bpm \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e2\u003c/span\u003eA\u003cstrong\u003e)\u003c/strong\u003e. Metoprolol administration failed to control the ventricular rate; therefore, intravenous amiodarone was administered at a dose of 150 mg infused over 10 minutes, followed by a continuous infusion at 1 mg/min for 24 hours. Sinus rhythm was restored within 2 hours of amiodarone initiation \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e2\u003c/span\u003eB\u003cstrong\u003e)\u003c/strong\u003e, and the patient was subsequently switched to oral amiodarone 200 mg three times daily for maintenance therapy.\u003c/p\u003e\n\u003cp\u003eEmergency coronary angiography (CAG) was performed 6 hours after admission \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e3\u003c/span\u003e\u003cstrong\u003e)\u003c/strong\u003e. The angiographic findings were as follows: the coronary circulation was right-dominant; the left main coronary artery was normal; the proximal segment of the left circumflex artery (LCX) was chronically occluded with a Thrombolysis in Myocardial Infarction (TIMI) flow grade of 0, with collateral circulation supplied by the first diagonal branch; the left anterior descending artery (LAD) had mild proximal calcification and an acute occlusion in the mid-segment (TIMI 0); the proximal segment of the right coronary artery (RCA) was diffusely chronically occluded (TIMI 0) with minimal collateral circulation. Intra-aortic balloon pump (IABP) support (2:1 counterpulsation) was implemented prior to the interventional procedure. A 2.75×23 mm drug-eluting stent (Abbott Xience Alpine) was successfully implanted at the occluded segment of the LAD, resulting in the restoration of TIMI flow grade 3 in the target vessel. Two hours postoperatively, the patient's hemodynamic status improved (blood pressure 125/75 mmHg), lung rales resolved, and the IABP was removed. Elective revascularization of the LCX and RCA was planned for a later stage.\u003c/p\u003e\n\u003cp\u003eDuring hospital days 2–4, the patient's hemodynamic status remained stable; however, serial ECGs showed progressive prolongation of the corrected QT interval (QTc): 435 ms on day 2, 472 ms on day 3, and 498 ms on day 4 \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e2\u003c/span\u003eC\u003cstrong\u003e)\u003c/strong\u003e. Electrolyte analysis on day 4 revealed hypokalemia (serum potassium: 3.07 mmol/L) and hypomagnesemia (serum magnesium: 0.85 mmol/L). Intravenous potassium supplementation was initiated immediately, with 15 mL of 10% potassium chloride diluted in 500 mL of 5% glucose solution infused at a rate of 20 drops/min, targeting a serum potassium level of 4.0–4.5 mmol/L.\u003c/p\u003e\n\u003cp\u003eOn hospital day 5, ECG monitoring revealed torsades de pointes (TdP) \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e4\u003c/span\u003e\u003cstrong\u003e)\u003c/strong\u003e, accompanied by syncope and convulsions. Immediate asynchronous electrical defibrillation with a biphasic shock of 200 J was performed. Subsequent interventions included: immediate discontinuation of both oral and intravenous amiodarone; intravenous injection of 2 g 25% magnesium sulfate (diluted in 20 mL of 5% glucose solution); and continuous intravenous infusion of isoproterenol at an initial dose of 1 µg/min, with titration to maintain the ventricular rate at 90–100 bpm. Within 2 hours of the initial TdP episode, four recurrent episodes occurred, all of which were successfully converted to sinus rhythm by electrical defibrillation \u003cstrong\u003e(\u003c/strong\u003eFig. \u003cspan\u003e5\u003c/span\u003e\u003cstrong\u003e)\u003c/strong\u003e. After 24 hours of continuous isoproterenol infusion, the patient's sinus rhythm stabilized without further arrhythmic events. Re-examination showed a QTc interval of 425 ms and a serum potassium level of 3.8 mmol/L. The isoproterenol infusion was then gradually tapered and eventually discontinued.\u003c/p\u003e\n\u003cp\u003eThe patient was discharged on hospital day 10. Discharge evaluations showed: LVEF 52% (by TTE), troponin I \u0026lt; 0.04 ng/mL, and N-terminal pro-brain natriuretic peptide 2150 pg/mL. The discharge medication regimen was as follows: spironolactone 20 mg once daily, rivaroxaban 15 mg once daily, clopidogrel 75 mg once daily, atorvastatin 20 mg once nightly, dapagliflozin 10 mg once daily, potassium magnesium aspartate 1 tablet three times daily, and sacubitril/valsartan 50 mg twice daily.\u003c/p\u003e\n\u003cp\u003eDuring the 6-month follow-up period, the patient remained asymptomatic with stable vital signs and good medication adherence. Repeat ECGs showed no QT interval prolongation or arrhythmias. Repeat TTE demonstrated an improved LVEF of 55%. The patient declined the planned elective PCI for revascularization of the LCX and RCA.\u003c/p\u003e\n"},{"header":"Discussion and conclusions","content":"\u003cp\u003eThis case describes an elderly female with AMI who developed ES due to amiodarone-related TdP post-PCI. Key clinical features include multiple TdP risk factors (advanced age, female gender, AMI, hypokalemia), progressive QTc prolongation after amiodarone administration, and successful rescue with targeted interventions.\u003c/p\u003e\u003cp\u003eAmiodarone blocks the rapid component of the delayed rectifier potassium current (IKr), prolonging ventricular repolarization and QT interval [\u003cspan\u003e6\u003c/span\u003e]. Unlike high-risk QT-prolonging drugs, amiodarone usually uniformly prolongs repolarization across all myocardial layers, resulting in a low intrinsic TdP risk. However, in patients with reduced repolarization reserve (e.g., AMI, electrolyte disturbances), the proarrhythmic risk increases significantly [\u003cspan\u003e7\u003c/span\u003e]. This patient had AMI-induced myocardial ischemia and hypokalemia (3.07 mmol/L), which further impaired repolarization reserve by inhibiting IKr and increasing myocardial repolarization heterogeneity [\u003cspan\u003e8\u003c/span\u003e]. The combination led to progressive QTc prolongation (from 392 ms to 498 ms) and finally triggered TdP. ES development was attributed to persistent arrhythmic triggers: delayed amiodarone withdrawal during QTc prolongation and incomplete correction of hypokalemia [\u003cspan\u003e9\u003c/span\u003e]. Recurrent TdP further activated the sympathetic nervous system, forming a vicious cycle of \"arrhythmia → sympathetic activation → further arrhythmia\", consistent with ES pathophysiology described in the literature [\u003cspan\u003e10\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eThe diagnosis of TdP mainly relies on ECG features and clinical context. TdP is characterized by polymorphic VT with twisting QRS morphology, accompanied by QTc \u0026gt; 500 ms or ≥ 60 ms increase from baseline [\u003cspan\u003e11\u003c/span\u003e]. Although the maximum QTc of this patient was 498 ms (not exceeding 500 ms), it increased by 106 ms from the baseline, combined with typical TdP morphology and hypokalemia, so the diagnosis was clear. Differential diagnosis is crucial to avoid mismanagement. Idiopathic ventricular fibrillation was excluded due to the presence of structural heart disease (AMI) and QT prolongation [\u003cspan\u003e12\u003c/span\u003e]. Congenital long QT syndrome was ruled out by normal baseline QTc and negative family history [\u003cspan\u003e13\u003c/span\u003e]. Ischemia-induced polymorphic VT was excluded by the absence of new coronary stenosis [\u003cspan\u003e14\u003c/span\u003e]. These differentiations are based on literature-described disease characteristics, enhancing diagnostic accuracy .\u003c/p\u003e\u003cp\u003eThe treatment of TdP-related ES should focus on trigger removal, substrate correction, and arrhythmia suppression. The treatment strategy in this case aligned with guidelines and literature recommendations[\u003cspan\u003e3\u003c/span\u003e, \u003cspan\u003e15\u003c/span\u003e]: Discontinuing QT-prolonging drugs is a Class I recommendation for drug-induced long QT syndrome. Amiodarone was immediately withdrawn after TdP diagnosis, eliminating the direct cause of QT prolongation. Magnesium sulfate (2 g intravenous) is first-line therapy for TdP regardless of serum magnesium level. Potassium supplementation targeted 4.0-4.5 mmol/L to improve repolarization reserve. Isoproterenol infusion (maintaining ventricular rate at 90–100 beats/min) shortened QT interval and reduced repolarization heterogeneity. This is consistent with literature showing that increasing heart rate can effectively suppress TdP. Immediate defibrillation for hemodynamically unstable TdP is mandatory, which maintained hemodynamic stability during recurrent episodes.\u003c/p\u003e\u003cp\u003eThis case highlights key considerations for AMI patients post-PCI: First, AMI patients receiving amiodarone require QTc monitoring every 8–12 hours and electrolyte surveillance. Timely intervention for QTc prolongation (e.g., QTc \u0026gt; 500 ms or ≥ 60 ms increase from baseline) or electrolyte disorders reduces TdP risk. Second, AMI patients should maintain potassium levels at 4.0-4.5 mmol/L. Even mild hypokalemia synergistically increases proarrhythmic risk with QT-prolonging drugs. Third, for drug-related TdP-induced ES, prioritize trigger removal over aggressive antiarrhythmic therapy. Beta-blockers may be used for sympathetic activation, while isoproterenol or overdrive pacing is effective for recurrent TdP [\u003cspan\u003e16\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eIn conclusion, amiodarone-related TdP is a rare but severe complication post-PCI for AMI. Comprehensive risk assessment, close monitoring of QTc and electrolytes, and evidence-based interventions improve patient outcomes. This case provides valuable insights for managing similar complications.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eES: Electrical storm; AMI: Acute myocardial infarction; PCI: Percutaneous coronary intervention; TdP: Torsades de pointes; VT: Ventricular tachycardia; VF: Ventricular fibrillation; NSTEMI: Non-ST-segment elevation myocardial infarction; ECG: Electrocardiogram; QTc: Corrected QT interval; CAG: Coronary angiography; TIMI: Thrombolysis in myocardial infarction; LAD: Left anterior descending artery; LCX: Left circumflex artery; RCA: Right coronary artery; IABP: Intra-aortic balloon pump; LVEF: Left ventricular ejection fraction; IKr: Rapid component of the delayed rectifier potassium current.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was conducted in strict accordance with the ethical principles of medical research and the Helsinki Declaration.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe confirm that informed consent was obtained from the participants for the use of clinical information within the scope that does not compromise their anonymity.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets analyzed during the current study are available from the corresponding author upon request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eGuangzhou Science and Technology Plan Project (No. 2025A03J3718),Medical Research Fund of Guangdong Province (No. B2024095), Teaching Reform Project of the First Affiliated Hospital (Clinical Medical School) of Guangdong Pharmaceutical University (No. 2024JX09),which has played a pivotal role in making this project possible.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eRong Chen: Writing\u0026ndash;original draft; Tudi Li: Data curation; Jiaying Zhang: Data curation; \u0026nbsp;Shiyang Zhang: Writing\u0026ndash;review \u0026amp; editing; Zhihuan Zeng, Xiuhong Weng: Supervision, Writing\u0026ndash;review \u0026amp; editing, Funding acquisition. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eCredner SC, Klingenheben T, Mauss O, et al. Electrical storm in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications. J Am Coll Cardiol. 1998;32(7):1909-1915. doi:10.1016/s0735-1097(98)00495-1\u003c/li\u003e\n \u003cli\u003eLiu B, Xie B, Chen X, et al. A successful case of electrical storm rescue after acute myocardial infarction. BMC Cardiovasc Disord. 2022;22(1):537. Published 2022 Dec 9. doi:10.1186/s12872-022-02982-2\u003c/li\u003e\n \u003cli\u003eZeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997-4126. doi:10.1093/eurheartj/ehac262\u003c/li\u003e\n \u003cli\u003eDrew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010;121(8):1047-1060. doi:10.1161/CIRCULATIONAHA.109.192704\u003c/li\u003e\n \u003cli\u003eRoden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022. doi:10.1056/NEJMra032426\u003c/li\u003e\n \u003cli\u003eKhan SA, Emmanuel S, Shantha Kumar V, et al. Long QT Syndrome With Drugs Used in the Management of Arrhythmias: A Systematic Review. Cureus. 2024;16(7):e65857. Published 2024 Jul 31. doi:10.7759/cureus.65857\u003c/li\u003e\n \u003cli\u003eFriedman A, Miles J, Liebelt J, et al. QT Dispersion and Drug-Induced Torsade de Pointes. Cureus. 2021;13(1):e12895. Published 2021 Jan 25. doi:10.7759/cureus.12895\u003c/li\u003e\n \u003cli\u003eGrune J, Lewis AJM, Yamazoe M, et al. Neutrophils incite and macrophages avert electrical storm after myocardial infarction. Nat Cardiovasc Res. 2022;1(7):649-664. doi:10.1038/s44161-022-00094-w\u003c/li\u003e\n \u003cli\u003eHan C, Qiu R, Li L, et al. Electrical storm refractory multiple antiarrhythmic medications was stopped by interatrial shunting procedure-A case report. Front Cardiovasc Med. 2022;9:1012916. Published 2022 Nov 17. doi:10.3389/fcvm.2022.1012916\u003c/li\u003e\n \u003cli\u003eElsokkari I, Tsuji Y, Sapp JL, Nattel S. Recent Insights Into Mechanisms and Clinical Approaches to Electrical Storm. Can J Cardiol. 2022;38(4):439-453. doi:10.1016/j.cjca.2021.12.015\u003c/li\u003e\n \u003cli\u003eEl-Sherif N, Turitto G, Boutjdir M. Acquired long QT syndrome and torsade de pointes. Pacing Clin Electrophysiol. 2018;41(4):414-421. doi:10.1111/pace.13296\u003c/li\u003e\n \u003cli\u003eBelhassen B. Idiopathic ventricular fibrillation. Heart Rhythm. 2024;21(4):509-511. doi:10.1016/j.hrthm.2024.01.012\u003c/li\u003e\n \u003cli\u003eKaufman ES, Eckhardt LL, Ackerman MJ, et al. Management of Congenital Long-QT Syndrome: Commentary From the Experts. Circ Arrhythm Electrophysiol. 2021;14(7):e009726. doi:10.1161/CIRCEP.120.009726\u003c/li\u003e\n \u003cli\u003eKuroda S, Mizukami A, Hayashi T, Yoshioka K, Suzuki M, Matsumura A. Verapamil-sensitive ventricular tachycardia demonstrating multiform QRS morphology in a patient with ischemic cardiomyopathy. HeartRhythm Case Rep. 2019;5(12):573-577. Published 2019 Sep 6. doi:10.1016/j.hrcr.2019.08.013\u003c/li\u003e\n \u003cli\u003eAl-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2018;15(10):e73-e189. doi:10.1016/j.hrthm.2017.10.036\u003c/li\u003e\n \u003cli\u003eThomas SH, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes. Br J Clin Pharmacol. 2016;81(3):420-427. doi:10.1111/bcp.12726\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table","content":"\u003cp\u003eTable1 \u0026nbsp;Summary of Laboratory Findings on Admission\u003c/p\u003e\n \u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"568\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eParameter\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAdult Reference Range\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAdmission Value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eWhite blood cell count (\u0026times;10⁹/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e3.5-9.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e11.62\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eNeutrophil proportion\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e0.40-9.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e0.771\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eHemoglobin (g/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e115-150\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e116\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eCardiac troponin I (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e＜0.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e11.27\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eCreatine kinase-MB (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e＜5.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e69.64\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eMyoglobin (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e＜70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e＞600\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eD-dimer (mg/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e＜0.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e1.45\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eNTpro-BNP（ng/ml）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e＜300\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e5052\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eCreatinine (\u0026mu;mol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e41-81\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e89\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003ePotassium (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e3.5-5.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e3.07\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eAST（U/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e7-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e15\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eALT（U/L）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e13-35\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e75\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eTotal cholesterol (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e3.6-5.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e8.61\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eTriglycerides (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e0.33-1.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e1.42\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eHigh-density lipoprotein (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e0.91-1.95\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e1.29\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eLow-density lipoprotein (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e5.43\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eFasting blood glucose (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e3.9-6.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e10.32\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003e2-hour postprandial blood glucose (mmol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e3.89-7.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e12.09\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eGlycated hemoglobin (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e4.2-6.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e7.7\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003eArterial blood gas analysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003ePH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e7.25-7.45\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e7.505\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003ePCO2(mmHg)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e32-45\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e29.3\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 292px;\"\u003e\n \u003cp\u003ePO2（mmHg）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 158px;\"\u003e\n \u003cp\u003e80-100\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 118px;\"\u003e\n \u003cp\u003e58.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Electrical storm, Amiodarone, Torsades de pointes, Percutaneous coronary intervention, Acute myocardial infarction ","lastPublishedDoi":"10.21203/rs.3.rs-8539511/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8539511/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: Electrical storm (ES) is a life-threatening complication of acute myocardial infarction (AMI) post-percutaneous coronary intervention (PCI), characterized by recurrent malignant ventricular arrhythmias. Amiodarone, a widely used class Ⅲ antiarrhythmic drug, may induce QT interval prolongation and torsades de pointes (TdP), especially in the presence of electrolyte disturbances and reduced myocardial repolarization reserve.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCase presentation: A 78-year-old female with a 20-year history of uncontrolled hypertension was admitted to the emergency department with \"chest tightness and retrosternal pain for 5 days, acute exacerbation for 4 hours\". Clinical evaluation confirmed acute non-ST-segment elevation myocardial infarction and acute decompensated heart failure. Emergency PCI was performed 6 hours after admission, with successful stenting of the left anterior descending artery (LAD). Amiodarone was administered for new-onset atrial fibrillation, which was followed by progressive QT interval prolongation and hypokalemia. On day 5 of hospitalization, the patient developed TdP-related ES, which was successfully managed with electrical defibrillation, immediate amiodarone withdrawal, electrolyte supplementation, and isoproterenol infusion.\u003c/p\u003e\n\u003cp\u003eConclusion: For AMI patients receiving amiodarone post-PCI, close monitoring of QT interval (corrected QT, QTc) and electrolyte levels is essential. Timely identification and intervention of modifiable risk factors can effectively improve outcomes of ES caused by amiodarone-related TdP.\u003c/p\u003e","manuscriptTitle":"Electrical Storm Secondary to Amiodarone-Related Torsades de Pointes Following PCI for Acute Myocardial Infarction: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-04 05:18:28","doi":"10.21203/rs.3.rs-8539511/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"20e90182-954f-4d87-8030-6d0a99f0a1d1","owner":[],"postedDate":"February 4th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-03-11T14:12:05+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-04 05:18:28","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8539511","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8539511","identity":"rs-8539511","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}