Spiked Helmet Sign: An Electrocardiographic Pattern Beyond Sepsis

Spiked Helmet Sign: An Electrocardiographic Pattern Beyond Sepsis | 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 Spiked Helmet Sign: An Electrocardiographic Pattern Beyond Sepsis Gustavo Rojas-Velasco, Andrés Arteaga-Arellano, Daniel Manzur-Sandoval, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8563794/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 The spiked helmet sign (SHS) is a rare ECG pattern classically associated with severe non-cardiac illness and high mortality. Its occurrence in primary cardiac conditions is uncommon and remains poorly characterized. Case Presentation A 62-year-old male undergoing elective non-cardiac surgery developed hypotension followed by ventricular arrhythmias and cardiac arrest during anesthetic induction. Post-resuscitation ECG demonstrated dynamic ST-segment changes with prominent R-wave and convex ST-segment elevation, consistent with SHS morphology. The patient remained in the intensive care unit for 7 days, during which clinical recovery was favorable and no condition known to be associated with SHS was identified. Seventy-two hours after discharge, the patient presented with recurrence of chest pain accompanied by reappearance of SHS morphology. Coronary angiography demonstrated severe spontaneous right coronary artery vasospasm, coinciding with ECG changes. Initiation of calcium channel blocker therapy led to resolution of symptoms and normalization of the ECG abnormalities. Conclusions This case documents SHS occurring in the setting of coronary vasospasm and cardiac arrest, expanding its clinical spectrum beyond sepsis, intra-abdominal or intrathoracic pathologies. Recognition of this atypical and novel presentation highlights the need for further investigation into the mechanisms and clinical implications of SHS in cardiac disease. Spiked helmet sign SHS vasospasm coronary artery vasospasm Figures Figure 1 Figure 2 Figure 3 CAPSULE SUMMARY We report a rare presentation of the spiked helmet sign associated with unexplained cardiac arrest and coronary vasospasm, with a favorable clinical course, expanding its spectrum and highlighting the need for further understanding of its pathophysiological mechanisms and prognostic implications. Introduction In 1842, the Prussian army adopted the Pickelhaube, a spiked helmet meant to deflect danger from enemy blades, rain, and wind [ 1 ]. Nearly two centuries later, the spiked helmet sign (SHS) served a similar warning function, alerting physicians to imminent clinical danger [ 2 ]. This electrocardiographic sign, characterized by elevation of the isoelectric line followed by a sharp R-wave and convex ST-segment elevation, has been associated with severe systemic, non-cardiac illness and high mortality since its first description [ 2 , 3 ]. We report a case of SHS occurring in the context of cardiac arrest and coronary vasospasm, with favorable clinical evolution and current asymptomatic status. This case highlights the diagnostic challenges that arise when SHS appears in a cardiac context and reinforces the need to clarify its mechanisms and clinical implications, which remain poorly understood. Case presentation A 62-year-old male with a 15-year history of hypertension, treated with metoprolol 100 mg/day, and major depressive disorder managed with duloxetine 30 mg/day, was scheduled for functional rhinoplasty. During anesthetic induction, the patient developed hypotension, for which intravenous epinephrine was administered. Subsequently, frequent ventricular premature complexes were observed, which resolved following administration of 60 mg of 2% lidocaine. Shortly after, the rhythm progressed to monomorphic ventricular tachycardia and ventricular fibrillation, requiring advanced cardiopulmonary resuscitation. Four biphasic 200 J defibrillations were delivered, and after ten cycles of resuscitation, return of spontaneous circulation was achieved. The post-resuscitation ECG demonstrated ST-segment depression in leads DII, DIII, aVF, and V6 ( Fig. 1 , Panel A) . The patient was placed on invasive mechanical ventilation and maintained on norepinephrine at 0.1 µg/kg/min. During transfer to the intensive care unit (ICU), prominent R-wave and convex ST-segment elevation were noted in leads DII, DIII, aVF, V5, and V6 ( Fig. 1 , Panel B) . Point-of-care transthoracic echocardiography revealed inferolateral wall motion abnormalities with a left ventricular ejection fraction of 40%. Acute coronary syndrome was suspected. Coronary angiography performed two hours after the initial event demonstrated angiographically normal coronary arteries without obstructive lesions. The patient remained in the ICU for 7 days. During this period, recurrent transient sharp R-waves and ST-segment elevations consistent with SHS morphology were observed, along with self-limited episodes of non-sustained ventricular tachycardia. A follow-up transthoracic echocardiogram conducted seven days after the first study showed resolution of wall motion abnormalities and preserved LVEF. Cardiac magnetic resonance imaging revealed no evidence of myocarditis or myocardial infarction. Following clinical improvement, extubation was achieved, and vasopressor and inotropic support were discontinued. Coronary vasospasm was considered the most likely cause of the recurrent ECG changes. Although an acetylcholine provocation test was considered, it could not be performed due to the unavailability of the agent. Hyperventilation and an ajmaline provocation test were carried out, yielding negative results. The patient evolved favorably and was discharged on a calcium channel blocker and a beta blocker without recurrence of ECG abnormalities. Seventy-two hours after discharge, the patient presented with an episode of poorly defined chest pain associated with hypotension. On arrival at the emergency department, the ECG demonstrated ST-segment elevation of up to 10 mm in the inferior and lateral leads with SHS morphology, which resolved spontaneously. Coronary angiography with vasoreactivity testing was scheduled 24 hours after the last administration of beta-blocker therapy. Coronary angiography once again revealed no obstructive lesions. During the procedure, a spontaneous severe vasospasm occurred in the right coronary artery ( Fig. 2 ) (Supplementary Material 1) , coinciding with chest pain and recurrence of ST-segment elevation (Fig. 3 , Panel A) . The vasospasm was self-limited; leading to complete resolution of symptoms and normalization of the ECG changes ( Fig. 3 , Panel B) . Calcium channel blockers were initiated. The patient was later discharged and remains asymptomatic at three-month follow-up. Discussion Since its first description in 2011 by Littman, SHS has been reported predominantly in the context of critical illness, with a mortality rate of 75% in the initial case series [ 3 ]. Several reports have indicated that it is not suggestive of cardiac pathology and is generally a self-limited finding [ 4 , 5 ]. In a systematic review of clinical cases published in 2023, Mahmoudi et al described SHS in patients with intracranial hemorrhage, pneumothorax, severe pneumonia, acute respiratory distress syndrome, bowel ischemia, bowel obstruction, and sepsis. Only 8.6% of patients included in the review presented a coronary event, and overall mortality was 59% [ 6 ]. Wang et al in 2024 described 20 cases of patients who died, with 90% of these deaths due to non-cardiac causes and 95% occurring less than one week after admission [ 7 ]. More recently, in 2025, Bosnjak et al reviewed 43 published cases, with a mean age of 59.4 years and a mortality rate of 58.1%, notably higher in males at 69.6% compared with 45% in females [ 8 ]. These findings underscore its association with high-risk conditions, infrequent linkage to primary cardiac disease, and an adverse outcome profile. Timely recognition of the sign and differentiation from obstructive myocardial infarction has been deemed critical for accurate diagnosis and proper management, as misinterpretation may lead to unnecessary testing and interventions [ 6 – 8 ]. Nevertheless, clinicians should maintain a high index of suspicion for cardiac pathology, as our case demonstrates that, although uncommon, it is a possible cause of SHS. Several mechanisms have been proposed for the development of SHS [ 6 ]: Increased intrathoracic (V3-V5 lead involvement) and intra-abdominal (inferior lead) pressure Adrenergic stimulation with QT prolongation Pulsatile diaphragmatic contractions Electrical and mechanical artifacts. In our case, SHS was observed in the inferolateral leads in the absence of conditions known to increase abdominal or intrathoracic pressure. There was no evidence of sepsis or other systemic processes previously associated with this ECG sign. Conclusions This case represents a rare presentation of SHS, expanding its clinical spectrum beyond previously reported etiologies. It demonstrates that SHS may occur in the setting of unexplained cardiac arrest, in the absence of infectious or systemic inflammatory disease, and in association with coronary vasospasm. Recognition of this atypical presentation may aid clinicians in prompt identification of the sign without ruling out cardiac illness, and underscores the need for further investigation into the underlying pathophysiological mechanisms and clinical implications of SHS. Declarations Competing interests The authors have no relevant financial or non-financial interests to disclose. Consent to participate Informed consent was obtained from the patient. Consent to publish The participant has consented to the submission of the case report to the journal. Author Contribution G.R: Writing – review & editing, Writing – original draft, Validation, Supervision. A.A: Writing – review & editing, Writing – original draft, Validation, Conceptualization. D.M: Writing – review & editing, Writing – original draft. G.J: Writing – review & editing, Writing – original draft. S.G: Writing – review & editing, Visualization, Validation. A.B: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Conceptualization. All authors reviewed the manuscript. References Heinemann SM. About the invention and introduction of the Pickelhaube in Prussia in 1842 [Internet]. Bassum: Historien-Kabinett; 2021 [cited 2025 Nov 12]. Available from: https://historien-kabinett.de/About-the-invention-and-introduction-of-the-Pickelhaube-in-Prussia-in-1842 Crinion D, Abdollah H, Baranchuk A. An ominous ECG sign in critical care. Circulation. 2020;141(25):2106–9. 10.1161/CIRCULATIONAHA.120.047427 . Littmann L, Monroe MH. The spiked helmet sign: a new electrocardiographic marker of critical illness and high risk of death. Mayo Clin Proc . 2011;86:1245–1246. 10.4065/mcp.2011.0647 Hamade H, Jabri A, Yusaf A, Nasser MF, Karim S. The Spiked Helmet Sign: A Concerning Electrocardiographic Finding. JACC Case Rep. 2021;3(11):1370–2. 10.1016/j.jaccas.2021.04.048 . PMID: 34505073; PMCID: PMC8414533. Tomcsányi J, Frész T, Proctor P, Littmann L. Emergence and resolution of the electrocardiographic spiked helmet sign in acute noncardiac conditions. Am J Emerg Med. 2015;33(1):127.e5-7. 10.1016/j.ajem.2014.06.023 . Epub 2014 Jun 26. PMID: 25066910. Mahmoudi E, Hui JMH, Leung KSK, Satti DI, Lee YHA, Li KHC, Lau DHH, Kot TKM, Ciobanu A, Bazoukis G, Chan JKK, Baranchuk A. Spiked helmet electrocardiographic sign — a systematic review of case reports. Curr Probl Cardiol. 2022;49:101535. 10.1016/j.cpcardiol.2022.101535 . Wang G, Zhong S, Chu H, Zhong L. Spiked Helmet Sign: An Uncommon Electrocardiographic Marker. Rev Cardiovasc Med. 2023;24(9):272. 10.31083/j.rcm2409272 . PMID: 39076406; PMCID: PMC11270090. Bosnjak M, Nottingham T, Strey G. A Distinctive Electrocardiographic Pattern: Unveiling the Spiked Helmet Sign. JACC Case Rep. 2025;30(12):103412. 10.1016/j.jaccas.2025.103412 . Epub 2025 May 6. PMID: 40447374; PMCID: PMC12235485. Additional Declarations No competing interests reported. Supplementary Files SM1.mp4 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-8563794","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":584455648,"identity":"94dd79d1-b8a9-44fa-81a5-9cea06d108f3","order_by":0,"name":"Gustavo Rojas-Velasco","email":"","orcid":"","institution":"Instituto Nacional de Cardiología","correspondingAuthor":false,"prefix":"","firstName":"Gustavo","middleName":"","lastName":"Rojas-Velasco","suffix":""},{"id":584455649,"identity":"d585976b-8909-43ed-938b-3a2b291206df","order_by":1,"name":"Andrés Arteaga-Arellano","email":"","orcid":"","institution":"Axxis Hospital de Especialidades","correspondingAuthor":false,"prefix":"","firstName":"Andrés","middleName":"","lastName":"Arteaga-Arellano","suffix":""},{"id":584455650,"identity":"a104878e-0308-4e78-b8e2-c66f9d65ed54","order_by":2,"name":"Daniel Manzur-Sandoval","email":"","orcid":"","institution":"Instituto Nacional de Cardiología","correspondingAuthor":false,"prefix":"","firstName":"Daniel","middleName":"","lastName":"Manzur-Sandoval","suffix":""},{"id":584455651,"identity":"0a41de19-dc41-4341-af7c-40fa4f41e514","order_by":3,"name":"Gian Manuel Jiménez-Rodríguez","email":"","orcid":"","institution":"Instituto Nacional de Cardiología","correspondingAuthor":false,"prefix":"","firstName":"Gian","middleName":"Manuel","lastName":"Jiménez-Rodríguez","suffix":""},{"id":584455652,"identity":"23f75594-0562-4b52-bce9-ea620ebfea2d","order_by":4,"name":"Shyla Gupta","email":"","orcid":"","institution":"University of Ottawa","correspondingAuthor":false,"prefix":"","firstName":"Shyla","middleName":"","lastName":"Gupta","suffix":""},{"id":584455653,"identity":"52ae7690-7b6d-45ea-8497-6ed778c56e8b","order_by":5,"name":"Adrián Baranchuk","email":"data:image/png;base64,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","orcid":"","institution":"Universidad Abierta Interamericana","correspondingAuthor":true,"prefix":"","firstName":"Adrián","middleName":"","lastName":"Baranchuk","suffix":""}],"badges":[],"createdAt":"2026-01-09 19:08:15","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8563794/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8563794/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":101792540,"identity":"a456792c-79a4-486c-9990-14a7d84ae5c0","added_by":"auto","created_at":"2026-02-03 16:12:45","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":967101,"visible":true,"origin":"","legend":"\u003cp\u003eInitial\u003cstrong\u003e \u003c/strong\u003eST-segment morphology changes\u003c/p\u003e\n\u003cp\u003ePanel A: ST-segment depression in leads DII, DIII, aVF and V6 observed after cardiac arrest\u003c/p\u003e\n\u003cp\u003ePanel B: Sharp R-wave followed by convex ST-segment elevation in leads DII, DIII, aVF, V5 and V6, compatible with spiked helmet sign, observed moments after ST-segment depression\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8563794/v1/dce6f1f7367ba6185b2df397.png"},{"id":101792526,"identity":"9bd3e6d1-9234-45f4-95cd-05b3f8c8297d","added_by":"auto","created_at":"2026-02-03 16:12:43","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":365522,"visible":true,"origin":"","legend":"\u003cp\u003eCoronary angiography demonstrating right coronary artery vasospasm\u003c/p\u003e\n\u003cp\u003eRed arrow: Right coronary artery vasospasm\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8563794/v1/d23c10c3e89ccf439f8f534b.png"},{"id":101792574,"identity":"a64706ed-8cdb-4834-9286-52ae4290b3d5","added_by":"auto","created_at":"2026-02-03 16:12:50","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":890888,"visible":true,"origin":"","legend":"\u003cp\u003eST-segment morphology changes upon readmission\u003c/p\u003e\n\u003cp\u003ePanel A: Sharp R-wave followed by convex ST-segment elevation in leads DII, DIII, aVF, V5 and V6, compatible with spiked helmet sign in readmission\u003c/p\u003e\n\u003cp\u003ePanel B: Resolution of ECG changes after vasospasm treatment\u003c/p\u003e\n\u003cp\u003ePanel C: Spiked helmet \u003cem\u003ePickelhaube\u003c/em\u003e\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-8563794/v1/5b2dafeb3be670447273dda1.png"},{"id":107266870,"identity":"79491380-79ed-4c14-a4b6-fec1cb6aa623","added_by":"auto","created_at":"2026-04-19 16:10:12","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2334871,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8563794/v1/52ff422f-751d-4205-a80a-f2d88cb497f3.pdf"},{"id":101792588,"identity":"255d9f30-9631-4963-9c31-2e7b5a763172","added_by":"auto","created_at":"2026-02-03 16:12:52","extension":"mp4","order_by":0,"title":"","display":"","copyAsset":false,"role":"supplement","size":6824372,"visible":true,"origin":"","legend":"","description":"","filename":"SM1.mp4","url":"https://assets-eu.researchsquare.com/files/rs-8563794/v1/3aa94c02442e9e73d13e14ed.mp4"}],"financialInterests":"No competing interests reported.","formattedTitle":"Spiked Helmet Sign: An Electrocardiographic Pattern Beyond Sepsis","fulltext":[{"header":"CAPSULE SUMMARY ","content":"\u003cp\u003eWe report a rare presentation of the spiked helmet sign associated with unexplained cardiac arrest and coronary vasospasm, with a favorable clinical course, expanding its spectrum and highlighting the need for further understanding of its pathophysiological mechanisms and prognostic implications.\u003c/p\u003e"},{"header":"Introduction","content":"\u003cp\u003eIn 1842, the Prussian army adopted the Pickelhaube, a spiked helmet meant to deflect danger from enemy blades, rain, and wind [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Nearly two centuries later, the spiked helmet sign (SHS) served a similar warning function, alerting physicians to imminent clinical danger [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThis electrocardiographic sign, characterized by elevation of the isoelectric line followed by a sharp R-wave and convex ST-segment elevation, has been associated with severe systemic, non-cardiac illness and high mortality since its first description [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWe report a case of SHS occurring in the context of cardiac arrest and coronary vasospasm, with favorable clinical evolution and current asymptomatic status. This case highlights the diagnostic challenges that arise when SHS appears in a cardiac context and reinforces the need to clarify its mechanisms and clinical implications, which remain poorly understood.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 62-year-old male with a 15-year history of hypertension, treated with metoprolol 100 mg/day, and major depressive disorder managed with duloxetine 30 mg/day, was scheduled for functional rhinoplasty.\u003c/p\u003e \u003cp\u003eDuring anesthetic induction, the patient developed hypotension, for which intravenous epinephrine was administered. Subsequently, frequent ventricular premature complexes were observed, which resolved following administration of 60 mg of 2% lidocaine. Shortly after, the rhythm progressed to monomorphic ventricular tachycardia and ventricular fibrillation, requiring advanced cardiopulmonary resuscitation. Four biphasic 200 J defibrillations were delivered, and after ten cycles of resuscitation, return of spontaneous circulation was achieved. The post-resuscitation ECG demonstrated ST-segment depression in leads DII, DIII, aVF, and V6 \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, \u003cb\u003ePanel A)\u003c/b\u003e. The patient was placed on invasive mechanical ventilation and maintained on norepinephrine at 0.1 \u0026micro;g/kg/min.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eDuring transfer to the intensive care unit (ICU), prominent R-wave and convex ST-segment elevation were noted in leads DII, DIII, aVF, V5, and V6 \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, \u003cb\u003ePanel B)\u003c/b\u003e. Point-of-care transthoracic echocardiography revealed inferolateral wall motion abnormalities with a left ventricular ejection fraction of 40%. Acute coronary syndrome was suspected. Coronary angiography performed two hours after the initial event demonstrated angiographically normal coronary arteries without obstructive lesions.\u003c/p\u003e \u003cp\u003eThe patient remained in the ICU for 7 days. During this period, recurrent transient sharp R-waves and ST-segment elevations consistent with SHS morphology were observed, along with self-limited episodes of non-sustained ventricular tachycardia. A follow-up transthoracic echocardiogram conducted seven days after the first study showed resolution of wall motion abnormalities and preserved LVEF. Cardiac magnetic resonance imaging revealed no evidence of myocarditis or myocardial infarction. Following clinical improvement, extubation was achieved, and vasopressor and inotropic support were discontinued.\u003c/p\u003e \u003cp\u003eCoronary vasospasm was considered the most likely cause of the recurrent ECG changes. Although an acetylcholine provocation test was considered, it could not be performed due to the unavailability of the agent. Hyperventilation and an ajmaline provocation test were carried out, yielding negative results. The patient evolved favorably and was discharged on a calcium channel blocker and a beta blocker without recurrence of ECG abnormalities.\u003c/p\u003e \u003cp\u003eSeventy-two hours after discharge, the patient presented with an episode of poorly defined chest pain associated with hypotension. On arrival at the emergency department, the ECG demonstrated ST-segment elevation of up to 10 mm in the inferior and lateral leads with SHS morphology, which resolved spontaneously. Coronary angiography with vasoreactivity testing was scheduled 24 hours after the last administration of beta-blocker therapy. Coronary angiography once again revealed no obstructive lesions. During the procedure, a spontaneous severe vasospasm occurred in the right coronary artery \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cb\u003e) (Supplementary Material 1)\u003c/b\u003e, coinciding with chest pain and recurrence of ST-segment elevation (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e, \u003cb\u003ePanel A)\u003c/b\u003e. The vasospasm was self-limited; leading to complete resolution of symptoms and normalization of the ECG changes \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e, \u003cb\u003ePanel B)\u003c/b\u003e. Calcium channel blockers were initiated. The patient was later discharged and remains asymptomatic at three-month follow-up.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eSince its first description in 2011 by Littman, SHS has been reported predominantly in the context of critical illness, with a mortality rate of 75% in the initial case series [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Several reports have indicated that it is not suggestive of cardiac pathology and is generally a self-limited finding [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn a systematic review of clinical cases published in 2023, Mahmoudi et al described SHS in patients with intracranial hemorrhage, pneumothorax, severe pneumonia, acute respiratory distress syndrome, bowel ischemia, bowel obstruction, and sepsis. Only 8.6% of patients included in the review presented a coronary event, and overall mortality was 59% [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Wang et al in 2024 described 20 cases of patients who died, with 90% of these deaths due to non-cardiac causes and 95% occurring less than one week after admission [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. More recently, in 2025, Bosnjak et al reviewed 43 published cases, with a mean age of 59.4 years and a mortality rate of 58.1%, notably higher in males at 69.6% compared with 45% in females [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. These findings underscore its association with high-risk conditions, infrequent linkage to primary cardiac disease, and an adverse outcome profile.\u003c/p\u003e \u003cp\u003eTimely recognition of the sign and differentiation from obstructive myocardial infarction has been deemed critical for accurate diagnosis and proper management, as misinterpretation may lead to unnecessary testing and interventions [\u003cspan additionalcitationids=\"CR7\" citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Nevertheless, clinicians should maintain a high index of suspicion for cardiac pathology, as our case demonstrates that, although uncommon, it is a possible cause of SHS.\u003c/p\u003e \u003cp\u003eSeveral mechanisms have been proposed for the development of SHS [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]:\u003c/p\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003eIncreased intrathoracic (V3-V5 lead involvement) and intra-abdominal (inferior lead) pressure\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eAdrenergic stimulation with QT prolongation\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003ePulsatile diaphragmatic contractions\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eElectrical and mechanical artifacts.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003cp\u003eIn our case, SHS was observed in the inferolateral leads in the absence of conditions known to increase abdominal or intrathoracic pressure. There was no evidence of sepsis or other systemic processes previously associated with this ECG sign.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eThis case represents a rare presentation of SHS, expanding its clinical spectrum beyond previously reported etiologies. It demonstrates that SHS may occur in the setting of unexplained cardiac arrest, in the absence of infectious or systemic inflammatory disease, and in association with coronary vasospasm. Recognition of this atypical presentation may aid clinicians in prompt identification of the sign without ruling out cardiac illness, and underscores the need for further investigation into the underlying pathophysiological mechanisms and clinical implications of SHS.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors have no relevant financial or non-financial interests to disclose.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from the patient.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to publish\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe participant has consented to the submission of the case report to the journal.\u003c/p\u003e\n\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\n\u003cp\u003eG.R: Writing \u0026ndash; review \u0026amp; editing, Writing \u0026ndash; original draft, Validation, Supervision. A.A: Writing \u0026ndash; review \u0026amp; editing, Writing \u0026ndash; original draft, Validation, Conceptualization. D.M: Writing \u0026ndash; review \u0026amp; editing, Writing \u0026ndash; original draft. G.J: Writing \u0026ndash; review \u0026amp; editing, Writing \u0026ndash; original draft. S.G: Writing \u0026ndash; review \u0026amp; editing, Visualization, Validation. A.B: Writing \u0026ndash; review \u0026amp; editing, Writing \u0026ndash; original draft, Visualization, Validation, Supervision, Conceptualization. All authors reviewed the manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eHeinemann SM. About the invention and introduction of the Pickelhaube in Prussia in 1842 [Internet]. Bassum: Historien-Kabinett; 2021 [cited 2025 Nov 12]. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://historien-kabinett.de/About-the-invention-and-introduction-of-the-Pickelhaube-in-Prussia-in-1842\u003c/span\u003e\u003cspan address=\"https://historien-kabinett.de/About-the-invention-and-introduction-of-the-Pickelhaube-in-Prussia-in-1842\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCrinion D, Abdollah H, Baranchuk A. An ominous ECG sign in critical care. Circulation. 2020;141(25):2106\u0026ndash;9. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1161/CIRCULATIONAHA.120.047427\u003c/span\u003e\u003cspan address=\"10.1161/CIRCULATIONAHA.120.047427\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLittmann L, Monroe MH. The spiked helmet sign: a new electrocardiographic marker of critical illness and high risk of death. \u003cem\u003eMayo Clin Proc\u003c/em\u003e. 2011;86:1245\u0026ndash;1246. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.4065/mcp.2011.0647\u003c/span\u003e\u003cspan address=\"10.4065/mcp.2011.0647\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHamade H, Jabri A, Yusaf A, Nasser MF, Karim S. The Spiked Helmet Sign: A Concerning Electrocardiographic Finding. JACC Case Rep. 2021;3(11):1370\u0026ndash;2. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.jaccas.2021.04.048\u003c/span\u003e\u003cspan address=\"10.1016/j.jaccas.2021.04.048\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. PMID: 34505073; PMCID: PMC8414533.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTomcs\u0026aacute;nyi J, Fr\u0026eacute;sz T, Proctor P, Littmann L. Emergence and resolution of the electrocardiographic spiked helmet sign in acute noncardiac conditions. Am J Emerg Med. 2015;33(1):127.e5-7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.ajem.2014.06.023\u003c/span\u003e\u003cspan address=\"10.1016/j.ajem.2014.06.023\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. Epub 2014 Jun 26. PMID: 25066910.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMahmoudi E, Hui JMH, Leung KSK, Satti DI, Lee YHA, Li KHC, Lau DHH, Kot TKM, Ciobanu A, Bazoukis G, Chan JKK, Baranchuk A. Spiked helmet electrocardiographic sign \u0026mdash; a systematic review of case reports. Curr Probl Cardiol. 2022;49:101535. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.cpcardiol.2022.101535\u003c/span\u003e\u003cspan address=\"10.1016/j.cpcardiol.2022.101535\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang G, Zhong S, Chu H, Zhong L. Spiked Helmet Sign: An Uncommon Electrocardiographic Marker. Rev Cardiovasc Med. 2023;24(9):272. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.31083/j.rcm2409272\u003c/span\u003e\u003cspan address=\"10.31083/j.rcm2409272\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. PMID: 39076406; PMCID: PMC11270090.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBosnjak M, Nottingham T, Strey G. A Distinctive Electrocardiographic Pattern: Unveiling the Spiked Helmet Sign. JACC Case Rep. 2025;30(12):103412. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.jaccas.2025.103412\u003c/span\u003e\u003cspan address=\"10.1016/j.jaccas.2025.103412\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. Epub 2025 May 6. PMID: 40447374; PMCID: PMC12235485.\u003c/span\u003e\u003c/li\u003e\u003c/ol\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":"Spiked helmet sign, SHS, vasospasm, coronary artery vasospasm","lastPublishedDoi":"10.21203/rs.3.rs-8563794/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8563794/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe spiked helmet sign (SHS) is a rare ECG pattern classically associated with severe non-cardiac illness and high mortality. Its occurrence in primary cardiac conditions is uncommon and remains poorly characterized.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase Presentation\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA 62-year-old male undergoing elective non-cardiac surgery developed hypotension followed by ventricular arrhythmias and cardiac arrest during anesthetic induction. Post-resuscitation ECG demonstrated dynamic ST-segment changes with prominent R-wave and convex ST-segment elevation, consistent with SHS morphology. The patient remained in the intensive care unit for 7 days, during which clinical recovery was favorable and no condition known to be associated with SHS was identified. Seventy-two hours after discharge, the patient presented with recurrence of chest pain accompanied by reappearance of SHS morphology. Coronary angiography demonstrated severe spontaneous right coronary artery vasospasm, coinciding with ECG changes. Initiation of calcium channel blocker therapy led to resolution of symptoms and normalization of the ECG abnormalities.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case documents SHS occurring in the setting of coronary vasospasm and cardiac arrest, expanding its clinical spectrum beyond sepsis, intra-abdominal or intrathoracic pathologies. Recognition of this atypical and novel presentation highlights the need for further investigation into the mechanisms and clinical implications of SHS in cardiac disease.\u003c/p\u003e","manuscriptTitle":"Spiked Helmet Sign: An Electrocardiographic Pattern Beyond Sepsis","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-03 16:11:40","doi":"10.21203/rs.3.rs-8563794/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":"cf11f57c-f82d-4af0-85d5-1465d12c24cf","owner":[],"postedDate":"February 3rd, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-04-19T16:09:44+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-03 16:11:40","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8563794","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8563794","identity":"rs-8563794","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}