Ondansetron-induced cardiac arrest and cardiomyopathy with successful reversal: a case report
Highlight box
Key findings
• Cardiac arrest and cardiomyopathy resulted from a single dose of 8 mg intravenous (IV) ondansetron, where contributing factors included hypomagnesemia and borderline serum potassium level.
What is known and what is new?
• The Food and Drug Administration issued a warning that ondansetron is known to cause normal corrected QT interval prolongation in high-risk patients.
• Cardiac arrest and cardiomyopathy from a single 8 mg IV dose of ondansetron in a patient with no past medical illness are considered rare. Moreover, achieving return of spontaneous circulation after five cycles of cardiopulmonary resuscitation and then complete recovery after discontinuation of the offending agent (ondansetron) and proper interventions is considered an achievement in treatment success.
What is the implication, and what should change now?
• Such a serious incident raised awareness among clinicians and hence mandates preventive measures prior to ondansetron administration, such as electrocardiogram checking, electrolyte screening, and correction. It is also essential that clinicians remain vigilant for any unfavorable ondansetron-associated incidents that may arise and take quick interventions.
Introduction
Background
Ondansetron, a 5-hydroxytryptamine 3 (5-HT3) receptor antagonist, is a medication used to prevent and treat nausea and vomiting (1). Although ondansetron is generally well tolerated and considered safe, there have been case reports where its use has led to severe allergic reactions (anaphylaxis) or cardiac arrhythmias, which could be further complicated by cardiac arrest (2-12). Considering anaphylaxis, there are two underlying mechanisms related to ondansetron use. The first one is the traditional type I immune-mediated allergic reaction [immunoglobulin E (IgE)-mediated], typically associated with the drug. The other one is through an alternative pathway, the Mas-related G protein-coupled receptor X2 (MRGPRX2) stimulating histamine release (7,8).
Cardiac arrhythmias resulting from ondansetron administration, on the other hand, may occur from several mechanisms. Ondansetron can block the rapid repolarizing current (IKs), which may lead to the prolongation of repolarization and thus result in cardiac disturbances (10). Another mechanism is related to suppressing the Bezold-Zarish reflex, which is mediated by 5-HT3 receptors leading to tachyarrhythmia (11).
Ondansetron-induced QT interval prolongation and cardiac arrhythmias are considered rare and dose-dependent (13-17), and there are some reports on their occurrence that have been published (5,9,11), and our case is the first case reported in the Middle East addressing the consequences of a single dose of ondansetron in terms of cardiac arrhythmias, cardiomyopathy, and suspected anaphylaxis. Therefore, it is essential that clinicians consider such serious incidents upon ondansetron use and undergo preventive measures in checking serum electrolytes and electrocardiogram (ECG) accordingly, particularly in patients with electrolyte imbalance and other risk factors.
Rationale and knowledge gap
Our case report findings would highlight the possibility of cardiac arrhythmias and cardiomyopathy as a complication of ondansetron administration and hence raise awareness among clinicians to make preventive measures and take quick interventions if required before and after the administration of ondansetron, respectively.
Objective
To analyze the clinical features related to serious complications due to ondansetron administration and create a comprehensive protocol among clinicians for the early detection of electrolyte imbalance or other factors that may lead to ondansetron-associated cardiac arrest and cardiomyopathy and hence mandate quick interventions prior to ondansetron use in all patients. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-25-3/rc).
Case presentation
A 43-year-old female patient with a negative medical and psycho-social history arrived on August 30th, 2023 to the hospital’s emergency room (ER) with a fully conscious level with Glasgow Coma Score (GCS) 15/15 (18) complaining of nausea, vomiting, and headache. Vital signs upon arrival were normal (Table 1). As a usual clinical management approach done in the ER in patients with persistent vomiting and requiring a fast-acting antiemetic agent, blood extraction was done to check serum electrolytes (Table 2), and the patient received an intravenous (IV) dose of 8 mg of ondansetron (usual IV dose is 8–16 mg). Ten minutes later, she started experiencing palpitations pulse rate reaching 156 beats per minute (bpm) with a drop in oxygen saturation (SatO2) 86%, followed by unexplained convulsions for which she was given midazolam 5 mg IV. Seven minutes thereafter, there was a marked drop in the level of consciousness (GCS reaching 3), where she went into cardiac arrest and developed polymorphic ventricular fibrillation, necessitating cardiopulmonary resuscitation (CPR) as per advanced cardiac life support (ACLS) protocol (19). Pharmacological interventions in the ER included IV fluid (IVF) NaCl 0.9% a total of 1,000 mL, Ringer’s lactate (RL) 500 mL, and sodium bicarbonate 8.4% 100 mL IV bolus, adrenaline 1 mg, and amiodarone 150 mg, with doses repeated as protocol. After 5 cycles of CPR with three direct current defibrillator shocks (DC shocks), the patient achieved return of spontaneous circulation (ROSC), was intubated and started on IV vasopressor therapy (norepinephrine IV infusion 1.5 mcg/kg/min) and sedation (propofol 30 mg IV stat and fentanyl 60 mcg IV stat then 50 mcg/h IV infusion) and was kept under monitoring in the ER then shifted to intensive care unit (ICU) with normal vital signs (Tables 1,3).
Table 1
| Time | Vital sign | Result | Reference range |
|---|---|---|---|
| Before receiving ondansetron | BP (mmHg) | 112/78 | 90/60–120/80 |
| Pulse (bpm) | 78 | 60–100 | |
| Temperature (℃) | 37 | 36.5–37.3 | |
| SatO2 (%) | 98 | 95–100 | |
| 10 minutes after receiving ondansetron | BP (mmHg) | 100/50 | 90/60–120/80 |
| Pulse (bpm) | 156 | 60–100 | |
| Temperature (℃) | 37 | 36.5–37.3 | |
| SatO2 (%) | 86 | 95–100 | |
| ROSC achieved | BP (mmHg) | 100/50 | 90/60–120/80 |
| Pulse (bpm) | 155 | 60–100 | |
| Temperature (℃) | 37 | 36.5–37.3 | |
| SatO2 (%) | 100 | 95–100 | |
| Upon shifting to ICU | BP (mmHg) | 99/67 | 90/60–120/80 |
| Pulse (bpm) | 114 | 60–100 | |
| Temperature (℃) | 37 | 36.5–37.3 | |
| SatO2 (%) | 98 | 95–100 |
BP, blood pressure; bpm, beats per minute; ICU, intensive care unit; ROSC, return of spontaneous circulation; SatO2, oxygen saturation.
Table 2
| Day | Lab parameter | Result | Reference range |
|---|---|---|---|
| On the day of arrest and prior to receiving ondansetron | Magnesium (mg/dL) | 1.57 | 1.9–2.5 |
| Calcium (mg/dL) | 8.16 | 8.8–10.6 | |
| Potassium (mmol/L) | 3.54 | 3.5–5.1 | |
| Sodium (mmol/L) | 139 | 136–146 | |
| On the day of arrest and ~30 minutes after developing the reaction to ondansetron | Troponin-I (ng/mL) | 2.056 | 0.01–0.02 |
| CK-MB (ng/mL) | 18.1 | 0.6–6.3 | |
| CK (μ/L) | 357.63 | <145 | |
| Tryptase (ng/mL) | 2.4 | <11.5 | |
| IgE (IU/mL) | 274.5 | 0–100 | |
| On the second day after arrest and after being shifted to ICU | Magnesium (mg/dL) | 1.79 | 1.9–2.5 |
| Calcium (mg/dL) | 7.27 | 8.8–10.6 | |
| Potassium (mmol/L) | 4.17 | 3.5–5.1 | |
| Sodium (mmol/L) | 137.12 | 136–146 | |
| Magnesium (mg/dL) | 2.2 | 1.9–2.5 | |
| Calcium (mg/dL) | 7.44 | 8.8–10.6 | |
| Potassium (mmol/L) | 4.03 | 3.5–5.1 | |
| Sodium (mmol/L) | 132 | 136–146 | |
| On the third day after arrest and in the ICU after being extubated | Magnesium (mg/dL) | 2.07 | 1.9–2.5 |
| Calcium (mg/dL) | 8.01 | 8.8–10.6 | |
| Potassium (mmol/L) | 4.21 | 3.5–5.1 | |
| Sodium (mmol/L) | 141 | 136–146 | |
| CK (μ/L) | 2,718 | <145 | |
| Potassium (mmol/L) | 3.1 | 3.5–5.1 | |
| Sodium (mmol/L) | 143 | 136–146 | |
| Albumin (g/dL) | 2.94 | 3.5–5.2 | |
| On the fourth day after arrest and in the ICU after further stabilization | CK (μ/L) | 1,888 | <145 |
| Magnesium (mg/dL) | 2.28 | 1.9–2.5 | |
| Calcium (mg/dL) | 7.97 | 8.8–10.6 | |
| Potassium (mmol/L) | 4.28 | 3.5–5.1 | |
| Sodium (mmol/L) | 141 | 136–146 | |
| Magnesium (mg/dL) | 2.02 | 1.9–2.5 | |
| Calcium (mg/dL) | 7.78 | 8.8–10.6 | |
| Potassium (mmol/L) | 3.25 | 3.5–5.1 | |
| Sodium (mmol/L) | 142 | 136–146 | |
| On the fifth day after arrest and in the ICU prior to discharge | Magnesium (mg/dL) | 2.14 | 1.9–2.5 |
| Calcium (mg/dL) | 7.77 | 8.8–10.6 | |
| Potassium (mmol/L) | 3.73 | 3.5–5.1 | |
| Sodium (mmol/L) | 140 | 136–146 | |
| CK (μ/L) | 520 | <145 |
CK, creatine kinase; CK-MB, creatine kinase-MB; ICU, intensive care unit; IgE, immunoglobulin E.
Table 3
| Time | Clinical event | Interventions | Outcome |
|---|---|---|---|
| Presenting to ER | Nausea, vomiting | 8 mg IV ondansetron | Convulsions then cardiac arrest |
| Course of management in the ER | Convulsions then cardiac arrest | Midazolam 5 mg IV stat, IVF NaCl 0.9% a total of 1,000 mL, RL 500 mL and sodium bicarbonate 8.4% 100 mL IV bolus, adrenaline 1 mg and amiodarone 150 mg with doses repeated as protocol. Then norepinephrine IV infusion reaching 1.5 mcg/kg/min and sedation (propofol 30 mg IV stat and fentanyl 60 mcg IV stat then 50 mcg/h IV infusion) | ROSC |
| Upon admission to the ICU | Shock state | Norepinephrine IV infusion (1.5 mcg/kg/min), vasopressin 0.04 IU/h, and fentanyl 50 mcg/h IV infusion. Hydrocortisone 200 mg IV followed the second day by methylprednisolone 125 mg IV every 6 hours. Enoxaparin 40 mg SC once daily | Shock resolved |
| Hypomagnesemia, hypokalemia, hypocalcemia | Magnesium sulfate 50% 2 g IV on the day of admission followed the second day by 4 g IV, calcium gluconate 2 g IV followed by a maintenance of 1 g IV every 8 hours on the second day, Potassium chloride 40–80 mEq IV daily according to the MOH protocol | Electrolyte correction was achieved, with documented clinical improvement (improved vital signs, normalization of QTc, patient extubation) | |
| After extubation and stabilization | Cardiomyopathy | Furosemide 20 mg IV daily, bisoprolol 1.25 mg orally daily and captopril 6.25 mg orally every 8 hours | Patient stabilization with normalization of laboratory and ECG findings; patient discharge |
This timeline table summarizes the sequence of events starting from presenting to ER with the complaint of nausea and vomiting, with the course of management done in the ER and ICU that includes CPR, electrolyte correction, shock and cardiomyopathy management until reaching complete recovery and then being discharged in a stable clinical condition. CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ER, emergency room; ICU, intensive care unit; IV, intravenous; IVF, intravenous fluid; MOH, Ministry of Health; QTc, normal corrected QT; RL, Ringer’s lactate; ROSC, return of spontaneous circulation; SC, subcutaneous.
Essential pharmacological interventions done during hospitalization in the ICU included the following: magnesium sulfate 50% 2 g IV on the day of admission followed the second day by 4 g IV, calcium gluconate 2 g IV followed by a maintenance of 1 g IV every 8 hours on the second day, potassium chloride 40–80 mEq IV daily according to the hospital protocol (20) norepinephrine IV infusion reaching 1.5 mcg/kg/min, vasopressin 0.04 IU/h, fentanyl 50 mcg/h IV infusion, hydrocortisone 200 mg IV followed the second day by methylprednisolone 125 mg IV every 6 hours, enoxaparin 40 mg subcutaneous (SC) once daily, furosemide 20 mg IV daily, bisoprolol 1.25 mg orally daily and captopril 6.25 mg orally every 8 hours.
The possibility of anaphylactic shock was addressed, and the reaction to ondansetron was considered possible and classified as severe according to the Naranjo Probability Scale and the Hartwig Severity Assessment Scale, respectively (13,14).
After additional assessment and lab tests, results showed: a high level of IgE antibodies 274.5 IU/mL (explained by her allergic rhinitis), a tryptase level of 2.8 ng/mL, within the normal range, strongly suggesting that anaphylaxis was unlikely, especially since the sample was drawn 30 minutes after the cardiac arrest and medication administration.
Furthermore, the patient exhibited low levels of serum magnesium 1.57 mg/dL and low levels of potassium 3.58 mmol/L indicating concurrent hypomagnesemia and hypokalemia upon ER admission (Table 2), which greatly contributed to QT interval prolongation normal corrected QT (QTc) 582 ms (Figure 1) and hence polymorphic ventricular fibrillation and cardiac arrest.
After 48 hours of ICU hospitalization, intense clinical workup, and interventions including electrolyte correction, resuscitation, and arrhythmia control, the patient showed marked clinical improvement. Echocardiography results also revealed sequential improvement where findings first revealed severely reduced left ventricular (LV) function and hence ejection fraction (EF 20%) with mild to moderate mitral regurgitation. Three days later, findings revealed a significant improvement in LV function (EF 40%) where the transmitral spectral Doppler flow pattern was suggestive of pseudo-normalization (Figure 2), got successfully extubated with a level of consciousness reaching GCS 15/15, and then discharged in a stable clinical condition.
Other relevant cardiology investigations revealed LV dysfunction with EF 20% (Figure 2). Interestingly, coronary angiogram investigations ruled out ischemia, and cardiomyopathy resolved quickly after taking proper interventions in the post-arrest period.
The patient was scheduled an appointment as soon as possible for a potential Electrophysiology Study (EPS) and discussion of implantable cardioverter-defibrillator (ICD) placement, if indicated.
She followed up after 6 months in the cardiology clinic, was assessed for adherence to therapy and underwent ECG, echocardiography, and Holter testing which revealed normal results (Figures 2,3) with complete recovery. However, she refused to do the EPS study.
She was also scheduled a follow-up appointment with the immunologist for further evaluation and management, but she did not follow up in the immunology clinic.
All procedures performed in this study were in accordance with the ethical standards of SMC Hospital Ethics Committee (No. 005-2024) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.
Patient perspective
To start from the beginning, we would have to go back to August 2023 when I came to the hospital ER with nausea and vomiting for which I received a certain medication that resulted in palpitations, convulsions and loss of consciousness after a while; I was then intubated and shifted to the ICU. I remember that I regained my consciousness in the ICU when I got successfully extubated. I have been told that I had cardiac arrest and cardiomyopathy which required intensive care management, but luckily, I was discharged in a stable condition. I followed up later in the outpatient clinic, and I am satisfied that I ended up in full recovery.
Discussion
Our case emphasizes the causality between ondansetron and the risk of serious complications such as cardiac arrest and cardiomyopathy, particularly when hypomagnesemia and hypokalemia are documented.
According to a systemic review done by Freedman et al., no reports identified cardiac arrhythmias occurring from a single oral dose of ondansetron (21). However, 67% of the cases that developed cardiac arrhythmias upon ondansetron use had significant medical history or were on concomitant use of a QT-prolonging medications such as chemotherapeutic agents; such findings were identified in 83% of published reports. It was then stated that current evidence does not support routine ECG and electrolyte screening before single oral ondansetron dose administration to individuals without known risk factors. Screening should be targeted to high-risk patients and those receiving ondansetron intravenously (21). Another cross-sectional study conducted by Tabrizi et al., investigated the effect of low-dose ondansetron (4 mg) concluded that low-dose ondansetron (4 mg) IV administration among non-cardiac patients was not associated with QT interval prolongation (22). On the other hand, a case report by Orozco et al. showed similar findings to our case where a single dose of 4 mg IV ondansetron was associated with QTc prolongation with contributing factors such as hypomagnesemia and hypokalemia (23). Although the mentioned solid evidence suggests that the risk of cardiac arrhythmias associated with ondansetron use in medically free patients is unlikely, there have still been few case reports documenting this occurrence after single and multiple ondansetron doses (6,9,21,23), but none reported the occurrence of cardiomyopathy.
The interesting findings of torsade de pointes after the administration of low doses of ondansetron were further highlighted in other case reports by Orozco et al. and Patel et al. where risk factors included hypomagnesemia and hypokalemia (23,24).
The findings observed in our case would in fact necessitate serum electrolyte checking in patients presenting with vomiting prior to receiving IV or oral ondansetron. Therefore, we created a protocol accordingly in the hospital to necessitate ECG and magnesium/potassium checking with appropriate preventive measures prior to receiving ondansetron. Up to our knowledge, no studies were done in Saudi Arabia to confirm such findings, and further research is required to build strong recommendations.
Conclusions
The use of ondansetron even in low doses can result in serious life-threatening cardiac arrhythmias and cardiomyopathy with LV dysfunction particularly in patients with electrolyte imbalance. Complete recovery can be achieved upon discontinuation of ondansetron and undergoing quick cardiopulmonary and pharmacological interventions. It is therefore crucial to exercise caution when administering this drug, correct electrolytes prior to and during ondansetron administration and be watchful for any adverse events that might occur.
Acknowledgments
We would like to express our sincere gratitude to the echocardiography consultant Dr. Emadaldin Musa Ahmed for his support and guidance throughout cardiology workup and assessment done in this case and Mr. Amjad Naji from the catheterization laboratory for providing us with all the relevant echocardiography images. We would also like to thank Jida Al-Mulki for her meticulous review of the final draft of this case report.
Footnote
Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-25-3/rc
Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-25-3/prf
Funding: None.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-25-3/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of SMC Hospital Ethics Committee (No. 005-2024) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
References
- Ye JH, Ponnudurai R, Schaefer R. Ondansetron: a selective 5-HT(3) receptor antagonist and its applications in CNS-related disorders. CNS Drug Rev 2001;7:199-213. [Crossref] [PubMed]
- Weiss KS. Anaphylactic reaction to ondansetron. Arch Intern Med 2001;161:2263. [Crossref] [PubMed]
- Mehra KK, Gogtay NJ, Ainchwar R, et al. Hypersensitivity to intravenous ondansetron: a case report. J Med Case Rep 2008;2:274. [Crossref] [PubMed]
- Fernando SL, Broadfoot AJ. Ondansetron anaphylaxis: a case report and protocol for skin testing. Br J Anaesth 2009;102:285-6. [Crossref] [PubMed]
- Sapkota K, Bhagat R. Fatal anaphylaxis to intravenous ondansetron: A case report. Clin Case Rep 2021;9:e04110. [Crossref] [PubMed]
- Leung KSK, Ahmad F, Mahmood A, et al. Ondansetron and hypothermia induced cardiac arrest in a 97-year-old woman: a case report. Cardiovasc Innov Appl 2022;7:990.
- Suzuki Y, Liu S, Iwata M, et al. Ondansetron-Induced Anaphylactic Shock: An In-Depth Analysis of a Rare Adverse Event. Cureus 2023;15:e42894. [Crossref] [PubMed]
- Baldo BA. Allergic and other adverse reactions to drugs used in anesthesia and surgery. Anesthesiol Perioper Sci 2023;1:16. [Crossref] [PubMed]
- Lee DY, Trinh T, Roy SK. Torsades de Pointes after Ondansetron Infusion in 2 Patients. Tex Heart Inst J 2017;44:366-9. [Crossref] [PubMed]
- Kuryshev YA, Brown AM, Wang L, et al. Interactions of the 5-hydroxytryptamine 3 antagonist class of antiemetic drugs with human cardiac ion channels. J Pharmacol Exp Ther 2000;295:614-20.
- Kasinath NS, Malak O, Tetzlaff J. Atrial fibrillation after ondansetron for the prevention and treatment of postoperative nausea and vomiting: a case report. Can J Anaesth 2003;50:229-31. [Crossref] [PubMed]
- Charbit B, Alvarez JC, Dasque E, et al. Droperidol and ondansetron-induced QT interval prolongation: a clinical drug interaction study. Anesthesiology 2008;109:206-12. [Crossref] [PubMed]
- Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239-45. [Crossref] [PubMed]
- Hartwig SC, Siegel J, Schneider PJ. Preventability and severity assessment in reporting adverse drug reactions. Am J Hosp Pharm 1992;49:2229-32.
- UpToDate Inc. Ondansetron [drug information]. Lexi-Drugs. UpToDate Lexidrug. 2024. Available online: https://online.lexi.com/Ico/action/login
- Medicines and Healthcare Products Regulatory Agency (MHRA). Zofran Injection - Summary of Product Characteristics (SmPC). 2024. Available online: https://www.medicines.org.uk
- US Food and Drug Administration. FDA Drug Safety Communication: Abnormal heart rhythms may be associated with use of Zofran (ondansetron). 2016. Available online: https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-abnormal-heart-rhythms-may-be-associated-use-zofran-ondansetron
- Jain S, Margetis K, Iverson LM. Glasgow Coma Scale. In: StatPearls. Treasure Island: StatPearls Publishing; 2025.
- Perman SM, Elmer J, Maciel CB, et al. 2023 American Heart Association Focused Update on Adult Advanced Cardiovascular Life Support: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2024;149:e254-73. [Crossref] [PubMed]
- Ministry of Health (MOH). Adult Electrolyte Replacement Therapy Protocol. 2025. Available online: https://www.moh.gov.sa/Ministry/MediaCenter/Publications/Documents/Adults-Electrolyte-Replacement-Therapy-protocol.pdf
- Freedman SB, Uleryk E, Rumantir M, et al. Ondansetron and the risk of cardiac arrhythmias: a systematic review and postmarketing analysis. Ann Emerg Med 2014;64:19-25.e6. [Crossref] [PubMed]
- Tabrizi S, Heidari S, Rafiei H. Investigation role of ondansetron on long QT interval among non-cardiac patients. Ann Med Surg (Lond) 2021;71:102971. [Crossref] [PubMed]
- Orozco BS, Lee SC, Fuchs RT, et al. QT prolongation, torsades des pointes, and cardiac arrest after 4 mg of IV ondansetron. Am J Emerg Med 2023;68:214.e3-6. [Crossref] [PubMed]
- Patel E, Rosemond D, Afzal A. Ondansetron induced torsades de pointes. Clin Case Rep 2019;7:1557-8. [Crossref] [PubMed]
Cite this article as: Tafish R, Elsayed R, Alsolamy S, Aljuaid W, Yaseen R, Kuhail A. Ondansetron-induced cardiac arrest and cardiomyopathy with successful reversal: a case report. AME Case Rep 2025;9:122.
