Safety and Efficacy of Intravenous Magnesium for Torsade de Pointes　― A Scoping Review ―

Mutsuko Sangawa; Hiroki Shiomi; Eiji Hiraoka; Kazuo Sakamoto; Kenichi Iijima; Tetsuma Kawaji; Takayuki Kitai; Yukio Hosaka; Masashi Yokose; Teruo Noguchi; Hiroshi Takahashi; Tetsuya Matoba; Migaku Kikuchi; Yoshio Tahara; Hiroshi Nonogi; Toshikazu Funazaki; for the Japan Resuscitation Council (JRC) Emergency Cardiovascular Care (ECC) Arrhythmia Task Force and the Guideline Editorial Committee on behalf of the Japanese Circulation Society (JCS) Emergency and Critical Care Committee

doi:10.1253/circrep.CR-25-0175

Abstract

Intravenous magnesium is commonly used in clinical practice for treating Torsade de Pointes (TdP), although supporting evidence remains limited. This scoping review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension guidelines. Four online databases were searched for relevant studies published as of November 27, 2024, but only 4 observational studies met the inclusion criteria. TdP resolved in a substantial proportion of patients treated with intravenous magnesium (78.3% [N=36/46]), although most studies lacked a control group. No serious adverse events related to magnesium were reported (0% [N=0/46]). Despite several limitations that preclude firm conclusions, intravenous magnesium appears to be a relatively safe and effective treatment for TdP. However, TdP progressed to ventricular fibrillation (VF) in 21.7% (N=10/46) of patients, underscoring the need for readiness to perform immediate electrical defibrillation during treatment. Further high-quality studies are warranted to validate these findings.

Central Figure

Torsade de Pointes (TdP), first described in 1966 by Dessertenne, is a potentially life-threatening, polymorphic, and repetitive form of ventricular tachycardia (VT).¹ Typical ECG features of TdP are nonuniform yet organized, with progressive changes in the morphology, amplitude, and polarity of ventricular complexes that appear to twist around the isoelectric baseline before terminating spontaneously.² TdP often arises in the setting of prolonged QT intervals and is commonly associated with antiarrhythmic drugs, electrolyte imbalances, and bradycardia.³

In addition to potassium supplementation in cases of hypokalemia,⁴^,⁵ treatment of TdP includes cardiac pacing³^,⁶^–⁸ and administration of isoproterenol⁹ to increase heart rate, thereby shortening the QT interval. Intravenous magnesium is widely used in clinical practice for the treatment of TdP. Current Japanese and Western clinical guidelines, recommend intravenous magnesium as a treatment option, although no randomized clinical trials (RCTs) have evaluated its safety and efficacy.¹⁰^–¹²

In JCS/JHRS 2020 Guideline on pharmacotherapy of cardiac arrhythmias, magnesium administration for polymorphic VT associated with QT prolongation is recommended by Grade B (scientific evidence is available and it is recommended) in accordance with the Minds Clinical Practice Guideline Development Manual 2007.¹² In 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death, intravenous magnesium with supplementation of potassium is recommended in patients with TdP by Class I.¹¹

In 2020, the International Liaison Committee on Resuscitation (ILCOR) reviewed available evidence on pharmacologic interventions for TdP by analyzing observational studies and RCTs indexed in PubMed through December 19, 2019. However, no studies met the inclusion criteria, and no systematic review was conducted.¹⁰ Therefore, we conducted a scoping review to assess the available clinical evidence regarding the safety and efficacy of intravenous magnesium for TdP. Our findings did not identify sufficient high-quality evidence to justify a systematic review or meta-analysis.

Methods

The Japan Resuscitation Council (JRC) Arrhythmia Task Force and the Editorial Committee for the JRC Guideline 2025 initially conducted a systematic review using the Population, Intervention, Comparator, Outcome, Study design, and Timeframe framework, as follows:

P (Population): patients aged ≥18 years with TdP

I (Intervention): intravenous magnesium

C (Comparator): no magnesium

O (Outcomes):

Critical outcomes: short-term mortality (harms), progression to ventricular fibrillation (VF) (harms)

Important outcomes: termination of TdP (benefits), fatal side effects (harms)

S (Study design): RCTs, observational studies with or without control group, cohort studies, and case series with ≥5 cases. All relevant publications in any language included if an English abstract was available. Unpublished studies (e.g., conference abstracts, trial protocols) and grey literature were excluded.

T (Timeframe): all literature published up to November 27, 2024. However, no RCTs or observational studies with adequate sample size and control groups were identified to support a meta-analysis. Therefore, a scoping review was conducted, focusing on cohort and case series studies with ≥5 cases.

This scoping review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) guidelines.¹³^,¹⁴ Institutional Review Board approval was not required, as the study used publicly available data.

Identification of the Research Question

Does intravenous magnesium improve clinical outcomes in the acute treatment of TdP?

Study Selection and Definitions

All cohort and case series studies that included ≥5 patients with TdP treated with intravenous magnesium were included if they met both of the following criteria: (1) patients received intravenous magnesium alone as the initial treatment for TdP, and (2) the study assessed the safety and efficacy of intravenous magnesium for TdP.

The clinical outcomes included: termination of TdP (benefit); short-term mortality (harm); progression to VF (harm); and fatal side effects (harm).

Short-term mortality was defined as all-cause death during hospitalization. Progression to VF was defined as the occurrence of VF or electrical cardioversion after intravenous magnesium administration. Serious side effects associated with intravenous magnesium were considered fatal. If no side effects were described in the included studies, they were interpreted as having no reported fatal side effects.

Extraction of Relevant Studies

Literature search strategies were developed using Medical Subject Headings (MeSH) and relevant keywords related to TdP and magnesium. The complete search strategy is provided in the Supplementary Appendix. A systematic search of published studies was performed in MEDLINE, the Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, and Igaku Chuo Zasshi to identify relevant articles from database inception to November 27, 2024. Extracted data included author names, article title, journal name, publication year, URL, and abstract. After removing duplicates, titles and abstracts were independently screened by 2 reviewers (M.S. and H.S.) using predefined inclusion criteria. In cases of uncertainty, the full texts were independently reviewed by the same 2 reviewers. Disagreements regarding study eligibility were resolved through discussion, with final adjudication by a third independent reviewer (E.H.).

Results

Among the 1,568 articles screened by title and abstract, 919 duplicates and 642 articles were excluded for not meeting the inclusion criteria. After excluding 3 additional papers during full-text review, 4 studies were identified as eligible for inclusion in this scoping review (Figure).

Figure.

Study flow chart.

Study Characteristics

A summary of the 4 studies is presented in the Table. All were single-center, retrospective observational studies, including 1 case series without a control group. The studies collectively included 46 patients with TdP treated with intravenous magnesium alone. TdP resolved in 36 patients (78.3%), while 10 patients (21.7%) progressed to VF. None of the studies reported deaths or serious adverse effects related to intravenous magnesium.

Table.

Summary of Studies Evaluating the Safety and Efficacy of Intravenous Magnesium for TdP

Study name	Study design	Sample size (Mg alone: N)	Summary	Clinical outcomes
				Benefits	Harms
				Termination of TdP by Mg alone	Mortality (short term)	Progression to VF	Serious side effects
Gowda et al. (Int J Cardiol 2004)¹⁵	Cohort study	18	Patients: TdP after the infusion of ibutilide (N=58) Treatment: Mg administration (N=21: study group) 　– MgSO₄ alone: N=18 (31%) 　– MgSO₄+lidocaine: N=3 (5%) No Mg administration (N=37: control group) 　– EC alone: N=11 (19%) 　– Precordial thump: N= 2 (3%) 　– Without treatment: N=24 (41%) Results: progression to VF: study group (N=10), control group (N=11) 　Survival: no deaths (N=58)	8/18 (44.4%)	0/18 (0%)	10/18 (55.6%)	0/18 (0%)
Manz et al. (Herz 1997)¹⁶	Cohort study	4	Patients: TdP (N=4: study group) Persistent monomorphic VT (N=25: control group) Treatment: magnesium glutamate (2×1,000 mg IV): – study group (N=4), – control group (N=25) Results: (Study group) TdP terminated: N=4 (100%) 　　　　(Control group) TdP terminated: N=8 (32%)	4/4 (100%)	0/4 (0%)	0/4 (0%)	0/4 (0%)
Perticone et al. (Clin Drug Invest 1997)²	Case series reports	12	Patients: TdP with acquired prolonged QT interval (N=12) Treatment: MgSO₄ infusion in 0.9% sodium chloride at a slow rate (50 mg/min) 　MgSO₄ infusion continued for 2 h 　Prophylactic infusion b.i.d. over the next 3–4 days Other treatment: potassium therapy after MgSO₄ infusion: N=2 Results: TdP disappeared within 20–30 min: N=12 (100%) 　Progression to VF: N=0 (0%) 　Serious side effects: N=0 (0%)	12/12 (100%)	0/12 (0%)	0/12 (0%)	0/12 (0%)
Tzivoni et al. (Circulation 1988)¹⁷	Cohort study	12	Patients: TdP with QT prolongation (N=12: study group) 　Polymorphous VT normal QT interval (N=5: control group) Treatment: MgO₄ administration: N=17 (100%) 　– Bolus infusion: N=17 (100%) 　– Continuous infusion after bolus infusion (3–20 mg/min): N=9 　(75%: preventive [N=6], not preventive [N=3]) Other therapies: supplementation of potassium (study group: N=8) Results: Disappearance of TdP: 　(Study group: N=12) TdP terminated after a single MgO₄ bolus injection: N=9 (75%) 　TdP terminated after second MgO₄ bolus injection: N=3 (25%) 　(Control group: N=5) TdP was not terminated by MgO₄ bolus injection in all 5 cases: N=0 (0%) 　Survival: no deaths (N=17)	12/12 (100%)	0/12 (0%)	0/12 (0%)	0/12 (0%)
All	–	46	–	36/46 (78.3%)	0/46 (0%)	10/46 (21.7%)	0/46 (0%)

b.i.d., twice a day; TdP, torsades de pointes; VF, ventricular fibrillation.

Patient selection, presence or absence of a control group, study methods, magnesium dosing, and reported outcomes varied across the 4 studies.

Gowda et al.¹⁵ investigated the effects of intravenous magnesium sulfate in 58 patients with TdP, drawn from a cohort of 1,096 patients who had received the Class III antiarrhythmic agent ibutilide for atrial arrhythmias. Of them, 21 patients received intravenous magnesium sulfate and were compared with 37 patients who did not. Among the 21 treated patients, 18 received intravenous magnesium sulfate alone and 3 received a combination of magnesium sulfate and lidocaine. Among the 18 patients treated with intravenous magnesium sulfate alone, TdP terminated in 8 (termination rate: 44.4%), and 10 required electrical cardioversion due to VF (progression rate: 55.6%). In the overall study population, 24 of the 58 patients experienced spontaneous TdP termination without any treatment (self-termination rate: 41%). No deaths were reported in the study.

Manz et al.¹⁶ investigated the effectiveness of magnesium sulfate in 29 patients with VT. Among them, 4 had TdP, and the remaining 25 had sustained monomorphic VT. In all 4 patients, TdP resolved after intravenous administration of magnesium glutamate (2×1,000 mg) (termination rate: 100%), with no progression to VF or reported side effects. In the 25 patients with sustained monomorphic VT, VT terminated following intravenous magnesium glutamate in 8 patients (termination rate: 32%). The authors concluded that intravenous magnesium was ineffective as emergency therapy for monomorphic VT, but effective for terminating and suppressing TdP.

Perticone et al.² reported 12 consecutive cases of TdP (9 men, 3 women, aged 49–78 years) with acquired QT prolongation (QTc: 500–640 ms). Of them, 5 patients received Class IA antiarrhythmic drugs (disopyramide in 2, quinidine plus disopyramide in 1, quinidine in 2). All patients were treated with magnesium sulfate diluted in 0.9% sodium chloride and infused at 50 mg/min, continued for 2 h after TdP resolution. A prophylactic infusion of 30 mg/min was administered twice daily for 90 min over the next 3–4 days. Before treatment, 109 episodes of TdP (mean 9.1±2.4 per patient) lasting 2–16 s were recorded. In all 12 patients, TdP terminated within 20–30 min (termination rate: 100%) and did not progress to VF. Arrhythmic suppression was not associated with changes in QT interval. No side effects were reported, and intravenous magnesium sulfate did not affect heart rate or blood pressure.

Tzivoni et al.¹⁷ described 12 consecutive patients with TdP and QT prolongation treated over a 4-year period. In 9 of the 12 cases, TdP was induced by antiarrhythmic agents. All patients received a 2 g bolus of magnesium sulfate intravenously. In 9 patients, TdP resolved within 1–5 min after a single bolus; in the remaining 3 patients, TdP resolved 5–15 min later following a second bolus (termination rate: 100%). Nine patients received a continuous infusion of magnesium sulfate (3–20 mg/min) for 7–48 h until the QT interval decreased to <0.50 s. Two patients experienced TdP recurrence 1–6 h after initial treatment; an additional bolus was effective in both cases. No adverse effects were reported. The authors also noted that magnesium sulfate boluses were ineffective in 5 patients with polymorphic VT who did not have QT prolongation.

Discussion

Main Findings in Our Scoping Review

In 2020, the ILCOR reviewed and updated the evidence on whether medications improve outcomes in TdP by evaluating human observational studies and RCTs indexed in PubMed through December 19, 2019. No systematic review was conducted, as no human RCTs or observational studies met the inclusion criteria.¹⁰ Although no randomized studies have been conducted on drugs for the treatment of TdP, the ESC 2022 guidelines¹¹ strongly recommend the combination of intravenous magnesium and potassium supplementation for adult patients with TdP, based on a case report of 12 patients reported in 1988.¹⁷ However, because there has been no sufficient evidence-based study and magnesium is widely used in the treatment of TdP both in Japan and overseas, we conducted a scoping review by the JRC with expanded search conditions and inclusion criteria. The inclusion criteria for papers were expanded to case series of ≥5 cases to examine the effect of magnesium. Consistent with these findings, our scoping review, which extended the scope to include small observational studies, identified only 4 eligible studies.

The main findings of this review are as follows.

1. Only 4 small observational studies without a control group met the eligibility criteria to evaluate the safety and efficacy of intravenous magnesium alone for TdP.

2. TdP resolved in a substantial proportion of patients treated with intravenous magnesium (78.3% [N=36/46]).

3. No serious adverse effects related to intravenous magnesium were reported.

4. TdP progressed to VF in 10 of the 46 cases (21.7%).

Based on these findings, the TdP termination rate with intravenous magnesium was substantial (78.3%). Although the precise mechanism remains unclear, proposed mechanisms include stabilization of the cardiac cell membrane and suppression of early afterdepolarizations. Importantly, none of the studies reported serious side effects associated with intravenous magnesium. Given its favorable safety profile and potential therapeutic benefit, intravenous magnesium may represent a reasonable treatment option for TdP. However, given that a notable proportion of patients experienced progression to VF, it is essential to ensure readiness for immediate electrical defibrillation during TdP management.

Literature Review of TdP Treatment

Magnesium is the second most abundant intracellular cation after potassium. It is an essential element involved in regulating membrane stability and supporting neuromuscular, cardiovascular, immune, and hormonal functions. Magnesium plays a critical role in various cellular processes. Ventricular arrhythmias in patients with hypomagnesemia are commonly associated with prolonged QT intervals.¹⁸^–²⁰ Hypomagnesemia is frequently linked to a prolonged action potential duration (APD) at the cellular level.¹⁹ Shimaoka et al. provided evidence that chronic magnesium deficiency reduces the expression of Kir2.1 and Kv4.2 channels, resulting in decreased IK1 and Ito currents and consequent APD prolongation in cardiomyocytes, along with QT interval prolongation in intact rats.¹⁸

Magnesium also acts as a natural endogenous blocker of calcium (Ca²⁺) channels. A reduction in extracellular magnesium concentration can increase inward Ca²⁺ currents, further prolonging the QT interval.¹⁸^,¹⁹

TdP is typically caused by either congenital or acquired long QT syndrome (LQTS). It is a form of polymorphic VT characterized by beat-to-beat changes in the polarity and amplitude of the QRS complexes, producing a waveform that appears to twist around the isoelectric line.

In congenital LQTS, the initiating mechanism of premature ventricular contractions in TdP is believed to involve triggered activity resulting from early afterdepolarizations, while the maintenance of TdP is supported by reentry mechanisms due to heterogeneity in APD across ventricular regions.⁹^,²¹

The RR interval pattern immediately preceding TdP onset often follows a short–long–short sequence,²² which is considered a hallmark of LQT2. Additionally, in some cases there is an increased sinus rate pattern, where the RR interval gradually shortens. This altered depolarization pattern is regarded as a variant of the short–long–short sequence.²³

Acquired LQTS is often drug-induced, but other causes include electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia; QT prolongation following myocardial infarction;²⁴ takotsubo cardiomyopathy;²⁵^,²⁶ pheochromocytoma;²⁷ and intracranial bleeding. TdP in acquired LQTS commonly arises due to an R-on-T pattern, in which premature ventricular contractions occur during the prolonged T wave following a pause. TdP may also be initiated by a short–long–short sequence of the RR interval.²³^,²⁸^,²⁹

The proposed mechanism of TdP involves triggered activity caused by early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs), as well as re-entry resulting from significant heterogeneity in myocardial repolarization.²^,⁹^,²¹^,³⁰

In vitro studies have demonstrated that EADs, DADs, and the arrhythmias they induce can be suppressed by magnesium.²⁰ TdP can be experimentally induced in animal models by prolonging the QT interval using agents such as quinidine³¹ or cesium chloride,³² which promote the development of EADs and arrhythmias. Notably, magnesium administration has been shown to suppress both EADs and TdP without shortening the QT interval.³¹^,³²

Acquired LQTS is frequently accompanied by bradycardia, regardless of the underlying cause, and bradycardia is recognized as a contributing factor in the onset of TdP. Therefore, increasing the heart rate through temporary pacing is considered an effective management strategy.³^,⁶^–⁸^,¹² Although continuous intravenous infusion of isoproterenol may be used to raise the heart rate, it is typically reserved as a bridge to pacing. Caution is warranted when a congenital form of LQTS is suspected, as isoproterenol may worsen QT prolongation.⁹^,¹² In addition, if contributing factors such as QT-prolonging medications, bradycardia or electrolyte imbalances are present; they should be corrected promptly.¹²

Hypokalemia is a known contributor to QT prolongation, and potassium supplementation is commonly used as an adjunctive treatment. Maintaining serum potassium levels at ≥4.0 mEq/L is considered effective in preventing cardiac events.⁴^,⁵^,¹²

Because hereditary arrhythmias can be fatal at first onset, the international consensus supports early diagnosis and intervention during childhood, before symptom onset for hereditary disorders such as congenital LQTS. Genetic counseling plays a crucial role in this process.³³^–³⁵ Recently, Yoshinaga et al. reported that the maximum QTc value on Holter monitoring may predict symptom onset in pediatric patients with LQTS.³⁶ Although this parameter is not currently included in the LQTS risk score, it may be helpful for diagnosing LQTS in individuals whose QT interval does not prolong during exercise testing, particularly in those with LQT2 or LQT3.

Therefore, diagnostic and treatment strategies for LQTS should incorporate age, sex, clinical presentation, genetic findings, and QT/QTc intervals from follow-up 12-lead and Holter ECG recordings.³⁷

In recent years, advances in catheter-based therapies have enabled attempts at 3-dimensional electroanatomic mapping of the short-coupled variant of TdP (sc-TdP).³⁸

Although there is not enough evidence yet, and it is not recommended in the current clinical practice guidelines due to insufficient evidence,³⁹ Steinfurt et al.³⁸ reported favorable short- and long-term outcomes following 3D mapping and catheter ablation of the culprit premature ventricular contraction at the free wall junction. This technique may offer a potential therapeutic option for patients with recurrent sc-TdP or electrical storm.

Currently, the ILCOR Consensus on Science with Treatment Recommendations no longer provides formal treatment guidance for arrhythmias and acute coronary syndromes. In response, the JRC has been working to generate evidence to support guideline development in cardiogenic shock and arrhythmias, in addition to ACS.⁴⁰ The JRC Resuscitation Guidelines emphasize early responses to acute clinical deterioration in undiagnosed patients, and are primarily designed for noncardiologists, trainees in emergency medicine and critical care, and other frontline medical staff.

There is little evidence on magnesium therapy for TdP, and further high-quality reports are needed.

Study Limitations

First and most importantly, only 4 small observational studies were identified, making it difficult to draw definitive conclusions. Second, all studies were relatively old, and their applicability to current clinical practice may be limited. Third, the possibility of reporting bias cannot be excluded, as most studies included only a small number of reported cases.

Given the limited and dated nature of the available evidence, there remains considerable uncertainty regarding the efficacy of intravenous magnesium therapy for TdP. Further high-quality research is warranted to clarify its therapeutic value.

Conclusions

Despite several limitations that hinder the ability to draw definitive conclusions, intravenous magnesium appears to be a relatively effective and safe treatment option for TdP. In some cases, TdP does not resolve even after magnesium administration, so electric shock may be required immediately and a defibrillator must be kept ready at all times. Further accumulation of high-quality evidence is necessary to validate its clinical utility.

Acknowledgments

The authors thank Mr. Shunya Suzuki and Ms. Tomoko Nagaoka, librarians at Dokkyo Medical University Tochigi, Japan, for their assistance with the article search.

This work was supported by the Japan Resuscitation Council, the Japanese Circulation Society, and JSPS KAKENHI Grant Number JP23K08454.

Disclosures

T.M. is a member of the Editorial Team for Circulation Reports.

All authors declare that they have no conflicts of interest regarding this paper.

IRB Information

Not applicable.

Data Availability

All data generated or analyzed during this study are included in this published article.

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circrep.CR-25-0175

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