What side effects are associated with this type of intervention?

Magnesium Sulphate, used to stabilize cardiac cell membranes, can cause side effects such as hypotension, bradycardia, and respiratory depression, especially at high doses. Digoxin, which increases vagal tone and decreases AV node conduction, may lead to nausea, vomiting, dizziness, and in severe cases, digoxin toxicity, which can cause arrhythmias and visual disturbances. Other common treatments for AF include beta blockers, which can cause fatigue, hypotension, and bradycardia; calcium channel blockers, which may lead to peripheral edema, constipation, and hypotension; and antiarrhythmic drugs like amiodarone and dronedarone, which have significant side effects including thyroid dysfunction, pulmonary toxicity, and liver enzyme abnormalities.

What prior FDA approvals exist?

The FDA has approved several drugs for the treatment of Atrial Fibrillation that have mechanisms similar to Magnesium Sulphate and Digoxin. Magnesium Sulphate is used to stabilize cardiac cell membranes and reduce excitability, while Digoxin increases vagal tone and decreases conduction through the AV node. Other FDA-approved drugs for AF include beta blockers (e.g., metoprolol, propranolol) which reduce heart rate and decrease myocardial oxygen demand, and calcium channel blockers (e.g., diltiazem, verapamil) which slow AV nodal conduction. Additionally, antiarrhythmic agents like amiodarone and sotalol are used to maintain sinus rhythm and prevent AF recurrence.

What other types of research exist?

Promising novel alternatives for Atrial Fibrillation treatment include KB-944 and Sulcardine. KB-944 is a new calcium antagonist that has shown potent antiarrhythmic effects in experimental models, being more effective than diltiazem and comparable to verapamil. Sulcardine, a sulfamide analogue, has demonstrated significant antiarrhythmic activity by increasing the threshold for aconitine-induced arrhythmias. Both agents offer different mechanisms of action compared to Magnesium Sulphate and Digoxin, potentially providing new therapeutic options for AF patients.

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Antiarrhythmic Agent

Magnesium vs Amiodarone for Atrial Fibrillation (MAGNAM Trial)

Q: What is the mechanism of action of this treatment?

Magnesium Sulphate stabilizes cardiac cell membranes and reduces excitability, helping to prevent abnormal electrical activity that can lead to Atrial Fibrillation (AF). Digoxin increases vagal tone and decreases conduction through the AV node, which slows the heart rate and helps control the ventricular response in AF. These mechanisms are crucial for AF patients as they directly address the irregular heart rhythms and high heart rates that characterize AF, improving symptoms and reducing the risk of complications.

Phase 3

Recruiting

Led By Brian H Cuthbertson, MD

Research Sponsored by Sunnybrook Health Sciences Centre

Eligibility Criteria Checklist

Specific guidelines that determine who can or cannot participate in a clinical trial

Must have

A newly documented episode of fast AF with HR >120/min confirmed by a 12-lead ECG assessment regardless of baseline rhythm (note- The AF can be acute or chronic diagnosis)

Be older than 18 years old

Timeline

Screening 3 weeks

Treatment Varies

Follow Up 90 days

Awards & highlights

MAGNAM Trial Summary

This trial will compare magnesium sulfate to magnesium sulfate + digoxin to see which is more effective in treating atrial fibrillation.

Who is the study for?

The MAGNAM trial is for adults in critical care with a new or existing diagnosis of fast atrial fibrillation (heart rate over 120/min) who need medical treatment. They must be able to have heart monitoring and not have used certain heart medications recently, nor should they have specific heart conditions, be pregnant, or critically ill with life expectancy under 12 hours.Check my eligibility

What is being tested?

This study tests if high-dose Magnesium Sulfate followed by Digoxin can more effectively restore normal heart rhythm compared to Amiodarone in patients with rapid atrial fibrillation. It's a randomized controlled trial across multiple centers where patients are chosen at random to receive one of the treatments.See study design

What are the potential side effects?

Possible side effects include flushing and sweating from Magnesium Sulfate; nausea, vomiting, and confusion from Digoxin; and Amiodarone may cause lung issues, liver problems, thyroid dysfunction or skin changes due to sun exposure.

MAGNAM Trial Eligibility Criteria

Inclusion Criteria

You may be eligible if you check “Yes” for the criteria below

Select...

I have had a recent episode of fast heart rate over 120 beats per minute due to atrial fibrillation.

MAGNAM Trial Timeline

Screening ~ 3 weeks3 visits

Treatment ~ Varies

Follow Up ~ 90 days

Screening ~ 3 weeks

Treatment ~ Varies

Follow Up ~90 days

This trial's timeline: 3 weeks for screening, Varies for treatment, and 90 days for reporting.

Treatment Details

Study Objectives

Outcome measures can provide a clearer picture of what you can expect from a treatment.

Primary outcome measures

Heart rate control (<110 beats per minute) and/or restoration of normal sinus

ICU free days

Secondary outcome measures

Avoidance of amiodarone

Continuation of trial intervention

Heart rate

+3 more

MAGNAM Trial Design

2Treatment groups

Experimental Treatment

Active Control

Group I: Experimental armExperimental Treatment1 Intervention

Intravenous magnesium sulphate as first line followed by digoxin IV loading as second line and then amiodarone IV as third line treatments for fast Atrial Fibrillation

Group II: Standard of care armActive Control1 Intervention

Intravenous amiodarone as compactor group intervention

0 / 1Eligibility criteria met

Research Highlights

Information in this section is not a recommendation. We encourage patients to speak with their healthcare team when evaluating any treatment decision.

Mechanism Of Action

Side Effect Profile

Prior Approvals

Other Research

Magnesium Sulphate stabilizes cardiac cell membranes and reduces excitability, helping to prevent abnormal electrical activity that can lead to Atrial Fibrillation (AF). Digoxin increases vagal tone and decreases conduction through the AV node, which slows the heart rate and helps control the ventricular response in AF. These mechanisms are crucial for AF patients as they directly address the irregular heart rhythms and high heart rates that characterize AF, improving symptoms and reducing the risk of complications.