Magnesium is a powerful anti-arrhythmic drug . It has a well established role in controlling VT when administered Intravenously especially in polymorphic VT .
Mechanism of action
- It acts at the cell membrane.
- It has a unique action of blocking calcium channels that reduces the number of oscillations of both early and late after potentials
Link for more on mechanism of action
https://drsvenkatesan.wordpress.com/2010/01/13/how-does-magnesium-acts-as-an-antiarrhythmic-drug/
How often cardiologists administer oral magnesium for long-term control of VT ?
As for as I know , no one uses it ! but dietary supplements are used for general well being .
Why ? Is it because
- Magnesium does not get absorbed in the gut
- Magnesium levels are un- predictable in plasma if administered orally
Answer : No one has really tried it as a chronic therapy in VT yet !
Final Message
Tablet Magnesium can give a tough fight to Amiodarone and Flecanaide in refractory VT at a fraction of the cost !
Who has the audacity to compare Magnesium with Amiodarone head on ?
Reference
Magnesium as health supplement .
Magnesium is available in tablet form as Malate , Stearate, Taurate and Aspartate along with calcium and Zinc etc .
Dr.S.Venkatesan MD 
good concept and i wanna add these facts also :
1- as such that magnesium acts on cerebral motor cortical neurons , the molecular basis of cellular excitability is similar for every cell and thus it’s great anti arrhythmic .
2- mg is a co-factor in the enzyme Na/K ATPase in the myocyte cell membrane , integrity of this enzyme essential for proper maintenance of the intracellular K.
3- further , mg competes with Ca++ ions to enter the cell and thus it’s a natural calcium blocker , this properly also helps in controlling refractory ca++ dependent cardiac arrhythmias , exerts some of it’s anti ischemic effects by limiting Na i by Na stimulating Ca influx or ( facilitating Ca efflux ) and hence , preventing intracellular Ca overload , that it’s not only cardioplegic be effective against detrimental effects of ischemia by antagonizing Ca overload .
4- upon re perfusion and so impair the return of normal contractile function the ability of mg to limit the K efflux form is of importance , not only in the prevention of ischemia induced calcium loss but also in the treatment of digitalis induced arrhythmias .
5- mg in cardiac cell are complex with high energy phosphate compounds and loss mg during ischemia may restrict the repletion of ATP .
6- it’s slightly negative inotropic .
7- it suppress sinoatrial automaticity while increase atriohisal and hisoventricular conduction time . there is weak data that mg increase coronary blood flow ,
many thanks