The Impact of Magnesium Oxide Monohydrate Compared to Placebo on Exercise Tolerance, Quality of Life and Clinical Outcomes in Chronic Heart Failure Patients

Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function. Patients with chronic heart failure (CHF) are magnesium deficient. The activation of the renin-angiotensin-aldosterone system and the use of diuretics are associated with depletion of potassium and magnesium in CHF. Magnesium deficiency stimulates aldosterone production and secretion, while magnesium infusion decreases aldosterone production production by inhibiting cellular calcium influx. Adamopoulos et al recently found that CHF in patients [mainly New York Heart Association (NYHA) II-II] with low serum magnesium ≤ 2 mEq/L was associated with increased cardiovascular mortality (but had no association with cardiovascular hospitalization) compared to those with serum magnesium > 2 mEq/L in a long-term follow-up of 36 months, suggesting that most of these deaths were likely sudden (arrhythmic) in nature.

Furthermore, Stepura and Martynow demonstrated that oral magnesium orotate used as adjuvant therapy in severe NYHA IV CHF patients increased 1-year survival rate and improved clinical symptoms and patient's quality of life compared to placebo. The investigators hypothesized that 1-year supplementation of oral magnesium compared to placebo to CHF patients will improve exercise duration time and quality of life.