Magnesium treatment for 3 months in patients with ischaemic heart disease increases the apolipoprotein A1:apolipoprotein B ratio by 13%, decreases the apolipoprotein B concentrations by 15%, and decreases very-low-density lipoprotein concentrations by 27%.118 Magnesium therapy also tended to increase high-density lipoprotein. The authors of the study concluded: ‘…magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis’.118 In hypomagnesaemic kidney transplant recipients, magnesium supplementation significantly decreases total cholesterol, low-density lipoprotein and total cholesterol:high density lipoprotein ratio.119 Magnesium deficiency may enhance vascular endothelial injury, promoting the development and progression of atherosclerosis.120
Magnesium deficiency may supersaturate bodily fluids with octacalcium phosphate calcifying soft tissues, whereas magnesium therapy may stop or even prevent soft tissue calcifications.121 Magnesium deficiency in Yorkshire swine induces numerous calcifications and smooth muscle cell degeneration, and promotes atherosclerosis in combination with an atherogenic diet.122 Hamsters fed a magnesium-deficient diet develop myocardial necrosis, calcifications and cardiomyopathy. These effects of magnesium deficiency seem to be secondary to the inhibition of the Na-K-ATPase and the calcium overload that follows in cardiac myocytes.123 Triglyceride-rich lipoproteins from magnesium-deficient rats are more susceptible to oxidation.124 Thus, magnesium deficiency predisposes to lipoprotein peroxidation and atherosclerosis. Perhaps most importantly, patients in the intensive cardiac care unit have been noted to have low blood mononuclear cell magnesium levels.125 The authors summarised their findings as the following: ‘We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the serum magnesium would lead one to suspect, and may contribute to clinical cardiovascular morbidity’.125