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Epidemiological studies of populations living in areas of low magnesium (Mg) intake have consistently shown a higher cardiovascular morbidity. Several hypotheses have been advanced to explain the cardioprotective properties of magnesium. Few studies, however, have analysed the relation of magnesium to haemostasis. The overall purpose of this project was to assess the association between certain haemostatic variables and magnesium deficiency. This experiment was designed to assess the effect of magnesium deficiency on various haemostatic variables which may relate to cardiovascular morbidity. Twelve female Yorkshire swine were fed for seven weeks on an Mg-sufficient or an Mg-deficient diet. Blood samples were obtained at baseline and after the termination of feeding in order to evaluate platelet aggregability and concentrations of antithrombin-III (AT-III), protein C, total protein S, fibronectin, endothelin-1 (ET-1), as well as the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1 alpha). In animals on an Mg-sufficient diet, there were no significant differences in any of the investigated haemostatic variables. In the Mg-deficient group, a significant decrease in serum magnesium was noted after the feeding period (from 2.0 +/- 0.1 to 1.3 +/- 0.1; P < 0.01). Mg-deficient swine showed significant increases in ADP-induced (33.3 per cent and 59.6 per cent) and collagen-induced (36.6 per cent) platelet aggregation, and decreased plasma antithrombin-III (17.7 per cent) and protein S (14.4 per cent) when compared to baseline. Plasma concentrations of TxB2 (28.7 per cent), protein C (57.2 per cent), and ET-1 (74.9 per cent) were dramatically increased. There were no significant differences in plasma fibronectin and 6-keto-PGF1 alpha levels in the magnesium-depleted animals. We conclude that magnesium deficiency is associated with significant proaggregatory and coagulation alterations. This may contribute to the increased cardiovascular morbidity found in magnesium-deficient populations. The beneficial effects of magnesium supplementation in an expanding array of clinical conditions including cardiovascular disease may, in part, be related to the improved haemostatic profile in such patients.

The aim of the present study was to evaluate the relationship between coronary vascular tone and serum magnesium concentration in patients with ischaemic heart disease. Thirty-seven patients were subjected to intracoronary injection of 200 micrograms nitroglycerine after discontinuation of anti-anginal medication for 24 h (group I, n = 23), except if they received calcium channel blockers (group II, n = 14). Coronary angiographic images were acquired before and 2 min after the nitroglycerine injection. Using quantitative coronary arteriography, the luminal diameter of one middle-sized non-stenotic coronary artery segment in each patient was measured before and after nitroglycerine injection, and the percentual increase was computed. In group I, coronary artery diameter changed from 3.0 +/- 0.7 to 3.5 +/- 0.6 mm (mean +/- SD), representing a 16.3 per cent increase. As expected, a more blunted response was observed in group II (from 3.5 +/- 0.8 to 3.7 +/- 1.0 mm, 6.5 per cent increase). However, neither of the groups displayed significant correlation between serum magnesium levels and the measured response to intracoronary nitroglycerine. In conclusion, this study fails to provide any correlation between serum magnesium levels within the normal physiological range and coronary vascular reactivity in patients with ischaemic heart disease.

The effect of magnesium sulphate infusion on ex vivo platelet aggregation in 11 female Yorkshire swine was observed using platelet-rich plasma and different agonists (ADP 5 mM; ADP 10 mM and collagen 1 mg/ml). Infusion of 1 g MgSO4 over 1 h produced a significant decrease in platelet aggregability. A dose-dependent effect of different ADP concentrations on platelet aggregation was noticed. Platelet inhibition was most consistent when using ADP 5 mM. We estimate this concentration of agonist as optimal in swine. The swine model is a good choice for investigation of in vivo platelet activation, especially with regard to cardiovascular research. We conclude that there is an inhibitory effect of supplemental magnesium on ex vivo platelet aggregation in swine with initial normomagnesaemia.