At present no consensus exists on the role of magnesium in acute myocardial infarction and this is primarily due to conflicting results from recent clinical trials. The ISIS-4 trial clearly showed that magnesium infusion is without benefit when given after thrombolysis or many hours after symptom onset. In contrast, the LIMIT-2 study provided strong evidence that early magnesium administration, given before any thrombolytic therapy protects the myocardium and improves long-term survival. Debate on the interpretation of the trial results is still ongoing, and is particularly focused on the time-dependency of magnesium, which has emerged from recent experimental studies. Candidate mechanisms, by which magnesium might modify the outcome of acute myocardial infarction, includes antiarrhythmic properties, improved coronary perfusion and haemodynamics, protection of the ischaemic myocardium, and an antithrombotic effect. So far animal models have shown a time-dependent effect of magnesium when given for both myocardial protection in experimental ischaemia-reperfusion injury and for antithrombotic purposes. Additional clinical trials are warranted and these must be carefully designed and implemented in the light of the laboratory evidence now available. In the present review magnesium's antithrombotic properties is discussed with respect to its effect on platelets, coagulation, fibrinolysis, and endothelial mediators with vasodilating and antithrombotic qualities. Observations from studies in patients with preeclampsia, another clinical condition where platelet hyperreactivity is well-recognized and where magnesium therapy is well-established, are briefly discussed in the present paper.