[Antithrombocytic effectiveness of magnesium].

Platelet activation and subsequent intravascular thrombus formation play a central role in the pathophysiology of acute coronary syndromes. Extracellular magnesium has an antithrombotic action due mainly to its antiplatelet effect. High concentrations of magnesium inhibit platelet aggregation and adhesion in vitro and reduce the generation of prothrombotic eicosanoids. In addition, magnesium modulates the intracellular platelet activation cascade and decreases calcium influx. The function of major platelet membrane receptors, such as the fibrinogen receptor GP-IIb-IIIa and P-selectin are also inhibited by extracellular magnesium. Intravenous magnesium inhibits platelet function in vivo-additive to aspirin. The antiplatelet effect of intravenously administered magnesium might be of benefit to patients with acute coronary syndromes when given before the development of an occlusive thrombotic plug.