Society of Cardiovascular Anesthesiologists

Magnesium and Platelet Dysfunction

Reviewer: Mark A. Chaney, MD
Associate Professor
University of Chicago

Magnesium is a critical cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Magnesium therapy and/or prophylaxis is useful in a wide variety of cardiovascular disorders. Beneficial physiologic effects include coronary and systemic vasodilation, improved cardiac function (increased cardiac index, increased left ventricular stroke work index), decreased incidence of supraventricular and ventricular arrhythmias, and even improved mortality following myocardial infarction. Hypomagnesemia is commonly observed in patients following cardiac surgery requiring cardiopulmonary bypass (with an incidence of approximately 70%). Hypomagnesemia in this setting has been shown to increase the incidence of atrial and ventricular dysrhythmias and may prolong requirement for postoperative mechanical ventilatory support. In patients undergoing cardiac surgery requiring cardiopulmonary bypass, magnesium supplementation decreases the incidence of atrial and ventricular dysrhythmias and improves cardiac function (increases cardiac index, increases left ventricular stroke work index). Thus, many patients now routinely receive magnesium supplementation either intraoperatively or during the immediate postoperative period following cardiac surgery requiring cardiopulmonary bypass.

Until recently, the only known major adverse physiologic effect of magnesium supplementation was potentiation of neuromuscular blockade. However, accumulating evidence indicates that magnesium supplementation may adversely affect platelet function in clinically relevant ways.

Magnesium has been shown to inhibit platelet function in vitro and in vivo at clinically relevant concentrations, perhaps by interacting with the platelet glycoprotein IIb/IIIa receptor to inhibit fibrinogen binding (required for platelet adhesion and aggregation). In noncardiac patients, magnesium administration has been shown to prolong bleeding time and inhibit platelet aggregation. The quantitative and qualitative platelet defect in patients following exposure to cardiopulmonary bypass is well known. Postoperative bleeding following cardiac surgery remains a substantial problem that increases morbidity and mortality. Any factor that accentuates platelet dysfunction in the postoperative period following cardiac surgery would thus be undesirable. The possibility that magnesium supplemen-tation accentuates the platelet dysfunction in patients following exposure to cardiopulmonary bypass is only now being studied. Gries, et al have recently shown that perioperative administration of magnesium to patients undergoing cardiac surgery and cardiopulmonary bypass does in fact inhibit platelet function. Their randomized, blinded, placebo-controlled investigation studied patients undergoing routine coronary artery bypass grafting. Blood samples were obtained before and after exposure to cardiopulmonary bypass and a wide variety of tests evaluating platelet function were then performed. Most importantly, these investigators revealed that magnesium supplementation caused dose-related inhibition of platelet aggregation, dose-related inhibition of fibrinogen binding to the platelet glycoprotein IIb/IIIa receptor, and prolonged bleeding time. These detrimental effects were observed in blood samples taken both before and after exposure to cardiopulmonary bypass. Furthermore, lower magnesium concentrations led to greater degrees of platelet dysfunction following cardiopulmonary bypass, indicating that exposure to cardiopulmonary bypass renders platelets more sensitive to the detrimental effects of magnesium.

These evolving investigations suggest that in patients undergoing cardiac surgery and cardiopulmonary bypass, perioperative supplementation of magnesium to maintain normal postoperative blood concentrations inhibits platelet function and may prolong bleeding time by as much as 20% to 40%. For routine cardiac surgery patients, this degree of added platelet dysfunction will likely not affect morbidity. However, in patients with pre-existing bleeding disorders (idiopathic and/or pharma-cologic), such additional platelet dysfunction may be detrimental.

References

Gries A, et al. The effect of intravenously administered magnesium on platelet function in patients after cardiac surgery. Anesth Analg 88: 1213-9, 1999.
Gomez MN. Magnesium and cardiovascular disease. Anesthesiology 89: 222-40, 1998.
Ravn HB, et al. Magnesium inhibits platelet activity: an infusion study in healthy volunteers. Thromb Haemost 75: 639-44, 1996.

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