Key result
Compared with placebo, intravenously administered magnesium significantly prolonged in vitro bleeding time by 22% and inhibited ADP- and collagen-induced platelet aggregation by 13% and 17%.
Why the study?
Does intravenously administered magnesium inhibit platelet function in patients after coronary revascularization with cardiopulmonary bypass?
RCT (n=69)
blinded
randomized
Does intravenously administered magnesium inhibit platelet function in patients after coronary revascularization with cardiopulmonary bypass?
Intravenous magnesium administration 24 hours after coronary artery bypass grafting significantly inhibits platelet function, suggesting a potential antithrombotic effect but warranting caution in patients with bleeding disorders.
May warrant bleeding caution after CABG; extends evidence of magnesium's antiplatelet effects to cardiac surgical patients.
UNLABELLED: After cardiac surgery, magnesium is often administered for prophylaxis and treatment of cardiac arrhythmias. Magnesium, however, inhibits platelet function in vitro and in healthy volunteers. We performed a randomized, blinded, and placebo-controlled study to investigate the effect of magnesium on platelet function in patients after cardiac surgery. We studied patients who underwent uneventful coronary revascularization with cardiopulmonary bypass on the first postoperative day. Before and after an infusion of either 5.4 mmol magnesium (n = 19) or saline (n = 20), platelet function was investigated by means of in vitro bleeding time, platelet aggregation, and flow-cytometric assays. In addition, to investigate platelet function in vitro, 1, 5, and 10 mM magnesium were added to platelet-rich plasma before and 24 h after surgery in 30 patients. Compared with the control group, magnesium prolonged the in vitro bleeding time (22%) and inhibited ADP- and collagen-induced platelet aggregation (13% and 17%), platelet P-selectin expression (18%), and the binding of fibrinogen to the platelet glycoprotein IIb/IIIa receptor (10%). Magnesium also led to significant dose-dependent inhibition of platelet aggregation (19%), P-selectin expression (14%), and fibrinogen binding (11%) before and after surgery in vitro. Although the antithrombotic effect of magnesium may be beneficial in patients after coronary revascularization, large-dose magnesium therapy should be carefully considered in patients with impaired platelet function and co-existing bleeding disorders. IMPLICATIONS: In a randomized, blinded, placebo-controlled study of patients 24 h after coronary artery bypass grafting, IV administered magnesium inhibited platelet function in vitro and in vivo.
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Gries et al. (1999) conducted an RCT in patients after cardiac surgery (n=69). Intravenously Administered Magnesium vs. saline was evaluated on platelet function (in vitro bleeding time, platelet aggregation, and flow-cytometric assays). Compared with placebo, intravenously administered magnesium significantly prolonged in vitro bleeding time by 22% and inhibited ADP- and collagen-induced platelet aggregation by 13% and 17%.
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