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Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease
Michael Shechter, MD, MAa, C. Noel Bairey Merz, MDa, Robert K. Rude, MDc, Maura J. Paul Labrador, MPHa, Simcha R. Meisel, MDb, Prediman K. Shah, MDb, Sanjay Kaul, MDb
(American Heart Journal 2000; 140: 212-8.) Copyright © 2000 by Mosby, Inc.
Background: Although reduced intracellular levels of magnesium have been described in patients with acute myocardial infarction, its significance as a regulator of thrombosis remains unknown.
Methods and Results: To determine whether reduced intracellular levels of magnesium enhance platelet-dependent thrombosis, we evaluated 42 patients with coronary artery disease (CAD) by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 minutes by using an ex vivo perfusion (Badimon) chamber. Baseline analysis demonstrated significant associations between intracellular levels of magnesium, platelet-dependent thrombosis (P = .02), and platelet P-selectin (CD62P) expression (P < .05). Patients were divided into 2 groups: below (n = 22) and above (n = 20) the median intracellular levels of magnesium (1.12 µg/mg protein). There were no significant differences in age, body mass index, serum lipids, fibrinogen, platelet count, or serum magnesium levels between the two groups. Platelet-dependent thrombosis was significantly higher in patients with intracellular levels of magnesium below compared with above median (150 ± 128 vs 45 ± 28 µm2/mm, P < .004). Neither platelet aggregation nor CD62P expression was significantly different between the two groups.
Conclusions: Platelet-dependent thrombosis was significantly increased in patients with stable CAD with low intracellular levels of magnesium, suggesting a potential role for magnesium supplementation in CAD.
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