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Circulation. 2000;102:2353-2358

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(Circulation. 2000;102:2353.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Oral Magnesium Therapy Improves Endothelial Function in Patients With Coronary Artery Disease

Michael Shechter, MD, MA; Michael Sharir, MD; Maura J. Paul Labrador, MPH; James Forrester, MD; Burton Silver, PhD; C. Noel Bairey Merz, MD

From the Preventive & Rehabilitative Cardiac Center and the Atherosclerosis Research Center, Cedars-Sinai Burns and Allen Research Institute, the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, and the University of California Los Angeles School of Medicine (M. Shechter, M. Sharir, M.J.P.L., J.F., C.N.B.M.); and IntraCellular Diagnostics, Inc (B.S.), Foster City, Calif.

Correspondence to Michael Shechter, MD, MA, FACC, Preventive & Rehabilitative Cardiac Center, Cedars-Sinai Medical Center, 444 San Vicente Blvd, Suite 901, Los Angeles, CA 90048. E-mail shechtes{at}netvision.net.il

Background—Magnesium blocks many of the physiological actions of calcium. Nevertheless, the impact of magnesium supplementation on endothelial function and exercise tolerance in stable coronary artery disease (CAD) patients has not been assessed.

Methods and Results—In a randomized, double-blind, placebo-controlled trial, 50 stable CAD patients (41 men and 9 women, mean±SD age 67±11 years, age range 42 to 82 years) were randomized to receive either magnesium (n=25) (30 mmol/d Magnosolv-Granulat; Asta Medica Company, Inc) or placebo (n=25) for 6 months. Before and after 6 months, endothelium-dependent brachial artery flow-mediated vasodilation (FMD) and endothelium-independent NTG-mediated vasodilation were assessed with high-resolution (10-MHz) ultrasound. Exercise stress testing was performed with use of the Bruce protocol. Intracellular magnesium concentrations ([Mg2+]i) were assessed from sublingual cells through x-ray dispersion (EXA) (normal mean±SD values 37.9±4.0 mEq/L). The magnesium therapy significantly increased postintervention ([Mg2+]i versus placebo (36.2±5.0 versus 32.7±2.7 mEq/L, P<0.02). There was a significant correlation in the total population between baseline [Mg2+]i and baseline FMD (r=0.48, P<0.01). The magnesium intervention resulted in a significant improvement in postintervention FMD (15.5±12.0%, P=0.02 compared with baseline), which was not evident with placebo (4.4±2.5%, P=0.78 compared with baseline). There was better exercise tolerance (9.3±2.0 versus 7.3±3.1 minutes, P=0.05) and less ischemic ST-segment changes (4 versus 10 patients, P=0.05) in the magnesium versus placebo groups, respectively.

Conclusions—Oral magnesium therapy in CAD patients is associated with significant improvement in brachial artery endothelial function and exercise tolerance, suggesting a potential mechanism by which magnesium could beneficially alter outcomes in CAD patients.


Key Words: magnesium • lipoproteins • endothelium • coronary disease




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