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Oral magnesium therapy, exercise heart rate, exercise tolerance, and myocardial function in coronary artery disease patients
  1. R Pokan1,
  2. P Hofmann2,
  3. S P von Duvillard3,
  4. G Smekal1,
  5. M Wonisch4,
  6. K Lettner1,
  7. P Schmid5,
  8. M Shechter6,
  9. B Silver7,
  10. N Bachl1
  1. 1Department of Sport and Exercise Physiology, University of Vienna, Vienna, Austria
  2. 2Department of Sports Sciences, University of Graz, Graz, Austria
  3. 3Human Performance Laboratory, Department of Health and Human Performance, Texas A&M University-Commerce, Commerce, TX, USA
  4. 4Department of Internal Medicine, University of Graz, Graz, Austria
  5. 5Center for Cardiac Rehabilitation, Bad Schallerbach, Austria
  6. 6The Heart Institute, Chaim Sheba Medical Center and the Tel Hashomer Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
  7. 7IntraCellular Diagnostics, Inc., Foster City, CA, USA
  1. Correspondence to:
 Serge P von Duvillard
 Department of Health and Human Performance, Texas A&M University-Commerce, PO Box 3011, Commerce, TX 75429-3011, USA; serge_vonduvillard{at}tamu-commerce.edu

Abstract

Background: Previous studies have demonstrated that in patients with coronary artery disease (CAD) upward deflection of the heart rate (HR) performance curve can be observed and that this upward deflection and the degree of the deflection are correlated with a diminished stress dependent left ventricular function. Magnesium supplementation improves endothelial function, exercise tolerance, and exercise induced chest pain in patients with CAD.

Purpose: We studied the effects of oral magnesium therapy on exercise dependent HR as related to exercise tolerance and resting myocardial function in patients with CAD.

Methods: In a double blind controlled trial, 53 male patients with stable CAD were randomised to either oral magnesium 15 mmol twice daily (n = 28, age 61±9 years, height 171±7 cm, body weight 79±10 kg, previous myocardial infarction, n = 7) or placebo (n = 25, age 58±10 years, height 172±6 cm, body weight 79±10 kg, previous myocardial infarction, n = 6) for 6 months. Maximal oxygen uptake (VO2max), the degree and direction of the deflection of the HR performance curve described as factor k<0 (upward deflection), and the left ventricular ejection fraction (LVEF) were the outcomes measured.

Results: Magnesium therapy for 6 months significantly increased intracellular magnesium levels (32.7±2.5 v 35.6±2.1 mEq/l, p<0.001) compared to placebo (33.1±3.1.9 v 33.8±2.0 mEq/l, NS), VO2max (28.3±6.2 v 30.6±7.1 ml/kg/min, p<0.001; 29.3±5.4 v 29.6±5.2 ml/kg/min, NS), factor k (−0.298±0.242 v −0.208±0.260, p<0.05; −0.269±0.336 v −0.272±0.335, NS), and LVEF (58±11 v 67±10%, p<0.001; 55±11 v 54±12%, NS).

Conclusion: The present study supports the intake of oral magnesium and its favourable effects on exercise tolerance and left ventricular function during rest and exercise in stable CAD patients.

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Footnotes

  • Published Online First 6 July 2006

  • Competing interests: none declared

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