Clinical Question:
Does oral magnesium theraphy beneficial on patient with coronary artery disease (CAD)?

Bottom Line:
The present study supports the intake of oral Mg and its favorable effects on exercise tolerance and left ventricular function during rest and exercise in stable CAD patients.

Reference:
Oral magnesium therapy, exercise heart rate, exercise tolerance, and myocardial function in coronary artery disease patients.Pokan R, Hofmann P, von Duvillard SP, Smekal G, Wonisch M, Lettner K, Schmid P, Shechter M, Silver B, Bachl N.Br J Sports Med. 2006 Jul 6

Study Design:
Randomized Controlled Trial (double blind)

Synopsis:
Previous studies have demonstrated that in patients with coronary artery disease (CAD) an upward deflection of the heart rate (HR) performance curve can be observed and that this upward deflection and the degree of the deflection is correlated with a diminished stress-dependent left ventricular function. Magnesium (Mg) supplementation improves endothelial function, exercise tolerance, and exercise-induced chest pain in patients with CAD. The author studied the effects of oral Mg therapy on exercise dependent HR as related to exercise tolerance and resting myocardial function in patients with CAD. They did a double-blind controlled trial, 53 male patients with stable CAD, were randomized to either oral Mg 15 mmol twice daily (N = 28, age = 61 inverted exclamation mark&Oacute9 yrs, height = 171 inverted exclamation mark&Oacute7, body weight = 79 inverted exclamation mark&Oacute10 kg, previous myocardial infarction (MI), N = 7) or placebo (N = 25, age = 58 inverted exclamation mark&Oacute10 yrs, height = 172 inverted exclamation mark&Oacute6, body weight = 79 inverted exclamation mark&Oacute10 kg, previous MI, 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 f not 0 (upward deflection) and the left ventricular ejection fraction (LVEF), were the outcomes measured. Six-month Mg therapy significantly increased intracellular Mg levels (32.7 inverted exclamation mark&Oacute2.5 vs. 35.6 inverted exclamation mark&Oacute2.1 mEq/L, p<0.001) compared to placebo (33.1 inverted exclamation mark&Oacute3.1.9 vs. 33.8 inverted exclamation mark&Oacute 2.0 mEq/L, n.s.), VO2max (28.3 inverted exclamation mark&Oacute6.2 vs. 30.6 inverted exclamation mark&Oacute7.1 ml/kg/min, p<0.001; 29.3 inverted exclamation mark&Oacute5.4 vs. 29.6 inverted exclamation mark&Oacute5.2 ml/kg/min, n.s.), factor k (-0.298 inverted exclamation mark&Oacute0.242 vs. -0.208 inverted exclamation mark&Oacute0.260, p<0.05; -0.269 inverted exclamation mark&Oacute0.336 vs. -0.272 inverted exclamation mark&Oacute0.335, n.s.), LVEF (58 inverted exclamation mark&Oacute11 vs. 67 inverted exclamation mark&Oacute10 %, p<0.001; 55 inverted exclamation mark&Oacute11 vs. 54 inverted exclamation mark&Oacute12 %, n.s.).