Since 1984, at least 10 randomized control trials (RCTs) of intravenous magnesium for acute MI have been reported. Several statistical models exist for pooling the data from multiple RCTs in a meta-analysis and estimating the treatment effect of magnesium. It is important to review the essential features of these models in order to place the RCT findings in proper perspective. The fixed effects model assumes that the RCTs are sampled from a homogenous group of trials. Under the homogeneity assumption, each RCT provides an estimate of the true treatment effect and differences between the estimates from the various RCTs are due only to experimental error (within-trial variability). The random effects model assumes the RCTs are heterogeneous and that differences between their estimates of the treatment effect are due both to experimental error (within-trial variability) and real differences among the trials such as trial design and characteristics of the patients enrolled (between-trial variability). The random effects model is generally favored since heterogeneity that cannot be explained by experimental error often exists among the RCTs, and this model takes such heterogeneity into account in estimation and hypothesis testing. Meta-analyses of the seven RCTs published between 1984-199l provided an estimated odds ratio (OR) for mortality of magnesium treated patients of 0.44 (0.27-0.71) using the fixed effects model and 0.45 (0.23-0.86) using the random effects model. The Leicester Intravenous Magnesium Intervention Trial (LIMIT-2), published in 1992, reported a 24 percent reduction in mortality with magnesium treatment (P<0.04), confirming the benefit of magnesium in reducing mortality in MI and inspiring many clinicians to advocate magnesium treatment programs in their coronary care units. The magnesium treated patients in LIMIT-2 experienced a 25 percent lower incidence of congestive heart failure in the coronary care unit, suggesting that magnesium exerts its beneficial effects, at least in part, via a direct protective action on the myocardium. Given the potent predictive power of left ventricular function on survival following MI one would anticipate that magnesium-treated patients in LIMIT-2 would have a lower long-term mortality. This hypothesis appears to have been confirmed by the recent long-term follow up report from LIMIT-2 showing a 21percent lower rate of ischemic heart disease related mortality in the magnesium group over a median follow up of 2.7 years. The LIMIT-2 investigators have recently examined the mortality rates over a five year follow up, and continue to document the same long term benefit of magnesium administered in the acute phase of infarction. The absence of any loss of the mortality benefit of magnesium over the long term is consistent with a significant myocardial protective effect achieved during the critical period of myocardial reperfusion.