ported in hypomagnesemic patients (Hollifield, 1987; Rude, 1993). Significantly higher retention rates after magnesium load tests have been reported in patients with ischemic heart disease compared to normal controls (Rasmussen et al., 1988). This suggests that a low magnesium concentration may also play a role in cardiac ischemia. However, the extent to which the disease modifies the indicators of magnesium deficiency rather than the deficiency resulting in the disease manifestations varies with the symptom and the individual studied.
The development of atheromatous disease has been associated with magnesium in epidemiological observational studies. Areas with increased water hardness (which is due to high calcium and magnesium content) tend to have lower cardiovascular death rates (Altura et al., 1990; Hammer and Heyden, 1980; Leoni et al., 1985; Luoma et al., 1983; Neri and Johansen, 1978; Neri et al., 1985; Rubenowitz et al., 1996). Problems with evaluating epidemiological studies have been identified (Comstock, 1979), and some studies have not found such an association (Hammer and Heyden, 1980; Leoni et al., 1985). However, as presented by Tucker (1996) and Beaton (1996), a congruence of positive studies may suggest an association of dietary intake and disease. Animals on low magnesium diets develop arterial wall degeneration and calcification as well as hypertriglyceridemia, hypercholesterolemia, and atherosclerosis (Altura et al., 1990; Orimo and Ouchi, 1990). Controlled human studies that support this relationship are lacking.
Magnesium depletion in patients with cardiac diseases may be due to concomitant medications, such as diuretics, as well as to dietary magnesium depletion. Although cardiac arrhythmia may be associated with the primary cardiac disorders, magnesium depletion may further predispose to cardiac arrhythmias by decreasing intracellular potassium.
Accumulation of magnesium may reduce the morbidity and mortality of patients in the period following myocardial infarction. Two large, placebo-controlled, randomized, double-blind studies of patients with myocardial infarction have shown that intravenous magnesium therapy reduces the incidence of therapy-requiring arrhythmias to approximately one-half that seen in control patients (Antman, 1996; Seelig and Elin, 1996). In one study of patients with acute myocardial infarction, magnesium therapy given before thrombolytic therapy decreased mortality by 24 percent (Woods and Fletcher, 1994). Another large study of myocardial infarction did not find favorable effects of magnesium that was administered after thrombolytic therapy (ISIS-4, 1995). Debate currently centers over