Intravenous Magnesium in Acute Myocardial Infarction

In recent decades, the management of patients with suspected acute myocardial infarction (MI) has progressed substantially through the testing (and acceptance or rejection) of a number of different hypotheses. In the 1960s, recognition of the risks of early ventricular fibrillation led to the establishment of coronary care units, emphasis on early hospitalization of patients, and often, the use of prophylactic antiarrhythmic agents (e.g., lidocaine).1,2 Various estimates suggest that these approaches were associated with a substantial reduction in early mortality, but the possibility that at least some part of this apparent benefit was due to the hospitalization of lower-risk individuals cannot be ruled out. In the 1970s and early 1980s, the concept of myocardial salvage was extensively evaluated by testing drugs with a variety of different mechanisms of action.3 This included early intravenous 83-blockers, hyaluronidase, nitrates, glucose-insulin potassium, calcium blockers, etc.4 Of these agents, the value of intravenous 13-blockers has been confirmed by large randomized trials5 and that of intravenous nitrates by meta-analyses of several smaller trials.6 However, the use of early intravenous X3-blockers in clinical practice is generally low, and this may relate chiefly to concerns about precipitating heart failure in patients with large MI.7 The late 1980s and early 1990s have seen a shift in focus to various antithrombotic strategies; of these, the value and efficacy of a thrombolytic agent and aspirin have been demonstrated and are widely accepted.8 The benefit of thrombolytic therapy is greater among patients treated early, with only modest benefits among patients treated within 6-12 hours after the onset of symptoms.9 Although the benefits of thrombolytic therapy are considered to be mediated by a reduction in infarct size and improvement in ventricular function, improvements in ejection fraction have not been dramatic.9 Moreover, some of the adverse effects result in permanent morbidity (e.g., reinfarction and strokes), and costs of some of these agents are substantial. Although the least expensive thrombolytic agent, streptokinase, is affordable in most Western societies, it still represents a large and