Intravenous magnesium sulphate in acute myocardial infarction--is the answer "MAGIC"?

The role of magnesium in coronary artery disease has been evaluated extensively during the last three decades. The intravenous application of magnesium in acute myocardial infarction is of major importance, the beneficial effects have been underlined in several studies. Magnesium is of significance in the pathomechanisms of reperfusion injury and reduction of malign arrhythmias in the critical acute phase of myocardial infarction, if applied intravenously. However, the promising results of LIMIT-2 could not be confirmed by the data of ISIS-4. The timing of magnesium therapy is probably the most important key factor. Similar to the guidelines of thrombolytic intervention, magnesium has to be administered as early as possible, at the latest before myocardial reperfusion has started. Nevertheless, because of conflicting results of prior trials doubts on the efficacy of intravenous magnesium in myocardial infarction still remain. The multinational, multicenter trial MAGIC has been set up to evaluate the optimal patient cohort as well as the ideal dose regimen for the application of intravenous magnesium sulphate in patients with acute myocardial infarction. The answer on the open questions on intravenous magnesium sulphate in myocardial infarction could be "MAGIC".

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque.

Defined angiographically, no-reflow (NR) manifests as an acute reduction in coronary flow in the absence of epicardial vessel obstruction. One candidate protein to cause coronary NR is tissue factor (TF), which is abundant in atherosclerotic plaque and a cofactor for activated plasma coagulation factor VII. Scrapings from atherosclerotic carotid arteries contained TF activity (corresponding to 33.03 +/- 13.00 pg/cm(2) luminal plaque surface). Active TF was sedimented, indicating that TF was associated with membranes. Coronary blood was drawn from 6 patients undergoing coronary interventions with the distal protection device PercuSurge GuardWire (Traatek, Miami, FL). Fine particulate material that was recovered from coronary blood showed TF activity (corresponding to 91.1 +/- 62.16 pg/mL authentic TF). To examine the role of TF in acute coronary NR, blood was drawn via a catheter from coronary vessels in 13 patients during NR and after restoration of flow. Mean TF antigen levels were elevated during NR (194.3 +/- 142.8 pg/mL) as compared with levels after flow restoration (73.27 +/- 31.90 pg/mL; P =.02). To dissect the effects of particulate material and purified TF on flow, selective intracoronary injection of atherosclerotic material or purified relipidated TF was performed in a porcine model. TF induced NR in the model, thus strengthening the concept that TF is causal, not just a bystander to atherosclerotic plaque material. The data suggest that active TF is released from dissected coronary atherosclerotic plaque and is one of the factors causing the NR phenomenon. Thus, blood-borne TF in the coronary circulation is a major determinant of flow.