High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase.

Abstract

This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.