Copyright © 1996 by the European Society of Cardiology.
© The European Society of Cardiology
lschaemic heart disease
High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase




*Departments of cardiology, Tel-Aviv Elias Sourasky Medical Centre, and The Sackier Faculty of Medicine, Tel-Aviv University Tel-Aviv, Israel
Departments of Internal Medicine A Tel-Aviv Elias Sourasky Medical Centre, and The Sackier Faculty of Medicine, Tel-Aviv University Tel-Aviv, Israel
the Laboratories of Cinical Immunology Tel-Aviv Elias Sourasky Medical Centre, and The Sackier Faculty of Medicine, Tel-Aviv University Tel-Aviv, Israel
the Laboratories of Biochemistry Tel-Aviv Elias Sourasky Medical Centre, and The Sackier Faculty of Medicine, Tel-Aviv University Tel-Aviv, Israel
Received 17 July 1995; accepted 7 August 1995.
Correspondence: Arie Roth, MD, Department of Cardiology, Tel-Aviv Elias Sourasky Medical Centre, 6 Weizman Street, Tel- Aviv. 64239, Israel
Abstract
OBJECTIVE: 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.
DESIGN: 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-l00 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion.
RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-l00 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-l00 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-l00 (P= 0·46).
CONCLUSION: (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.
Key Words: Acute myocardial infarction magnesium complement