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Published on: May 28, 2019
High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by
1Department of Cardiology, Tel-Aviv Elias Sourasky Medical Centre, Israel.
Insights
Magnesium sulphate (MgSO4) administration following acute myocardial infarction (AMI) with streptokinase treatment attenuates the complement response. High-dose MgSO4 delayed and reduced the consumption of complement factors C3, C4, and CH-100.
Area of Science:
- Immunology and Inflammation Research
- Cardiovascular Medicine
- Pharmacology
Background:
- Acute myocardial infarction (AMI) triggers a significant inflammatory response involving the complement system.
- Streptokinase is a common thrombolytic agent used in AMI treatment, which can activate the complement cascade.
- The role of magnesium sulphate (MgSO4) in modulating the post-AMI inflammatory and complement response is not fully understood.
Purpose of the Study:
- To investigate changes in complement levels (C3, C4, CH-100) after acute myocardial infarction treated with streptokinase.
- To evaluate the effect of intravenous magnesium sulphate (MgSO4) administration on the complement response post-AMI.
Main Methods:
- Twenty-nine patients with AMI treated with streptokinase were randomized into three groups.
- Groups A and B received intravenous MgSO4 (1g bolus followed by 4g/24h and 14g/24h, respectively).
- Group C received normal saline as a control; blood samples were collected for 48 hours to measure complement levels.
Main Results:
- A significant decrease in C3, C4, and CH-100 levels was observed in control (Group C) and low-dose MgSO4 (Group A) patients post-streptokinase.
- High-dose MgSO4 (Group B) attenuated this complement consumption, showing a delayed decrease in C3 and C4 (at 24h) and CH-100 (at 3h).
- Differences in C3 levels over time were significant between the three groups (P=0.021).
Conclusions:
- Complement factors are consumed following streptokinase-treated acute myocardial infarction.
- High-dose intravenous magnesium sulphate administration attenuates the complement activation process post-AMI.
- Magnesium may play a role in modulating the inflammatory response associated with myocardial infarction.
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-100 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-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).
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.
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