Related Experiment Videos
Serial changes of complement titers in the acute phase of myocardial infarction
Insights
This study found that complement activation may play a role in acute myocardial infarction. Complement levels (CH50, C4) increased, suggesting consumption by the damaged heart muscle.
Area of Science:
- Cardiovascular Medicine
- Immunology
Background:
- Limited evidence exists linking complement activation to acute myocardial infarction (AMI).
- Previous studies suggest complement involvement, but direct evidence in AMI patients is scarce.
Purpose of the Study:
- To investigate serial changes in complement system components during the acute phase of myocardial infarction.
- To determine if complement activation occurs and how it correlates with AMI development.
Main Methods:
- Serial measurements of total hemolytic complement titer (CH50), C3, C4, and total serum protein in 11 AMI patients up to 120 hours post-attack.
- Assessed C3 conversion and presence of Beta 1 A globulin.
Main Results:
- CH50 and C4 levels consistently increased in the acute phase of AMI.
- C3 levels showed no significant change, while total serum protein declined after 96 hours.
- Beta 1 A globulin, a C3 split product, was undetectable.
Conclusions:
- Infarcted or ischemic myocardium likely activates the complement system.
- Continuous consumption of C3 by myocardial tissue may stimulate complement production, leading to elevated C4 and CH50.
- Activated complement is suggested to play a significant role in the pathogenesis of myocardial infarction.
Abstract:
Although some studies suggest the involvement of a complement activation in the development of acute myocardial infarction, there has been little convincing evidence of the change of the complement in patients suffering from myocardial infarction. In 11 patients with acute myocardial infarction the serial changes of the total hemolytic complement titer (CH50), C3, C4, total serum protein and C3 conversion were investigated up to 120 hours after its attack. The level of CH50 and C4 increased consistently in the acute phase of myocardial infarction, but C3 did not show any change and total serum protein declined after 96 hours. Beta 1 A globulin, the split product of C3, could not be detected in the blood stream. These results suggest that the infarcted or ischemic myocardium would activate complements, and C3 might be consumed continuously by the infarcted or ischemic myocardium. Such consumption of complements should stimulate the production of complement and would give rise of an increase in C4 and CH50. It is suggested that activated complement might play a significant role in the development of myocardial infarction.