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Association between endogenous complement inhibitor and myocardial salvage in patients with myocardial infarction
Charlotte B Holt1, Steffen Thiel, Kim Munk
1Aarhus University Hospital, Aarhus, Denmark.
Insights
Plasma levels of MAp44, MASP-1, and MASP-3 are elevated in myocardial infarction (MI) patients but do not correlate with short-term outcomes like infarct size.
Area of Science:
- Complement system research
- Cardiovascular disease biomarkers
Background:
- Complement cascade dysregulation contributes to diseases.
- MAp44 (MAP1) is an endogenous complement inhibitor with protective effects in myocardial reperfusion injury.
- Investigating MAp44, MASP-1, and MASP-3 in acute myocardial infarction (MI) is crucial.
Purpose of the Study:
- To examine the association between plasma levels of MAp44, MASP-1, and MASP-3 and outcomes in first-time MI patients.
- To compare these plasma levels in MI patients versus healthy controls.
Main Methods:
- 192 MI patients and 140 controls were enrolled.
- Plasma levels of MAp44, MASP-1, and MASP-3 were measured using time-resolved immunofluorometric assays.
- Myocardial outcomes (salvage index, infarct size) were assessed via gated single-photon emission CT.
Main Results:
- MI patients exhibited significantly higher plasma MAp44 levels (18% increase) compared to controls (p<0.001).
- MASP-1 and MASP-3 levels were also elevated in MI patients (p=0.002 and p<0.001, respectively).
- No significant correlation was found between plasma levels of MAp44, MASP-1, MASP-3 and myocardial salvage index or final infarct size.
Conclusions:
- Plasma concentrations of MAp44, MASP-1, and MASP-3 are elevated in individuals with MI.
- These elevated levels are not associated with short-term outcomes such as salvage index and final infarct size in MI patients.
Background:
Many pathogenic processes and diseases are the result of an erroneous activation of the complement cascade and a number of inhibitors of complement have thus been examined for anti-inflammatory actions. It was recently demonstrated that supraphysiological concentrations of the endogenous complement inhibitor MAp44 (also denoted MAP1) protect against myocardial reperfusion injury. In the present study, we examined the association between outcome after acute myocardial infarction (MI) and the plasma levels of MAp44 and its related proteins MASP-1 and MASP-3 in patients with first-time MI. In addition, we compared plasma levels of MAp44, MASP-1, and MASP-3 in MI patients to levels in a healthy control group.
Methods:
A total of 192 MI patients and 140 control persons were included. Plasma samples were obtained and analysed with time-resolved immunofluorometric assays determining the plasma levels of MAp44, MASP-1, and MASP-3. The myocardial outcomes (salvage index and final infarct size) were measured by gated single-photon emission CT.
Results:
MI patients had 18 % higher plasma levels of MAp44 (IQR 11-25%) as compared to the healthy control group (p<0.001. However, neither salvage index (Spearman rho -0.1, p=0.28) nor final infarct size (Spearman rho 0.02, p=0.83) correlated with plasma levels of MAp44. Likewise, MASP-1 and MASP-3 were elevated in MI patients (p=0.002 and p<0.001), but the levels were not correlated to outcome.
Conclusions:
Plasma levels of MAp44, MASP-1, and MASP-3 are significantly higher in patients with MI compared to healthy control persons, but are not associated with short-term outcome measured as salvage index and final infarct.
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