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Published on: January 28, 2020
Level of complement activity predicts cardiac dysfunction after acute myocardial infarction treated with primary
Sune Haahr-Pedersen1, Mette Bjerre, Allan Flyvbjerg
1Department of Cardiology P, Gentofte University Hospital, Niels Andersens Vej 65, Copenhagen, Denmark. sunped01@geh.regionh.dk
Insights
High Mannose-binding lectin (MBL) and low soluble C5b-9 (sC5b-9) levels are linked to cardiac dysfunction after ST-elevation myocardial infarction (STEMI). These complement factors may predict poor outcomes in STEMI patients undergoing primary percutaneous coronary intervention.
Area of Science:
- Cardiology
- Immunology
- Complement System
Background:
- Ischemic/reperfusion (I/R) injury can reduce the benefits of reperfusion therapy for ST-elevation myocardial infarction (STEMI).
- Mannose-binding lectin (MBL) and soluble C5b-9 (sC5b-9) are implicated in complement-mediated cell lysis and may contribute to myocardial I/R injury.
- The study investigates the association between MBL, sC5b-9 levels, and cardiac dysfunction in STEMI patients treated with primary percutaneous coronary intervention (pPCI).
Purpose of the Study:
- To evaluate the potential association between plasma MBL and sC5b-9 levels.
- To determine the relationship between these complement factors and subsequent cardiac dysfunction in STEMI patients.
- To assess the predictive value of MBL and sC5b-9 for adverse cardiac outcomes post-pPCI.
Main Methods:
- The study included 74 STEMI patients with acute left anterior descending coronary artery occlusion treated with pPCI.
- Cardiac dysfunction was defined as a left ventricular ejection fraction (LVEF) below 35%.
- Plasma levels of MBL and sC5b-9 were measured and analyzed in relation to LVEF.
Main Results:
- Patients with LVEF < 35% exhibited significantly higher median MBL levels and lower sC5b-9 levels compared to those with LVEF ≥ 35%.
- Multivariate logistic regression analysis revealed that MBL ≥ 800 mcg/L was associated with an odds ratio of 5.5 for reduced LVEF (p=0.01).
- sC5b-9 ≤ 160 mcg/L was independently associated with an odds ratio of 5.0 for reduced LVEF (p=0.01).
Conclusions:
- Elevated plasma MBL and decreased plasma sC5b-9 are independently linked to an increased risk of cardiac dysfunction in STEMI patients treated with pPCI.
- These findings suggest increased complement system activity during the ischemic and reperfusion phases contributes to cardiac dysfunction.
- Low peripheral plasma sC5b-9 may indicate its accumulation and activation within the infarcted myocardium, serving as a potential biomarker.
Background:
The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human myocardial I/R injury. We evaluated the potential association between MBL and sC5b-9 in plasma and subsequent cardiac dysfunction in patients with STEMI treated with primary percutaneous coronary intervention (pPCI).
Methods:
The study included 74 STEMI-patients with acute occlusion of the left anterior descending coronary artery who were successfully treated with pPCI. Cardiac dysfunction was defined as left ventricular ejection fraction LVEF < 35%.
Results:
Patients with subsequent LVEF < 35% had significantly higher median MBL and lower sC5b-9 compared to patients with LVEF > or = 35%. After adjustment of the multivariate logistic regression analysis, the odds for reduced LVEF was 5.5 (95% CI:1.5-19.3; p = 0.01) for patients with MBL > or = 800 mcg/L, and 5.0 (95% CI 1.4-18.4; p = 0.01) for patients with sC5b-9 < or = 160 mcg/L.
Conclusion:
High plasma MBL and low plasma sC5b-9 are independently associated with increased risk of cardiac dysfunction in STEMI patients treated with pPCI, probably due to increased complement activity during the ischemic and reperfusion process. The predictive value of low peripheral plasma sC5b-9 may be explained by an accumulation and activation of sC5b-9 in the infarcted myocardium.
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