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Early Changes in Circulating Interleukins and Residual Inflammatory Risk After Acute Myocardial Infarction
Maria E R Coste1, Carolina N França2, Maria Cristina Izar1
1Universidade Federal de São Paulo, São Paulo, SP - Brasil.
Insights
Cytokine levels shift post-myocardial infarction, with improved pro- and anti-inflammatory balance except for IL-6, indicating residual inflammatory risk in STEMI patients.
Area of Science:
- Cardiology
- Immunology
- Biomarkers
Background:
- Acute myocardial infarction (MI) can lead to significant ventricular dysfunction.
- Early revascularization strategies may not fully mitigate infarct size and impaired heart function.
Purpose of the Study:
- To analyze circulating cytokine profiles in ST-segment elevation myocardial infarction (STEMI) patients.
- To determine the relationship between cytokine levels and ventricular function post-STEMI.
Main Methods:
- The BATTLE-AMI trial enrolled STEMI patients treated with a pharmacoinvasive strategy.
- Plasma cytokine levels (IL-1β, IL-4, IL-6, IL-10, IL-18) were measured via ELISA at baseline and 30 days.
- Left ventricular ejection fraction (LVEF) and infarct size were assessed using cardiac MRI.
Main Results:
- Post-STEMI, IL-1β and IL-18 decreased, while IL-4 and IL-10 increased (p<0.05).
- IL-6 levels showed no significant change (p=0.63).
- Baseline IL-6 correlated with LVEF (rho=-0.50, p=0.004) and hs-CRP.
Conclusions:
- A shift in cytokine balance occurs within the first month post-MI, excluding IL-6.
- Persistent IL-6 levels suggest ongoing inflammation and potential residual inflammatory risk.
Background:
Patients with acute myocardial infarction may have a large infarcted area and ventricular dysfunction despite early thrombolysis and revascularization.
Objective:
To investigate the behavior of circulating cytokines in patients with ST-segment elevation myocardial infarction (STEMI) and their relationship with ventricular function.
Methods:
In the BATTLE-AMI (B and T Types of Lymphocytes Evaluation in Acute Myocardial Infarction) trial, patients with STEMI were treated with a pharmacoinvasive strategy. The plasma levels of cytokines (IL-1 β , IL-4, IL-6, IL-10, and IL-18) were tested using enzyme-linked immunosorbent assay (ELISA) at baseline and after 30 days. Infarcted mass and left ventricular ejection fraction (LVEF) were examined by 3-T cardiac magnetic resonance imaging. All p-values < 0.05 were considered statistically significant.
Results:
Compared to baseline, lower levels were detected for IL-1 β (p = 0.028) and IL-18 (p < 0.0001) 30 days after STEMI, whereas higher levels were observed for IL-4 (p = 0.001) and IL-10 (p < 0.0001) at that time point. Conversely, no changes were detected for IL-6 levels (p = 0.63). The levels of high-sensitivity C-reactive protein and IL-6 correlated at baseline (rho = 0.45, p < 0.0001) and 30 days after STEMI (rho = 0.29, p = 0.009). At baseline, correlation between IL-6 levels and LVEF was also observed (rho = -0.50, p = 0.004).
Conclusions:
During the first month post-MI, we observed a marked improvement in the balance of pro- and anti-inflammatory cytokines, except for IL-6. These findings suggest residual inflammatory risk. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0).
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