Abstract
Aim To clarify the role of interleukin (IL) - 10 and members of its subfamily (IL-19 and IL-26) in cardiac remodeling during the post-myocardial infarction (MI) period.Material and methods A total of 45 patients with ST-segment elevation MI were enrolled. Serum cytokine concentrations were measured at the first day and 14 days post-MI. Left ventricular (LV) reverse remodeling (RR) was defined as the reduction of LV end-diastolic volume or LV end-systolic volume by ≥ 12 % in cardiac magnetic resonance images at 6‑mo follow-up. A 12 % increase was defined as adverse remodeling (AR).Results The post-MI first-day median IL-10 (9.7 pg / ml vs. 17.6 pg / ml, p<0.001), median IL-19 (28.7 pg / ml vs. 36.9 pg / ml, p<0.001), and median IL-26 (47.8 pg / ml vs. 90.7 pg / ml, p<0.001) were lower in the RR group compared to the AR group. There was a significant decrease in the concentration of anti-inflammatory cytokines in the AR group from the first to the 14 days post-MI. However, no significant change was observed in the RR group. Regression analysis revealed that a low IL-10 concentration on the post-MI first day was related to RR (OR=0.76, p=0.035). A 1 % increase in change of IL-10 concentration increased the probability of RR by 1.07 times.Conclusion The concentrations of cytokines were higher in the AR group, but this elevation was not sustained and significantly decreased for the 14 days post-MI. In the RR group, the concentrations of cytokines did not change and stable for the 14 days post-MI. As a reflection of this findings, stable IL-10 concentration may play a role the improvement of cardiac functions.
Highlights
Cardiac remodeling occurs as a result of inflammatory / anti-inflammatory homeostasis that develops after acute myocardial infarction (MI)
Mean LV ejection fraction (LVEF) was higher (50.5±8.0 % vs. 44.3±10.4 %, p=0.030) and mean LVEDV (144.7±31.0 ml vs. 186.1±33.1 ml, p
At the 6 mos post-MI, there was a significant worsening of Left ventricular (LV) volume and functions in AR group compared to RR group. (Table 2)
Summary
Cardiac remodeling occurs as a result of inflammatory / anti-inflammatory homeostasis that develops after acute myocardial infarction (MI). While an excessive inflammatory response induces adverse remodeling (AR), moderate inflammatory and strong anti-inflammatory responses can cause reverse remodeling (RR) [1] Proinflammatory cytokines, such as tumor necrosis factor (TNF) – α, interleukin (IL) – 1β, and IL-6, which increa se in the early post-MI period, are known to cause apoptosis, collagen production, matrix metalloproteinase (MMP) activation, fibrosis, and ventricular dilation that, in turn, cause ventricular failure [1,2,3]. One of the cytokines thought to play a major role in the anti-inflammatory balance in the post-MI period is IL-10 [5]. It inhibits the production of reactive oxygen species by TNF-α in cardiac myocytes [9]. Experimental studies in mice with IL-10 deficiency have confirmed that an increase in neutrophil infiltration increases myocardial infarct size [10]
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