Search

Objective: In this study, we aimed to investigate the relationship between smoking and adverse cardiac remodeling after ST-elevation MI (STEMI), and the association between smoking and inflammatory markers, including cytokine levels. Methods: Forty-three patients admitted to the emergency department between June 2015 and June 2020 who were diagnosed with STEMI for the first time and underwent successful primary percutaneous coronary intervention were included in the study. Inflammatory markers (interferon (IFN)-α, -γ, -β, interleukin (IL)-6R-α, and soluble tumor necrosis factor receptor (sTNFR)-1,-2) were measured on the first day and two weeks post-MI. Left ventricular volume and functions were evaluated using cardiac magnetic resonance imaging at two weeks and six months post- STEMI. Adverse remodeling (AR) was defined as an increase in left ventricular (LV) end-diastolic volume >12%. Results: The AR ratio (65% vs. 30.4%; p= 0.024) and the levels of each inflammatory marker on the first-day post- STEMI were higher in the smokers' group than in the non-smokers' group. Smoking (OR= 4.46; p= 0.032) and IFN-β (OR= 1.07; p=0.023) levels on the first-day post-MI were independent predictors of AR. Also, smoking (β(SE)= 8.96(2.74); p=0.002), increased neutrophil levels (β±SE= 1.72(0.66); p= 0.013) and increased LDL levels (β(SE) = 0.07(0.03); p=0.031) were independent predictors of elevated IFN-β levels. Conclusion: Baseline inflammatory marker levels and incidence of AR post-STEMI were higher in smokers. Smoking can contribute to the development of AR by increasing the severity of inflammation at the onset of acute STEMI. [ABSTRACT FROM AUTHOR]

Introduction: Increasing evidence supports the view that pro-inflammatory cytokines play a role in fibrosis after myocardial infarction (MI). It has been suggested that interleukin (IL)-12p40, a pro-inflammatory cytokine, can induce interferon g (IFN-γ) and matrix metalloproteinase (MMP). However, the role of IL-12p40 in adverse cardiac remodeling (AR) after ST-elevation MI (STEMI) is unclear. Aim: To examine the role of temporal changes of pro-inflammatory cytokines in the development of post-STEMI AR. Material and methods: A total of 43 patients with STEMI for the first time ever were prospectively analyzed. In cardiac magnetic resonance imaging at 6 months after STEMI, a decrease of left ventricular end-diastolic volume by = 12% was defined as reverse cardiac remodeling (RR), and a 12% increase was defined as AR. Cytokine concentrations were measured on the first day (baseline) and 2 weeks after STEMI. Results: Mean IL-12p40 (59.1 ±14.5 vs. 46.7 ±9.1 pq/ml, p = 0.001), median IFN-γ (20.4 vs. 16.2 pq/ml, p = 0.048) and median MMP-2 (33866 vs. 20691 pq/ml, p = 0.011) baseline concentrations were higher in AR than RR. In patients with AR, IL-12p40 level was lower at 2 weeks than baseline (p < 0.001). There was a positive correlation between the baseline concentrations of IL-12p40, IFN-γ, MMP-2, C-reactive protein and infarct size (p < 0.05). Increased IL-12p40 and MMP-2 baseline levels were independently associated with AR (OR = 1.14, p = 0.010; OR = 1.08, p = 0.035). Conclusions: In the initial phase of MI, greater release of pro-inflammatory cytokines was associated with increased MMP-2 levels. Elevated expression of IL-12 and MMP-2 had an independent association with AR. This may be related to the excessive inflammatory response in the initial phase of MI. [ABSTRACT FROM AUTHOR]

Introduction: Increasing evidence supports the view that pro-inflammatory cytokines play a role in fibrosis after myocardial infarction (MI). It has been suggested that interleukin (IL)-12p40, a pro-inflammatory cytokine, can induce interferon γ (IFN-γ) and matrix metalloproteinase (MMP). However, the role of IL-12p40 in adverse cardiac remodeling (AR) after ST-elevation MI (STEMI) is unclear., Aim: To examine the role of temporal changes of pro-inflammatory cytokines in the development of post-STEMI AR., Material and Methods: A total of 43 patients with STEMI for the first time ever were prospectively analyzed. In cardiac magnetic resonance imaging at 6 months after STEMI, a decrease of left ventricular end-diastolic volume by ≥ 12% was defined as reverse cardiac remodeling (RR), and a 12% increase was defined as AR. Cytokine concentrations were measured on the first day (baseline) and 2 weeks after STEMI., Results: Mean IL-12p40 (59.1 ±14.5 vs. 46.7 ±9.1 pq/ml, p = 0.001), median IFN-γ (20.4 vs. 16.2 pq/ml, p = 0.048) and median MMP-2 (33866 vs. 20691 pq/ml, p = 0.011) baseline concentrations were higher in AR than RR. In patients with AR, IL-12p40 level was lower at 2 weeks than baseline ( p < 0.001). There was a positive correlation between the baseline concentrations of IL-12p40, IFN-γ, MMP-2, C-reactive protein and infarct size ( p < 0.05). Increased IL-12p40 and MMP-2 baseline levels were independently associated with AR (OR = 1.14, p = 0.010; OR = 1.08, p = 0.035)., Conclusions: In the initial phase of MI, greater release of pro-inflammatory cytokines was associated with increased MMP-2 levels. Elevated expression of IL-12 and MMP-2 had an independent association with AR. This may be related to the excessive inflammatory response in the initial phase of MI., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2022 Termedia Sp. z o. o.)

Background: Copeptin is widely used as a predictor of an adverse prognosis in many clinical conditions. Reduced antegrade coronary flow in an infarct-related artery (IRA) is associated with adverse clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). The aim of this study was to investigate whether copeptin level on admission was associated with IRA patency in STEMI patients., Methods: A total of 88 patients were enrolled into the study and divided into two groups according to TIMI flow grade in the IRA before primary percutaneous coronary intervention., Results: White blood cell count (p = 0.015), neutrophils (p = 0.047), N-terminal pro-brain natriuretic peptide (NTproBNP) (p < 0.001), copeptin (p < 0.001) and peak troponin I (p = 0.001) were significantly higher in the occluded IRA group with a significantly lower serum sodium level (p < 0.001). Age- and gender-adjusted multivariate analysis revealed that copeptin (OR = 1.970; p = 0.001), peak troponin I (1.055; p = 0.005) and NTproBNP (OR = 1.003; p = 0.010) were independent predictors of an occluded IRA. A copeptin cut-off value of > 6.8 ng/mL was found to predict an occluded IRA with a sensitivity of 80% and specificity of 100% (area under the curve: 0.917; p < 0.001). Performance ranking of the biomarkers that could predict an occluded IRA showed copeptin > peak troponin I = NTproBNP., Conclusions: Copeptin levels were higher in the patients with an occluded IRA and STEMI. Higher levels of copeptin predicted an occluded IRA in the patients with STEMI who were admitted to the emergency department during the first three hours of chest pain.