Hypertension or hyperlipidemia did not have any associations with biomarkers’ levels. However, significant relationships existed between past medical history of diabetes mellitus and TGF-β-72 h (p = 0.033). Moreover, drug history of statins (HMG-CoA reductase inhibitors) had a significant Quizartinib in vivo association with GW786034 ic50 TGF-β-72 h (p = 0.009). Being a smoker had a relationship with the level of TNF-α-24 h (p = 0.049). There was not any association between type of reperfusion management and biomarker levels, while coronary angiographic findings showed a statistically

significant relationship with the TGF-β-72 h level (p = 0.014). The level of TGF-β-72 h had a statistically significant difference between patients with two-vessel disease and those with left main coronary artery (LMCA) disease (p = 0.001). Moreover, significant differences existed between patients with triple-vessel disease and those with LMCA disease (p = 0.021) as the latter had higher levels of TGF-β-72 h. In evaluating associations of echocardiographic findings and biomarker

levels, significant relationships existed between ejection fraction and TGF-β-72 h (p = 0.005) as well as between intraventricular septum abnormality and TNF-α-24 h (p = 0.038). 3.3 Correlations Between Biomarker Levels and Patient Characteristics We found significant correlations between the level of TNF-α-24 h and TGF-β-72 h (r = 0.231, p = 0.03). Significant correlation existed between the level of TNF-α-72 h and glycosylated hemoglobin (HbA1c) serum level SHP099 purchase (r = 0.655, p = 0.029). The level of TGF-β-24 h had significant correlations with ischemic time (r = −0.233, p = 0.037) as well as cardiac troponin T levels of patients within 6 h of admission Plasmin (r = 0.218, p = 0.042), white blood cell (WBC) count (r = 0.358, p = 0.001) and ALT serum levels (r = 0.377, p = 0.048). Finally, significant correlations existed between TGF-β-72 h levels and matrix metalloproteinase

(MMP)-9 measured after 72 h (r = 0.330, p = 0.003) in addition to patients’ ejection fraction (r = −0.311, p = 0.009). 4 Discussion Several physiologic pathways including inflammation and fibrosis may involve in the pathogenesis of post-myocardial infarction (MI) structural changes called remodeling. As TNF-α and TGF-β are known to be the major biomarkers that contribute to each of these mentioned mechanisms and NAC is proposed to have beneficial effects in acute cardiology, in this study we evaluated the impact of NAC on these biomarkers. TNF-α tends to peak within 24 h following MI, and decreased toward baseline 3 days after MI [28]. Although the TNF-α level trend was in favor of those who received NAC, the difference was not significant between groups. While we could not find any significant effect on the TNF-α level, NAC could prevent TGF-β from increasing.