Myocardial infarction (MI) is a major cause of morbidity and mortality and is a main etiology of heart failure. The process of MI is modulated by the inflammatory response. Many studies have shown a significant inflammatory response phenomenon in pathogenesis of MI.

The aim of this study is to discuss the role of pro-inflammatory (IL8, TNFα) and anti-inflammatory (IL10) cytokines that are among others decried involved in the process of remodeling post-myocardial infarction.

Prospective, monocentric case-control study that included 82 patients diagnosed with a first episode of myocardial infarction and low LVEF and 30 healthy subjects.The quantification of IL10 was based on the technique of sandwich ELISA. The CLIA technique was used for quantification of IL8 and TNFα.All patients were evaluated by an echocardiography after revascularisation and one month after to study cardiac remodeling.

The study shows that patients after MI had high levels of IL8 (1.54±0.6 vs 0.56±0.12, p<0.001) and TNFα (1.21±0.24 vs 0.77±0.14 p<0.001) contrasting with low levels of IL10(0.05±1.23 vs 0.12±0.10, p=0.06). Significant positive correlation between IL8 and TNFα with CRP was found (r=0.543, p=0.002 and r=0.458, p=0.034 respectively). The low level of IL10 was positively correlated with the ejection fraction of the left ventricle (LVEF), r=0.679, p=0.002 and negatively correlated with the diastolic diameter of left ventricle (LV) (r=-0.345, p=0.029) and the systolic volume of the LV (r=–0.377, p=0.022).One month after MI, a significant decrease of the level of TNFα (to 0.96) was observed the in the group of patients with a LVEF amelioration (34.7±5.6% vs 37.8±6%, p=0.017)and LVESV reduction (from76.9±15.8mL to 72.5±13.6mL, p=0.0017).

As a result, an increase in TNFα and IL8 associated with decreased IL10 after MI with low LVEF. A correlation was found between TNFα level decreased one month after MI and the LV remodeling.