Correlação de citocinas com marcadores biológicos no infarto agudo do miocárdio

• Autor(a) principal: Ribeiro, Larissa Nascimento
• Data de Publicação: 2015
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFMT
• Texto Completo: http://ri.ufmt.br/handle/1/2259
• topic: Doenças cardiovasculares; Marcador biológico; Inflamação; CNPQ::CIENCIAS DA SAUDE; Cardiovascular diseases; Biomarker; Inflammation

Cardiovascular diseases (CVDs) are the main noncommunicable diseases. Among them is coronary artery disease with a high prevalence today, with acute myocardial infarction (AMI) an ascension event of the disease. The IAM is due to insufficient blood flow caused by atherosclerosis, which leads to a prolonged ischemia. As a result, the heart muscle cells stimulates an inflammatory response through cytokine, especially pro-inflammatory (IL-2, IL-4, IL-6, TNF, INFγ). Accordingly, the assumption is that IL-10 and IL-17 is a regulatory feed-back mechanism for balancing the inflammation caused by pro-inflammatory cytokines in acute myocardial infarction, and also, that immune response to develop in reactions cascade of cytokines that may be correlated with each other, and between cardiac injury, displayed through the levels of cardiac markers (CPK, CK-MB and troponin). Another hypothesis is that there is a promising biomarker in patients suspected of AMI and confirmed AMI. This is a case-control study consisting of 3 groups: AMI, suspected AMI and control. The obtained samples hematologic, biochemical and immunologic assays were performed. The hematological parameters were analyzed in automated equipment BC-2800 (Mindray), biochemical parameters Bio-2000 (BioPlus) by the absorbance values and the serum levels of cytokines obtained by flow cytometry. The results of flow cytometry were generated using FCAP Array Software (BD) and statistical analyzes were performed using the BioEstat 5.0. Hematologic parameters only changed the group suspected AMI, while biochemical parameters showed elevated predominantly in patients with AMI confirmed. Cytokines such as IL-2, IL-6 and TNF-α have proved to change the suspect infarction, whereas in the AMI group were IL-2, IL-4, IL-6, TNF-α, IFN and IL- 17A. The correlation between cytokines and cardiac markers in AMI group was confirmed, in particular, TNF-α and INF. While the suspect group stood IL-4 and IL-6. In what regards the relationship between cytokines in patients with myocardial infarction, the INF correlated with IL-6, TNF -α and IL-17A. Our results suggest that the presence of AMI, or even suspected, was able to change the hematological, biochemical and immunological patterns. And the immune response to pro-inflammatory AMI was predominantly to reactions occurring cascade of cytokines and that these are related to the size of cardiac injury, especially INF. We can also conclude that high levels of IL-6 and TNF-α may represent a risk factor for AMI and that IL-17A does not act as a regulator of the inflammatory response, but plays a pro-inflammatory nature can be a promising marker for AMI.