The relation between interleukin 10 and acute coronary syndrome

Background Atherosclerosis is the one of leading causes of death in the advanced world. It is a disease of large and medium-sized muscular arteries that carries a significant health burden worldwide, Atherogenesis is not a fully understood process and many theories may participate in the etiology of atheromatous plaque formation such as inflammatory theory which states that atherosclerosis is a chronic inflammatory disease characterized by migration of monocytes and T lymphocytes to the area of arterial wall injury. Early investigators also noted that the lipid-rich atherosclerotic plaque may develop secondary to a primary inflammatory process. Although the inflammation is believed to be primarily defensive or protective, its principal aims are to neutralize and remove the initiating agent and to initiate the process of tissue repair and healing. However, the inflammatory mediators or cytokines associated with inflammatory cells are also potentially harmful because they may damage tissue and aggravate injury. Aim Was to explain the clinical and pathophysiologic meaning of Interleukin 10 (IL-10) elevation in acute coronary syndrome (ACS) by clarifying whether IL-10 release is a factor initiating the inflammatory process in Myocardial Infarction or is predominantly a response to that clinical condition. The other point is to assess the correlation between the level of IL-10 and other cardiac biomarkers for risk prediction in ACS. Methods Sixty patients were recruited to the study with a diagnosis of ACS as designed by American Heart Association (AHA) recommendations, all of them were admitted to the Intensive Care Units, Critical Care Medicine Department, Faculty of Medicine, University of Alexandria. Those patients were categorized into four groups: group I: Unstable Angina, group II: ST-segment elevation myocardial infarction with successful thrombolytic therapy, group III: STEMI with failed thrombolytic therapy, and a control group of matched age and sex (10 control persons). Full history and comprehensive clinical assessment, 12-lead ECG and biochemical analysis of CK-MB, troponin, c-reactive protein (CRP) and IL-10 were performed in all the patients and control groups. Blood samples were taken for all groups and control for cardiac biomarkers (by dimension RXL), CRP (Nephelometry Dade Behring), and IL-10 (ELISA). All the samples were stored for the study and processed in one setting by a clinical pathologist. Results IL-10 level showed a significant difference between all groups as IL-10 concentrations were significantly increased in ACS in comparison with the control group. We found a statistically significant inverse correlation between IL-10 and CRP in all patient groups. A full explanation of the results will be mentioned separately.