Immunological Window of Myocardial Infarction

Acute myocardial infarction (MI) describes as an irreversible death of heart muscle which is initiated by a shortage of myocardium oxygen supply and accompanies by a complex of pro and antiinflammatory events. During the last decades, innate and adaptive immune responses are considered more serious for controlling myocardial infarction. As, it was confirmed that deregulated immune system which triggers excessive local and systemic inflammatory events is responsible for serious adverse effects associated with acute MI. Bone marrow activation, spleen monocytopoiesis, a remarkable increase of circulating cytokines and adhesion molecules, in addition to elevated levels of active peripheral leukocytes and platelets are playing significant roles in determining the clinical outcome of patients with MI. The previous experience demonstrated the failure of traditional harsh antiinflammatory strategies. High mortality rate and poor quality of life observed for survivors of MI despite current progress in the field highlight the urgent need for such interdisciplinary studies in the context of molecular cardiology. Hence, unraveling the cellular and molecular events which are involved in the management of inflammatory responses postMI is of special focus. The concept of immune regulation after myocardial infarction is not new, but our perception for dealing with the challenge has been changed during the last decades with gaining more indepth molecular/immunological knowledge. It seems that finetuning the interplay between innate and adaptive immune responses and regulating their crosstalk should be in special focus to establish effective therapeutic strategies.