Acute myocardial infarction is the leading cause of morbidity and mortality in the
adult population of developed and developing nations. Although the prompt restoration
of antegrade blood flow in the infarct-related coronary artery is the mean therapy
for improving survival, reperfusion itself may cause damage to ischaemic myocardial
tissue. This event is well known as “reperfusion injury”. Crucial mediators for cardiac
damage in the reperfusion phases are oxidative stress, inflammation and leukocyte
infiltration. Already approved and novel therapies might directly reduce these inflammatory
processes. Treatments modulating chemokine secretion and activity should be considered
as very promising approaches to reduce myocardial reperfusion injury.
Keywords
Acute myocardial infarction - chemokines - inflammation