Background:
The inflammatory response to acute myocardial ischaemia/
reperfusion injury (IRI) plays a critical role in determining myocardial infarct (MI) size,
and subsequent post-MI left ventricular (LV) remodelling, making it a potential therapeutic
target for improving clinical outcomes in patients presenting with an acute myocardial infarction
(AMI). Recent experimental studies using advanced imaging and molecular techniques,
have yielded new insights into the mechanisms through which reactive oxygen species
(ROS) contribute to the inflammatory response induced by acute myocardial IRI - “adding
fuel to the fire”. The infiltration of inflammatory cells into the MI zone, leads to elevated
myocardial concentrations of ROS, cytokine release, and activation of apoptotic and
necrotic death pathways. Anti-oxidant and anti-inflammatory therapies have failed to protect
the heart against acute myocardial IRI. This may be, in part, due to a lack of understanding
of the time course, nature and mechanisms of the inflammation and redox dysregulation,
which occur in the setting of acute myocardial IRI.
Conclusion:
In this article, we examine the inflammatory response and redox dysregulation
induced by acute myocardial IRI, and highlight potential therapeutic options for targeting
redox dysregulation, in order to attenuate the detrimental effects of the inflammatory response
following an AMI, so as to reduce MI size and prevent heart failure.
P34 Adenosine a1 receptor activation can protect the myocardium from ischaemia reperfusion injury post reperfusion