Reperfusion Injury and Cardiac Remodelling after Acute Myocardial Infarction
Early recanalization of an occluded infarct vessel is the main target in the acute management of patients with an ST elevation myocardial infarction (STEMI) and can be obtained by primary percutaneous coronary intervention (pPCI). However, despite successful restoration of vessel patency, up to 40% of patients still fail to have a complete myocardial reperfusion due to a process of reperfusion injury at the microcirculatory level. Incomplete reperfusion results in a more extensive infarction and further dilatation of the heart (negative remodelling) and is associated with a poor prognosis in terms of cardiac failure and death.
Although the underlying mechanisms of reperfusion injury are still not fully elucidated, there is accumulating experimental evidence that inflammatory responses, overproduction of oxygen-derived free radicals and calcium overload play key roles and lead to microvascular dysfunction and, ultimately, to myonecrosis (see figure). Despite the large body of basic science research, translation into clinical practice has been disappointing until now.
Our team has been involved in many research projects targeting optimisation of reperfusion therapy in STEMI and is currently doing research both experimental, translational and clinical in the following fields of reperfusion injury:
- adiponectin in the process of reperfusion injury and apoptosis (FWO);
- dendritic cells in the process of remodelling post myocardial infarction (GOA);
- cyclosporine, a potent inhibitor of the mitochondrial permeability-transition pore, as novel treatment agent for the prevention of reperfusion injury (international research group).
