The coronary circulation is both culprit and victim of acute myocardial infarction.
The rupture of an epicardial atherosclerotic plaque with superimposed thrombosis causes
coronary occlusion, and this occlusion must be removed to induce reperfusion. However,
ischaemia and reperfusion cause damage not only in cardiomyocytes but also in the
coronary circulation, including microembolisation of debris and release of soluble
factors from the culprit lesion, impairment of endothelial integrity with subsequently
increased permeability and oedema formation, platelet activation and leukocyte adherence,
erythrocyte stasis, a shift from vasodilation to vasoconstriction, and ultimately
structural damage to the capillaries with eventual no-reflow, microvascular obstruction
and intramyocardial haemorrhage. Therefore, the coronary circulation is a valid target
for cardioprotection, beyond protection of the cardiomyocyte. Virtually all of the
above deleterious endpoints have been demonstrated to be favourably influenced by
one or the other mechanical or pharmacological cardioprotective intervention. However,
no-reflow is still a serious complication of reperfused myocardial infarction and
carries, independently from infarct size, an unfavourable prognosis. Microvascular
obstruction and intramyocardial haemorrhage can be diagnosed by modern imaging technologies,
but still await an effective therapy. The current review provides an overview of strategies
to protect the coronary circulation from acute myocardial ischaemia/reperfusion injury.
This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection
Beyond the Cardiomyocyte', and emerged as part of the discussions of the European
Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.
