Assessing perfusion and function in acute myocardial infarction: how and when?

REPERFUSION VERSUS NO REFLOW Immediate treatment usually restores patency of the occluded artery as a result of the infusion of a thrombolytic agent or preferably of direct percutaneous coronary intervention (PCI). Optimal angiographic recanalisation does not necessarily imply tissue reperfusion. Inadequate blood flow in the microcirculation despite recanalisation, termed “no reflow phenomenon”, was first studied experimentally and was observed in the clinical setting by Ito and colleagues, using myocardial contrast echocardiography (MCE) with intracoronary injection of sonicated microbubbles. No reflow or low reflow can be determined by several mechanisms. After thrombolysis, residual stenosis of the infarct related vessel is frequently severe and can be responsible for partial or complete reocclusion or for repetitive episodes of ischaemia and post-ischaemic myocardial and microvascular stunning. Primary PCI may be accompanied by distal embolisation of platelet aggregates, neutrophil accumulation, and capillary plugging inducing progressive microvascular obstruction despite initial reperfusion. In other patients, restoration of the blood supply leads to reactive hyperaemia, but also possibly to postreperfusion injury by oxygen-free radicals, inducing cellular oedema. After optimisation of vessel patency by successful stent placement, early and sustained improvement of coronary flow reserve is usually observed, consistent with gradual resolution of post-ischaemic vascular stunning. In other words, after early recanalisation, myocardial perfusion can dynamically evolve in two opposite directions: complete or at least partial recovery of microvascular integrity, or progressively irreversible microvascular damage, frequently accompanied by intramyocardial haemorrhage. SALVAGE VERSUS NECROSIS The transmural extent of myocardial and microvascular necrosis is highly variable from patient to patient. The major determinants are presence and adequacy of collateral circulation, time to treatment, and therapeutic efficacy. The time from symptom onset to the initiation of treatment is the sum of three individual periods of time: patient’s delay in seeking medical attention, transport time, and door-toneedle or door-to-balloon time. Patients should be educated to react early, the thrombolytic agent or the adjunctive treatment as a preparation for PCI can be given during transport, and door-toneedle or door-to-balloon times need to be improved.