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International audience; Primary percutaneous coronary intervention (PCI) is the best available reperfusion strategy for acute ST-segment elevation myocardial infarction (STEMI), with nearly 95% of occluded coronary vessels being reopened in this setting. Despite re-establishing epicardial coronary vessel patency, primary PCI may fail to restore optimal myocardial reperfusion within the myocardial tissue, a failure at the microvascular level known as no-reflow (NR). NR has been reported to occur in up to 60% of STEMI patients with optimal coronary vessel reperfusion. When it does occur, it significantly attenuates the beneficial effect of reperfusion therapy, leading to poor outcomes. The pathophysiology of NR is complex and incompletely understood. Many phenomena are known to contribute to NR, including leukocyte infiltration, vasoconstriction, activation of inflammatory pathways and cellular oedema. Vascular damage and haemorrhage may also play important roles in the establishment of NR. In this review, we describe the pathophysiological mechanisms of NR and the tools available for diagnosing it. We also describe the microvasculature and the endothelial mechanisms involved in NR, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients.

International audience; BACKGROUND: Cardiac magnetic resonance can detect myocardial oedema using myocardial transverse relaxation time (T2)-weighted sequences but quantitative data are lacking in patients evaluated early after acute myocardial infarction. AIM: To assess the spatial distribution of T2 in patients with recent acute myocardial infarction. METHODS: Twenty-four consecutive patients (mean age 60+/-11 years) with acute myocardial infarction (anterior, n=12; inferior, n=12) were evaluated prospectively. T2 was determined using a series of breath-hold T2-weighted segmented half-Fourier turbo-spin echo sequences. No-reflow was defined as the association of early hypoenhancement and delayed enhancement in an akinetic region after a bolus injection of DOTA-Gd (0.2 mmol/kg). RESULTS: No-reflow was present in 13 (54%) patients and absent in 11 (46%) patients. Mean T2 was increased in the infarct region (84.9+/-23.7 ms) compared with in the remote myocardium (62.8+/-10.3 ms, p=0.0001) and in control subjects (55.7+/-4.6 ms, p

SummaryTwo forms of reperfusion injury can occur in patients with ST-segment elevation acute myocardial infarction who are undergoing primary angioplasty: no-reflow phenomenon and reperfusion syndrome. No-reflow, defined as low or no distal perfusion despite removal of epicardial occlusion, can be detected by angiographic flow, myocardial blush grade and contrast echocardiography. Reperfusion syndrome involves haemodynamic and rhythmic disturbances, but an overall paradoxical ST-segment increase. A variety of mechanisms give rise to no-reflow, including distal embolization, leucocyte plugging and vasoconstriction. Reperfusion syndrome reflects, at least in part, the cardiomyocyte component of reperfusion injury. Reperfusion injury can be predicted from the initial electrocardiogram, especially when QRS complex distortion is observed. Pharmacological prevention of reperfusion injury has been tested in a number of trials; the most useful drugs available currently are glycoprotein IIb/IIIa receptor blockers and adenosine. Thrombus aspiration leads to faster and greater ST-segment resolution. Postconditioning (also called staccato reperfusion) is a new strategy that has produced highly encouraging results, although it has been tested only in a small randomized study. New tools are required to enable thrombus aspiration and postconditioning to be carried out simultaneously. Pharmacological postconditioning can be anticipated in the near future, as many drugs appear to achieve the same positive effect as mechanical modified reperfusion.