Modulation of individual susceptibility to the no-reflow phenomenon after acute myocardial infarction.

Coronary reperfusion using primary percutaneous coronary intervention (PCI) dramatically reduces morbidity and mortality among patients with acute myocardial infarction (AMI). Nevertheless, inadequate myocardial perfusion, known as the "no-reflow" phenomenon, is observed in approximately 15% of patients and is associated with poor outcomes. No-reflow is caused not only by mechanical occlusion of the microvasculature due to thromboembolism but also by myocardial injury. Transmural myocardial damage before PCI and the size of the associated area are major factors in the development of no-reflow. There is evidence indicating that inflammation, oxidative injury, morphological changes of endothelial cells, hyperglycemia, and absence of ischemic preconditioning also contribute to the development of no-reflow. Several strategies have been attempted to counteract these risk factors. To prevent microembolization related to PCI, thrombus aspiration appears promising, but distal protection devices have failed to demonstrate the expected results among patients with AMI. Most cardioprotective agents developed to modify the risk factors for no-reflow have been effective in animal experiments but have disappointed in clinical trials. Adjunctive treatments using statins, adenosine, atrial natriuretic peptide, nicorandil, or glycoprotein IIb/IIIa antagonists have been effective in reducing the infarct size or improving outcomes after AMI in clinical studies, although some have shown inconsistent results. It is probable that the relevance of each component associated with no-reflow is different for individual patients, and therefore the attempt to indiscriminately apply one treatment to all patients will not be as successful as expected. Individual susceptibility has to be evaluated when selecting an appropriate adjunctive treatment to prevent no-reflow in patients with AMI.