{'fraction_non_alphanumeric': 0.019528619528619527, 'fraction_numerical': 0.006734006734006734, 'mean_word_length': 5.723981900452489, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Noninvasive Evaluation of No-Reflow Phenomenon: Potential Role of Molecular Imaging

The primary treatment for acute myocardial infarction (MI) involves early revascularization, and millions of individuals each year presenting with acute MI are successfully treated with early and effective interventional reperfusion strategies. However, despite this initial strategy to reduce the ischemic injury post-MI, these patients are at significant risk for additional acute reperfusion injury and subsequent adverse left ventricular remodeling and heart failure.1 In this context, a period of ischemia that is followed by reperfusion initiates a cascade of biological events within the injured myocardium, leading to reperfusion injury. This reperfusion injury can be associated with the no-reflow phenomenon, which refers to the failure to restore perfusion to the microvasculature supplying the parenchyma of an organ after restoration of patency of the artery.2,3 In the heart, no reflow occurs on reperfusion after 30 to 90 minutes of coronary occlusion and progresses for about 2 hours after the restoration of epicardial flow. This phenomenon has been attributed to microvascular injury and microvascular plugging resulting in microvascular obstruction (MVO) after restoration of epicardial flow with a percutaneous coronary intervention (PCI) generally in the setting of acute MI. The presence of MVO is associated with late post-MI remodeling, heart failure, and higher mortality.4–7