1 Introduction Myocardial no-reflow occurs after primary percutaneous coronary interventions (PCI), as a consequence of microvascular clogging by microthrombi, microvascular spasm, edema formation, and interstitial hemorrhage [1] . It was initially described as an angiographic phenomenon, attenuating the efficacy of primary PCI especially in the setting of acute coronary syndromes (ACS) [2] . No-reflow has been linked to microvascular obstruction (MVO) as seen on cardiac magnetic resonance imaging (CMR) [3] , although MVO occurs in roughly 50 % of patients [4] whereas angiographic no-reflow is seen in around 30 % [2] . In a large individual pooled analysis, CMR-detected MVO was the strongest predictor of clinical outcomes including death [5] . Strategies to abate the consequences of no-reflow have focused on pharmacological strategies, including vasoactive substances and antithrombotic therapy. Importantly, the pharmaceutical target site is the microvasculature, which can only be reached in cases of at least partially restored coronary flow. Indeed, trials with positive results have employed medication after recanalization [67] .