Since medical school, we always heard that “time is muscle” and that the faster we reperfuse a culprit artery in acute coronary syndrome (ACS), the better for the patient. Over time, evidence-based cardiology has taught us that not every patent artery is the same. The fact that we have an artery with a “TIMI 3” flow seemed enough to define the patient’s prognosis, but after the concept of microvascular ischemia, we also started to care about small-vessel perfusion.^,

Based on this concern, came the concept of ‘no reflow’, which means that even after the recanalization of a culprit artery, the tissue flow related to that myocardial territory might not be reestablished. Going back in time, the phenomenon of slow flow has been described since 1972, defined as delayed coronary opacification in the absence of epicardial obstructive coronary disease, while maintaining myocardial perfusion. Slow flow seems to be more common in patients with metabolic syndrome, in the male gender and smokers. Both the phenomenon of no reflow and slow flow are associated with significant cardiovascular outcomes, the first being related to ventricular dysfunction and cardiac remodeling^, and the latter, to cases of ventricular arrhythmias or sudden death,^, in addition to refractory angina.

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