Many definitions have been given to this phenomenon based on individual’s area of specialty, but the definition that unites all fields was by Kloner et al in 1974 who described the condition as the inability to adequately perfuse myocardium after temporary occlusion of an epicardial coronary artery without evidence of persistent mechanical obstruction, thus implying ongoing myocardial ischaemia. When defined angiographically, it is an acute reduction in coronary flow (TIMI grade 0-1) in the absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion. In other words, it is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed.^[1][2] It has been clearly shown that a complete restoration of epicardial blood flow (TIMI Flow Grade 3) does not correlate with a better myocardial perfusion in achieving better clinical outcomes. Therefore, over the years, attention has shifted towards methods to evaluate myocardial perfusion. A lesser degree of obstruction to coronary blood flow (TIMI grade 2) is sometimes referred to as slow flow. No-reflow is the decline in TIMI flow from TIMI flow 3 or 2 to TIMI flow 1 or 0, which occurs >5 mm distal to the lesion. No-reflow is an important predictor of mortality after PCI ^[3].

This phenomenon was first described by Krug et al ^[4] during induced myocardial infarction in dog subjects in 1966, but the term ‘no-reflow’ was first used by Majno and colleagues in 1967 when they observed that brains of rabbits exposed to prolonged ischemia suffered significant changes in the microvasculature which impeded blood flow to the brain cells.

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