| Summary: | Ischemic postconditioning (iPost) was first described in 2003 as a strategy capable of reducing the size of infarction after prolonged coronary occlusion in dogs through the immediate application of reperfusion after 3 cycles of 30 seconds of coronary reocclusion followed by 30 seconds of reperfusion.1 These results were soon confirmed independently, and the potential mechanisms involved described including, among others, a delayed normalization of pH levels, less accumulation of intracellular calcium, inhibition of the mitochondrial permeability transition pore, and less oxidative stress.2 Compared to the robust protective effect of ischemic preconditioning, it was confirmed that iPost was only beneficial if the procedure started right after reperfusion. However, it was attenuated in elderly subjects or in the presence of comorbidities or certain drug therapies.2,3 Despite these limitations, iPost soon called the attention of interventional cardiologists because it was easy to apply during primary percutaneous coronary intervention. Back in 2005 the very first study ever conducted in humans was published. In this study, iPost reduced the size of creatine kinase release compared to the control group in patients with ST-segment elevation myocardial infarction (STEMI).4 However, successive trials that estimated the size of infarction using similar methods or was more reliably measured by contrast-enhanced...
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