ANGPT2 and myocardial infarction: The possible explanations for the differences in results of these two studies may include the following: Ang-2 is expressed weakly by resting endothelium but is highly upregulated following an inflammatory response.[2] In the acute period of myocardial infarction, especially in STEMI, the predominant inflammatory response peaks after 24 to 28 h and leads to a significant release of Ang-2.[24] In the subacute period, Ang-2 wanes gradually.