“…It is estimated that around 3% to 7% of AAD is concurrent with AMI [2,3], and mostly occurred in Stanford type A dissection. In type A AAD, the false lumen may extend proximally towards the coronary ostia producing various mechanisms of coronary occlusion, such as compression the proximal coronary by false lumen, ostium obstruction by intimal flap, dissection, avulsion and coronary artery spasm [4,5]. However, it cannot be explained by such mechanisms in our case which is infrequent seen in former reports.…”