“…It usually presents as acute STEMI, but compared to patients with early and late ST, patients with VLST had better prognosis with lower incidence of major adverse cardiac events and mortality [6][7][8]. The mechanism of VLST is not fully understood, but is thought to be related to delayed incomplete stent strut endothelialization [9,10], stent strut malapposition secondary to positive remodeling [10,11], stent fracture [12], hypersensitivity reaction to polymers [13,14], chronic inflammation [9,15], rupture of lipid-laden-like neointima within the DES [10], and discontinuation of antiplatelet therapy [16]. In our case, we did not notice anything from his medical history that known to contribute to VLST, and there was no delay in patient transfer or patient care.…”