Coronary angioplasty is commonly used as a treatment for myocardial infarction. Initial challenges of bare metallic stents (BMS), e.g., early thrombosis and in stent restenosis (ISR) from proliferation and migration of vascular smooth muscle cell (SMC) are treated with anticlotting drugs and drug eluting stents (DES), respectively. But very late stent thrombosis (ST) is another challenge which causes restenosis of the stenotic arteries [1]. Improvement of reduced in stent restenosis (ISR) rate from 20–25% to around 8.6% using DES instead of BMS is hampered by stent fracture (SF) associated with DES [2]. Moreover, BMS shows very late ST (>5 years), whereas improved DES shows late ST (>1 year). In addition, clinically silent DES SF is associated with ISR and ST and pathologic investigation indicates 29% incidence of SF with about additional 5% incidence associated with adverse effect, e.g., inflammation, ulceration, avulsion,...

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