Hideki Wada,1 Peter C. Mattson,2 *Hiroshi Iwata1
1. Department of Cardiovascular Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan
2. Warren Alpert Medical School, Brown University, Providence, Rhode Island, USA
*Correspondence to email@example.com
Disclosure: The authors have declared no conflicts of interest.
Received: 13.03.17 Accepted: 08.15.17
Citation: EMJ Int Cardiol. 2017;5:55-61.
Stent thrombosis (ST) is uncommon yet constitutes the most feared complication following percutaneous coronary intervention. Although its incidence is now <1% within a year after stenting in patients receiving second or later-generation drug-eluting stents (DES), compared to those in the first-generation DES-era, the clinical impact of ST is still high, because the majority of cases with ST are complicated by critical consequences, including myocardial infarction and even sudden cardiac death. Moreover, the pathophysiology and risk factors leading to ST were recently re-recognised, as bioresorbable scaffolds (or biodegradable vascular scaffolds) have now been developed, and concerns have arisen regarding scaffold thrombosis, which serves as another ‘ST’. Accumulating evidence through the bare-metal stent and DES-era has identified clinical factors associated with increased risk of ST, such as patient-related, lesion-related, procedure-related, and post-procedure-related risk factors. Therefore, this short review describes updated pathophysiology and contributing risk factors for stent (or scaffold) thrombosis, which are useful for risk stratification in patients with coronary artery disease in the late metallic DES-era or at the beginning of the bioresorbable scaffolds era.
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