What is the prevalence of stent thrombosis following percutaneous coronary intervention (PCI) and how is it treated?

Updated: Nov 27, 2019
  • Author: George A Stouffer, III, MD; Chief Editor: Karlheinz Peter, MD, PhD  more...
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Answer

Although DESs have significantly reduced the incidence of restenosis, early generations of these devices were linked with concerns regarding stent thrombosis. Currently, the thrombosis rate for a DES is virtually identical to that for a BMS at 1 year (0.5-0.7%). The NORSTENT study reported that the rates of definite stent thrombosis were 0.8% with DESs and 1.2% with BMSs (P = 0.05) over 6 years of follow-up. [117] Late stent thrombosis (>1 year), which occurred with early-generation DESs, is rarely seen with current DESs.

The factor that makes the greatest contribution to stent thrombosis is interruption of antiplatelet therapy. Current guidelines recommend a minimum of 1 year of DAPT for DES patients with acute coronary syndrome, 6 months of DAPT for stable DES patients, and 1 month of DAPT for BMS patients. [7] DESs take longer to endothelialize on the coronary vessel wall than BMSs do, and discontinuing DAPT may expose patients to an increased risk for stent thrombosis over time.

In some clinical situations (eg, before urgent noncardiac surgery in which antiplatelet therapy may have to be discontinued and when known or potential medicine compliance issues are present), implanting a bare-metal stent during PCI may be preferred to implanting a DES. Another important factor is final stent diameter and area.

Underdeployment or incomplete apposition of any stent increases the risk of stent thrombosis. Stone et al found that although stent thrombosis is infrequent, it results in higher rates of MI and death. [118]

An analysis of data from 7090 consecutive PCI-treated patients in the ISAR-ASPI (Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition) registry suggested that high platelet reactivity in patients on aspirin (HAPR) at the time of PCI was associated with a greater risk of death or stent thrombosis (6.2% vs 3.7% for non-HAPR) during the first year after PCI. [119] Moreover, HAPR independently predicted death or stent thrombosis at 1 year. These findings may support use of HAPR as a prognostic biomarker in PCI-treated patients.


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