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Predictors of stent thrombosis and their implications for clinical practice


Stent thrombosis (ST) is a rare but severe complication of coronary procedures with high mortality, high relapse rate and a very complex pathophysiology. An individual’s susceptibility to ST is multifactorial and results from interactions between clinical factors, endothelial biology, hypersensitivity and/or inflammatory reactions, blood rheology, platelet reactivity, clotting factors, physical and mechanical properties of the stent and from the effects of these different factors on the fluid dynamics of blood flow. Since the introduction of stents 32 years ago, continuous improvements in our understanding of the pathophysiology of ST have triggered important advances, including new therapies, new technologies and an increased awareness of the implications of implantation techniques. Furthermore, advances in medical imaging and in the mathematical processing of this information have allowed a more detailed assessment of the mechanisms of ST at the time of its onset. Evidence shows that addressing the risk factors for ST leads to a substantial reduction in its incidence, both early and late after stent implantation. A better knowledge of the mechanisms of this complication is, however, necessary to direct the choice of the most appropriate strategy for its prevention and treatment.

Key points

  • Although rare, stent thrombosis remains a major complication after stent implantation, with up to 45% mortality and a recurrence rate as high as 20%.

  • The mechanisms of stent thrombosis are multifactorial, and novel risk factors have been identified.

  • Multiple interactions between device-related factors, patient-related factors and procedure-related factors determine the risk of stent thrombosis at different time.

  • Although apparently complex, these concepts must be understood and applied in routine clinical practice given that their correction is associated with substantial reductions in the rate of stent thrombosis.

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Fig. 1: Strut dimensions, stent expansion and their haemodynamic effect.
Fig. 2: Stent footprint and stent thrombosis.
Fig. 3: Risk factors for stent thrombosis, clinical thresholds and recommended interventions.
Fig. 4: Short-term complications: early stent malapposition and dissections on OCT images.
Fig. 5: Long-term complications: uncovered struts, evaginations, endothelial bridges and dismantling.
Fig. 6: Long-term complications: restenosis, neoatherogenesis, peri-strut low-intensity areas, microchannels and strut fractures.


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Nature Reviews Cardiology thanks S.-J. Park and E. Brilakis for their contribution to the peer review of this work.

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T.G., A.P., L.R. and T.A. researched data for the article. T.G., C.I., L.R. and T.M. discussed its content. All the authors wrote the manuscript, and T.G., C.I., L.R., T.A. and T.M. reviewed and edited it before submission.

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Correspondence to Tommaso Gori.

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Competing interests

T.G. received a research grant from Abbott Vascular and speaker’s or consulting fees from Abbott Vascular, AstraZeneca, Biotronik, Braun, Novartis and Stentys. L.R. received research grants from Abbott Vascular, Regeneron and Sanofi, and speaker’s or consultation fees from Abbott Vascular, Amgen, AstraZeneca, Biotronik, CSL Behring, Novartis and Sanofi. T.A. received a research grant from Abbott Vascular and speaker’s or consulting fees from Abbott Vascular. The other authors declare no competing interests.

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Gori, T., Polimeni, A., Indolfi, C. et al. Predictors of stent thrombosis and their implications for clinical practice. Nat Rev Cardiol 16, 243–256 (2019).

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