In-Stent Restenosis: Is Low Shear Stress to Blame?

Vishal Nainesh Patel, Angshumonik Angbohang, Lingfang Zeng

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Cardiovascular disease is accountable for around 31% of all deaths worldwide. Percutaneous coronary intervention, particularly the use of stents has remarkably improved the management of moderate to severe cardiovascular disease since its introduction in 1977. However, in approximately 20-30% of patients clinical instent restenosis (ISR) can occur. ISR has a multifactorial aetiology, in which endothelial shear stress plays a major role. We aim to review the current evidence assessing the relationship between endothelial shear stress and ISR. The introduction of a stent can lead to changes in the mechanical environment of the artery, particularly at the inlet and the outlet of the stent which are susceptible to areas of low shear stress (LSS). In vivo studies have consistently associated LSS with a higher incidence of ISR whereas higher shear stress exerts a protective effect. The mechanisms underlying this association are not fully known, but ISR is likely to occur through neointimal hyperplasia (NIH). An endothelium dependent effect of LSS, endothelium-independent effect of LSS or the effect of LSS on smooth muscle cell phenotype may contribute to NIH progression. Factors relating to the stent design, patient specific characteristics and mechanical factors may also exacerbate NIH formation. Recent advances in the methodology for in vivo shear stress profiling may allow the early identification of patients at an increased risk of developing ISR clinically. This will then help guide novel treatment strategies towards an individual’s needs.
Original languageEnglish
JournalJournal of cardiology & clinical research
Issue number4
Early online date23 May 2017
Publication statusE-pub ahead of print - 23 May 2017


  • Shear stress
  • Atherosclerosis
  • In-stent restenosis


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