Influence of residual stenosis after percutaneous coronary intervention with stent implantation on development of restenosis and stent thrombosis

Sick, Peter; Hüttl, Tobias; Niebauer, Josef; Thiele, Holger; Lauer, Bernward; Hambrecht, Rainer; Hentschel, Bettina; Schuler, Gerhard

doi:10.1016/s0002-9149(02)03100-4

Cited by 20 publications

(13 citation statements)

References 28 publications

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“…In a large clinical trial, the effect of residual stenosis (various degrees of oversizing) after stent implantation on the rate of stent restenosis was evaluated in Ͼ2,000 patients (41). They found that even 10% oversizing led to excessive IH.…”

Section: Discussionmentioning

confidence: 99%

Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

Chen

Sinha

Choy

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation (R(2) = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed (R(2) = 0.48 and 0.50, respectively, P < 0.005). A linear relation (R(2) = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed (R(2) = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.

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Section: Discussionmentioning

confidence: 99%

Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

Chen

Sinha

Choy

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…For stent thrombosis, there was a 50% increase in GM (1.2% vs. 0.8%) 1 yr poststenting. For RGM, clinical trials showed that stent oversizing was associated with increased TVR, MI, and impaired myocardial perfusion (16,30). A greater propensity for disruptions of plaque associated with oversizing may also lead to increased distal microembolization (16).…”

Section: Discussionmentioning

confidence: 99%

“…The TVR rates in patients without GM were 45% lower than in patients with GM and the myocardial infarction rates were 60% lower for patients without GM. The STLLR report suggested that the lack of intimal hyperplasia in patients treated with DES likely contributed to a false perception that suboptimal percutaneous coronary intervention technique would no longer affect clinical outcomes (30). Another large clinical trial (2,157 patients) found negative residual stenosis (RGM) was associated with a higher extent of in-stent restenosis (30), consistent with the finding of another trial that negative residual stenosis was associated with impaired myocardial perfusion and increased mortality (16).…”

mentioning

confidence: 83%

Impact of stent mis-sizing and mis-positioning on coronary fluid wall shear and intramural stress

Chen

Koo

Bhatt

et al. 2013

Journal of Applied Physiology

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Stent deployments with geographical miss (GM) are associated with increased risk of target-vessel revascularization and periprocedural myocardial infarction. The aim of the current study was to investigate the underlying biomechanical mechanisms for adverse events with GM. The hypothesis is that stent deployment with GM [longitudinal GM, or LGM (i.e., stent not centered on the lesion); or radial GM, RGM (i.e., stent oversizing)] results in unfavorable fluid wall shear stress (WSS), WSS gradient (WSSG), oscillatory shear index (OSI), and intramural circumferential wall stress (CWS). Three-dimensional computational models of stents and plaque were created using a computer-assisted design package. The models were then solved with validated finite element and computational fluid dynamic packages. The dynamic process of large deformation stent deployment was modeled to expand the stent to the desired vessel size. Stent deployed with GM resulted in a 45% increase in vessel CWS compared with stents that were centered and fully covered the lesion. A 20% oversized stent resulted in 72% higher CWS than a correct sized stent. The linkages between the struts had much higher stress than the main struts (i.e., 180 MPa vs. 80 MPa). Additionally, LGM and RGM reduced endothelial WSS and increased WSSG and OSI. The simulations suggest that both LGM and RGM adversely reduce WSS but increase WSSG, OSI, and CWS. These findings highlight the potential mechanical mechanism of the higher adverse events and underscore the importance of stent positioning and sizing for improved clinical outcome.

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“…Stent diameter. Stents with increased diameter relative to the normal artery cross section pose a higher risk of clinical ISR (57). Although stent oversizing may induce ISR through marked arterial injury, oversized stents may also promote NIH by increasing the arterial cross section, reducing flow rate, and thus lowering ESS in the stented versus the proximal nonstented arterial segment.…”

Section: Modifiable Factors Thatmentioning

confidence: 99%

Role of Endothelial Shear Stress in Stent Restenosis and Thrombosis

Koskinas

Chatzizisis

Antoniadis

et al. 2012

Journal of the American College of Cardiology

284

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Restenosis and thrombosis are potentially fatal complications of coronary stenting with a recognized multifactorial etiology. The effect of documented risk factors, however, cannot explain the preponderance of certain lesion types, stent designs, and implantation configurations for the development of these complications. Local hemodynamic factors, low endothelial shear stress (ESS) in particular, are long known to critically affect the natural history of atherosclerosis. Increasing evidence now suggests that ESS may also contribute to the development of restenosis and thrombosis upon stenting of atherosclerotic plaques, in conjunction with well-appreciated risk factors. In this review, we present in vivo and mechanistic evidence associating ESS with the localization and progression of neointimal hyperplasia and in-stent clotting. Clinical studies have associated stent design features with the risk of restenosis. Importantly, computational simulations extend these observations by directly linking specific stent geometry and positioning characteristics with the post-stenting hemodynamic milieu and with the stent's thrombogenicity and pro-restenotic potential, thereby indicating ways to clinical translation. An enhanced understanding of the pathophysiologic role of ESS in restenosis and thrombosis might dictate hemodynamically favorable stent designs and deployment configurations to reduce the potential for late lumen loss and thrombotic obstruction. Recent methodologies for in vivo ESS profiling at a clinical level might allow for early identification of patients at high risk for the development of restenosis or thrombosis and might thereby guide individualized, risk-tailored treatment strategies to prevent devastating complications of endovascular interventions.

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Influence of residual stenosis after percutaneous coronary intervention with stent implantation on development of restenosis and stent thrombosis

Cited by 20 publications

References 28 publications

Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

Mis-sizing of stent promotes intimal hyperplasia: impact of endothelial shear and intramural stress

Impact of stent mis-sizing and mis-positioning on coronary fluid wall shear and intramural stress

Role of Endothelial Shear Stress in Stent Restenosis and Thrombosis

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