Author + information
- Received June 8, 2011
- Revision received September 13, 2011
- Accepted October 27, 2011
- Published online April 10, 2012.
- Konstantinos C. Koskinas, MD, MSc⁎,†,
- Yiannis S. Chatzizisis, MD, PhD⁎,†,
- Antonios P. Antoniadis, MD, PhD⁎,† and
- George D. Giannoglou, MD, PhD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. George D. Giannoglou, 1st Cardiology Department, AHEPA University Hospital, Aristotle University Medical School, 1 St. Kyriakidi Street, 54636 Thessaloniki, Greece
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.
This work was supported by the George D. Behrakis Cardiovascular Research Fellowships to Drs. Koskinas and Chatzizisis. All authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Koskinas and Chatzizisis are joint first authors.
- Received June 8, 2011.
- Revision received September 13, 2011.
- Accepted October 27, 2011.
- American College of Cardiology Foundation
- Stent-Induced Changes in ESS
- In Vivo Studies Associating Low ESS With ISR
- Role of Low ESS in the Pathobiology of Restenosis
- Endothelium-independent effect of low ESS
- Modifiable Factors That Influence the Pro-Restenotic Effect of Low ESS
- Role of ESS in ST
- Clinical Implications of Applying In Vivo ESS Profiling and Hemodynamically Favorable Stent Designs