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Monitoring the Wall Mechanics During Stent Deployment in a Vessel
Published on: May 8, 2012
Drug-eluting stent and coronary thrombosis: biological mechanisms and clinical implications
Thomas F Lüscher1, Jan Steffel, Franz R Eberli
1Cardiovascular Center, University of Zurich, Rämistrasse 100, 8091 Zürich, Switzerland. cardiotfl@gmx.ch
Insights
Drug-eluting stents (DES) can cause stent thrombosis, a serious complication. While evidence is inconclusive, factors like stent design and premature cessation of antiplatelet drugs increase risk, necessitating further research.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Biomaterials Science
Background:
- Stent thrombosis is a rare but severe complication following stent implantation, with higher incidence reported for drug-eluting stents (DES) compared to bare-metal stents.
- Factors contributing to stent thrombosis include procedural issues, patient characteristics, stent design, and premature cessation of antiplatelet therapy.
- The biological effects of drugs and polymers in DES may impair reendothelialization and promote a prothrombogenic environment, potentially increasing thrombosis risk.
Purpose of the Study:
- To review the pathophysiological mechanisms and pathological findings of stent thrombosis specifically in drug-eluting stents (DES).
- To synthesize current evidence regarding the risk of DES thrombosis and identify associated contributing factors.
- To highlight the need for further large-scale clinical trials and mechanistic studies to clarify the DES thrombosis risk.
Main Methods:
- Review of existing literature, including large registries, meta-analyses of randomized trials, and mechanistic studies.
- Analysis of pathophysiological pathways involved in DES-induced stent thrombosis.
- Examination of pathological findings associated with stent thrombosis in DES.
Main Results:
- DES may increase stent thrombosis risk due to impaired reendothelialization, delayed arterial healing, and induced prothrombogenic environments.
- Stent malapposition, underexpansion, multiple stents, stent length, slow coronary flow, dissections, patient factors, and premature cessation of antiplatelet drugs are associated with increased risk.
- Evidence remains inconclusive regarding the definitive higher risk of DES thrombosis, underscoring the need for more research.
Conclusions:
- Drug-eluting stents (DES) present complex pathophysiological mechanisms that can contribute to stent thrombosis.
- While contributing factors are identified, the overall risk of DES thrombosis compared to bare-metal stents requires further investigation.
- Additional large-scale, long-term clinical trials and mechanistic studies are crucial to definitively assess and understand DES-associated stent thrombosis.
Abstract:
Although rare, stent thrombosis remains a severe complication after stent implantation owing to its high morbidity and mortality. Since the introduction of drug-eluting stents (DES), most interventional centers have noted stent thrombosis up to 3 years after implantation, a complication rarely seen with bare-metal stents. Some data from large registries and meta-analyses of randomized trials indicate a higher risk for DES thrombosis, whereas others suggest an absence of such a risk. Several factors are associated with an increased risk of stent thrombosis, including the procedure itself (stent malapposition and/or underexpansion, number of implanted stents, stent length, persistent slow coronary blood flow, and dissections), patient and lesion characteristics, stent design, and premature cessation of antiplatelet drugs. Drugs released from DES exert distinct biological effects, such as activation of signal transduction pathways and inhibition of cell proliferation. As a result, although primarily aimed at preventing vascular smooth muscle cell proliferation and migration (ie, key factors in the development of restenosis), they also impair reendothelialization, which leads to delayed arterial healing, and induce tissue factor expression, which results in a prothrombogenic environment. In the same way, polymers used to load these drugs have been associated with DES thrombosis. Finally, DES impair endothelial function of the coronary artery distal to the stent, which potentially promotes the risk of ischemia and coronary occlusion. Although several reports raise the possibility of a substantially higher risk of stent thrombosis in DES, evidence remains inconclusive; as a consequence, both large-scale and long-term clinical trials, as well as further mechanistic studies, are needed. The present review focuses on the pathophysiological mechanisms and pathological findings of stent thrombosis in DES.
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