4 research outputs found

    Eight-year clinical outcome after radioactive stent implantation: A treatment failure without irreversible long-term clinical sequelae

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    Aims: To assess the long-term outcome of patients who underwent radioactive stent (RS) implantation. Methods and results: The RS study population consisted of 133 consecutive patients who underwent RS implantation between November 1997 and July 2000. They were matched using the propensity score method with 266 patients who underwent bare metal stenting (BMS) in the same span. Long-term survival status and information on MACE (death, non-fatal myocardial infarction or any re-intervention) was retrospectively obtained. Eight-year cumulative survival (90.2% vs. 87.4%, p=0.57) was similar between the RS and BMS group respectively, while 8-year cumulative MACE-free survival was significantly lower in RS patients (42.1% vs. 64.3%, p<0.001) due to the difference in events (mainly target lesion revascularisations [TLRs]) during the first year of follow-up (cumulative 1-year MACE-free survival: 59.4% vs. 86.7%, p<0.001); there was no difference in the MACE rate after the first year (p=0.71). The TLR rate at six months in the RS group was 29.3%, mainly due to edge restenosis and at one year 36.2% (control group: 9.5%, p<0.001). Conclusions: A high incidence of MACE and re-intervention was observed during the first year following RS implantation, mainly

    Patient-specific computational modeling of subendothelial LDL accumulation in a stenosed right coronary artery: Effect of hemodynamic and biological factors

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    Atherosclerosis is a systemic disease with local manifestations. Low-density lipoprotein (LDL) accumulation in the subendothelial layer is one of the hallmarks of atherosclerosis onset and ignites plaque development and progression. Blood flow-induced endothelial shear stress (ESS) is causally related to the heterogenic distribution of atherosclerotic lesions and critically affects LDL deposition in the vessel wall. In this work we modeled blood flow and LDL transport in the coronary arterial wall and investigated the influence of several hemodynamic and biological factors that may regulate LDL accumulation. We used a three-dimensional model of a stenosed right coronary artery reconstructed from angiographic and intravascular ultrasound patient data. We also reconstructed a second model after restoring the patency of the stenosed lumen to its nondiseased state to assess the effect of the stenosis on LDL accumulation. Furthermore, we implemented a new model for LDL penetration across the endothelial membrane, assuming that endothelial permeability depends on the local lumen LDL concentration. The results showed that the presence of the stenosis had a dramatic effect on the local ESS distribution and LDL accumulation along the artery, and areas of increased LDL accumulation were observed in the downstream region where flow recirculation and low ESS were present. Of the studied factors influencing LDL accumulation, 1) hypertension, 2) increased endothelial permeability (a surrogate of endothelial dysfunction), and 3) increased serum LDL levels, especially when the new model of variable endothelial permeability was applied, had the largest effects, thereby supporting their role as major cardiovascular risk factors
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