Stent strut

In contrast, in the current stent era, experimental studies indicated that a marked activation of inflammatory cells at the site of stent struts play a key role in the process of neointimal proliferation and restenosis (37-40), Indeed, interleukins I and 6 secreted by activated macrophages are powerful stimuli for smooth muscle cell proliferation and restenosis (41,42),... 

Hietala EM, Maasilta R Valimaa T et al. Platelet responses and coagulation activation on polylactide and heparin-polycaprolactone-L-lactide-coated polylactide stent struts. J Biomed Mater Res A2003 67(3) 785—791. 

Scanning electron micrograph showing continuous endothelial cell coverage of the stent struts after five-day implantation (preclinical study of clinical trial dose BiodivYsio Batimastat Stent). 

The one-month farm swine studies evaluated safety following implantation of two doses of batimastat loaded on the 18 mm BiodivYsio stent in comparison to control stent without batimastat. Two batimastat doses were evaluated as described in Table 2. No deaths occurred during the implantation procedure and no sub-acute death or stent thrombosis was observed during the follow-up period. Histological examination confirmed that all the vessels were patent, without the presence of thrombus in the vessel lumen, All sections showed stent struts to be completely covered, leading to a smooth endoluminal surface. There was no excessive inflammatory response at stent struts in BiodivYsio-Batimastat-treated sections compared with the control sections. Medial and adventitial layers appeared similar in all three groups. The perivascular nerve fibers, the adipose tissue, and adjacent myocardium appeared normal in control and Biod/VV s/o-Batimastat-treated sections. Therefore, these studies demonstrated that the Biod/VY s/o Batimastat stent at CTD and >CTD was well tolerated up to 28 days. 

Endothelialization between stent struts is noted (arrowed). 

BMSs are usually well covered by an intimal hyperplasia. But, with drug-eluting stents, because of the potency of the drug being eluted, sometimes struts are found that are thinly or barely covered by intimal hyperplasia. Hence, the concern is actually a vulnerable stent strut. The polymer around the metal of the strut is usually quite thin and usually next to the blood stream, providing the potential for some of the metal strut to be exposed to the blood stream. 

The stent struts are comprised of the metal and the polymer, and, overtime, the drug disappears (e.g., with the Cypher stent) or some drug will remain (e.g., with the Taxus stent). Thus, there is the potential for some metal, polymer, and drug to remain exposed to the blood stream. Using high-resolution imaging techniques, intimal hyperplasia is seen when looking at BMS in vivo. 

Factors that make a stent strut vulnerable, which may lead to thrombosis, jailing side branches, or breakage of the struts, include the following polymer/drug coating dissolution, incomplete apposition, stent fracture, and overlap region,... 

The use of Dacron-covered Gianturco-Rosch stents has been recommended to treat malignant SVC obstruction in patients with protrusion of tumor or thrombus trough the stent struts, which is a rare event (Chin et al. 1996). We have used Cragg stents in the past for these indications in a few patients. 

Interaction of the metalhc stent and the tracheobronchial wall is expected unlike plastic tube stents. This leads to specific problems. Removal of a metalhc stent, which is incorporated into the mucosa several weeks after deployment is extremely difficult and sometimes requires laser destruction of the stent struts in order to remove the stent piece by piece . Similarly, repositioning of an embedded metal stent is more difficult than relocation of a silicone stent. Covered metal stents exert less problems regarding removal and repositioning than uncovered mesh stents, where the open mesh design can lead to complete inoculation of the small stent wires into the mucosa. 

When using 3D C-arm imaging for the visualization of stents, physicians again found that access to 3D information during the intervention facilitated better clinical outcomes (Van Den Berg et al. 2002 Benndorf et al. 2005, 2006 Richter et al. 2007a). Benndorf et al, for example, valued the clear visualization of both the stent struts and their adaptation to arterial walls and aneurismal lumen. 

The deconvolution (or simply subtraction) of images adjacent to the K-edge of the contrast agent of interest allows visualization the lumen, without any overly. This concept has first been shown in simulation studies and subsequently been realized on a prototype scanner. First clinical proof-of-concept papers have shown the feasibility to separate gadolinium from stent struts and calcium in phantom studies (Feuerlein et al. 2008). 

Spectral CT could therefore have a major impact on the clinical value of CT coronary angiography. Without beam hardening artifacts, in-stent lumens become accessible and with partial volume averaging, reduced both vessel lumens adjacent to stent struts and densely calcified plaques are more accurately dehn-eated (Feuerlein et ah 2008). Overall, two new application scenarios could be feasible one is the foUow-up of patients after percutaneous coronary interventions with stent implantation the other is the evaluation of patients with known CAD or calcified vessels. Spectral detector technology may promote CT to become the primary tool for CAD imaging (Roessl and Proksa 2007 Feuerlein et al. 2008). 

FD-CT imaging in the angiography suite may enable adequate visuaHzation of stent position and especially the stent struts with a high spatial resolution (Richter et al. 2007). The acknowledged advance offered by FD-CT with respect to image quality is the improved spatial resolution (Fig. 40.5). 

The proximal and distal radiopaque markers are visible in fluoroscopy and provide gross overview of the stent position in situ. However, exact position of stent wall, adaptation of the stent to the vessel wall, and especially deployment of the stent struts at the aneurysm neck remain unclear. Even incomplete stent deployment or deficient fitting of the stent to the vessel wall may remain unnoticed. This deficit may play a role in complex aneurysms or curved vessel anatomy, especially, for instance, in cases with significant changing of parent vessel diameter and bifurcations. Additionally,... 

Arterial thrombotic events are the leading cause of MI and have recently been identified as a major contributing factor to plaque progression. The detection of thrombus in a coronary artery is crucially important, as it is used to verily plaque rupture, evaluate the efficacy of thrombolytic therapy, assess the need for thrombectomy and determine the risk for distal embolization and thrombus protrusion through stent struts if percutaneous coronary intervention is warranted [69]. Unfortunately, no FDA-approved technology can accurately detect intraluminal thrombus. 

Fig. 16 Results of the vascular response to stent implantation at 6 weeks postoperatively. CLSM images show (a-c) re-endothelialization and (d-f) macrophage inhltration after stent implantation (a,d) the empty stent (b,e) the control stent and (c,f) the experimental stent. The immunofluorescence was performed with mouse anti-human CD31 (PECAM-1, blue-, arrows indicate sites of re-endothelialization), mouse anti-rabbit macrophages (RAMll, green) and propidium iodide (PI, red). The insets of (a-c) are the same sections stained with hematoxylin-eosin. Sites of stent struts. Because of histological preparation, stent struts have been lost or migrated slightly. Arrow in inset to (b) indicates site of thrombus-like substance deposition. From [166] reproduced by permission of Elsevier...

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