Stent Site Research Articles

Is 40% to 70% diameter narrowing at the site of previous stenting or directional coronary atherectomy clinically significant?

Traditional binary definitions of coronary restenosls based on 6-month continuous angiographic measurements (e.g., >50% diameter stenosis) may give confusing results for lesions whose late percent stenosis falls near the arbitrary threshold. To determine the long-term clinical consequences of such lesions, the overall correlation between follow-up percent stenosis and the performance of subsequent ischemia-driven target vessel revascularization (triggered by significant angina or a positive exercise study result, or both) was examined in 443 consecutive lesions treated with directional coronary atherectomy or Palmaz-Schatz coronary stenting. Follow-up angiograms (available in 355 lesions, 82%) were stratified into 3 groups: severe late stenosis (>70% stenosis, n = 59), moderate late stenosis (40% to 70% stenosis, n = 72), and minimal late stenosis (<40% stenosis, n = 224). With an average clinical follow-up of 933 ± 394 days, 92% of lesions In the “severe late stenosis” group were treated with ischemia-driven target vessel revascularization, compared with 0% of the lesions in the “minimal late stenosis” group. Ischemia-driven target vessel revascularization was performed in 38% of patients in the “moderate late stenosis” group. However, patiente in this group who did not undergo revascularization (despite the fact that 43% of them had a late stenosis of >50%) showed a similarly favorable long-term clinical outcome to patiente with a minimal late stenosis. These results support a strategy of conservative management for the 20% of patiente who have a moderate (40% to 70%) late stenosis after stenting or atherectomy, but do not have evidence of ischemia.

Palmaz-Schatz stenting for treatment of focal vein graft stenosis: Immediate results and long-term outcome

Objectives. This study aimed to evaluate the effectiveness of Palmaz-Schatz stenting for the treatment of saphenous vein graft stenoses.Background. Failure of saphenous vein grafts is a common cause of recurrent ischemia after coronary bypass surgery. A second bypass surgery carries more risk than the initial procedure, and balloon angioplasty of vein grafts has yielded disappointing results. It has been hoped that starting might offer a better treatment option.Methods. We examined the results of stent placement in 200 saphenous bypass graft lesions consecutively treated with either coronary (n = 146) or biliary (n = 54) Palmaz-Schatz stents. Immediate outcome and clinical follow-up (median 15.5 months) were examined in all patients. To document angiographic outcome, a second angiography was performed at 3 to 6 months for the first 120 consecutively stented lesions and was successfully obtained for 94 (78%).Results. The mean graft age (±SD) was 8.7 ± 4 years. Stent placement was successful in 197 (98.5%) of 200 lesions, reducing the mean diameter stenosis from 74 ± 14% to 1 ± 15%. In 164 procedures, there was one in-hospital death (0.6%), no emergency bypass operations and no Q wave myocardial infarctions. There was one acute stent thrombosis (0.6%) but no subacute thromboses. Vascular repair was required after 14 procedures (8.5%), with transfusion in 23 additional cases (14%). Angiographic restenosta (diameter stenosis ≥ 50%) at 3- to 6-month follow-up was 17% (95% confidence interval 9% to 25%). By Kapian-Meier estimates, however, the 2-year second revascularization rate was 49%, refecting the predominant revascularization performed to treat progressive disease at other sites because failure at the stented site occurred in only 22% of lesions.Conclusions. Stenting resulted in exellent immediate and long-term angiographic resuls in this group of focally diseased, older saphenous vein grafts. Despite the high immediate success and very low (17%) angiographic restenesis rate at 6 months, approximately one half of these patients required farther revascularization in the following 2 years, mainly because of disease progression at other sites.

Treatment of malignant esophageal obstruction with silicone-coated metallic self-expanding stents

Six patients with high-grade malignant esophageal obstruction were treated with silicone-coated metallic self-expanding esophageal stents (Z stents). Endoscopic placement of stents was well tolerated. All patients achieved excellent palliation, defined by a decrease of at least two dysphagia grades, which was sustained. Complications occurred during follow-up in four patients and included stent migration, silicone disruption with tumor ingrowth, food impaction, and perforation (discovered at autopsy) at the distal stent site. Three of the four complications were promptly treated by endoscopic or radiologic intervention. Recent modification in stent design and placement technique will hopefully reduce complications. The self-expanding stent has several theoretical advantages over the rigid plastic stent and Nd:YAG laser for palliation of obstructing esophageal malignancy.

Coronary aneurysms after stent placement: A suggestion of altered vessel wall healing in the presence of anti-inflammatory agents

Coronary aneurysms are rare after conventional angioplasty and have not been reported after coronary stenting. Coronary artery stent sites were examined by follow-up angiography at a median of 4 months in 29 patients who received the Cook stent (Gianturco-Roubin) for acute coronary closure. Nineteen patients were treated with glucocorticoids administered intravenously or orally, or both, with or without colchicine and results were compared with those in 10 patients who were treated with neither agent. Standard therapy for all patients included routine administration of aspirin and heparin before and warfarin sodium (Coumadin) and aspirin after stent placement. Most patients also received dipyridamole and lovastatin during the follow-up period. Compliance with medications was confirmed by telephone conversation with each patient.Six (32%) of the 19 stented arteries showed evidence of coronary artery aneurysm, defined as expansion of the lumen outside the margins of the stent. None of the patients in the control group (who did not receive steroids or colchicine) developed aneurysm. This pattern of altered vascular healing in stented coronary segments appears to be due to the addition of multiple anti-inflammatory drugs rather than to stent presence alone. This observation demonstrates the possibility of medical impairment of normal vascular remodeling after acute injury and stent placement, which may be of benefit in designing future trials on restenosis.

Reduction in thrombus formation by placement of endovascular stents at endarterectomy sites in baboon carotid arteries.

Although antithrombotic therapies with aspirin, dipyridamole, and heparin have decreased thrombo-occlusive events, they have not abolished these complications. Endovascular mechanical support, first reported by Dotter in 1969, has been proposed as a means to reduce both acute and chronic vessel closure by providing a supporting framework for the disrupted and sometimes dissected arterial wall. To determine the effects of placing self-expanding stainless steel wire endoprostheses on the accumulation of thrombus at sites of carotid artery endarterectomy we measured platelet deposition continuously for 90 minutes and at 24 and 48 hours by gamma camera imaging of autologous 111In-labeled platelets in six stented and nonstented endarterectomized baboons that received heparin but no antiplatelet agents. At nonstented endarterectomy sites 5.36 +/- 1.25 x 10(8), 4.78 +/- 0.98 x 10(8), and 4.55 +/- 0.81 x 10(8) platelets per cm were deposited at 30, 60, and 90 minutes, respectively. In contrast, stented endarterectomy sites accumulated 0.99 +/- 0.31 x 10(8), 0.66 +/- 0.33 x 10(8), and 0.80 +/- 0.36 x 10(8) platelets per cm at 30 minutes (p = 0.02), 60 minutes (p = 0.004), and 90 minutes (p = 0.002), respectively. Platelet deposition remained reduced at 24 and 48 hours in stented endarterectomized carotid arteries (ECAs) when assessed as a ratio between net radioactivity in the endarterectomized region versus whole blood radioactivity (p = 0.006 and p = 0.009, respectively). Both stented and nonstented ECAs remained patent acutely, although two of six nonstented ECAs occluded by 30 days. By comparison 11 of 14 nonstented ECAs remained patent in another group of control animals. Scanning electron microscopy of control and stented arteries at 30 days demonstrated equivalently confluent endothelium. We postulate that endovascular stents reduce the thrombogenic effects of flap formation, tearing, dissection, and vasospasm in ECAs.

Intraluminal Ultrasound Assessment of Vascular Stent Deployment

This study assessed the utility of intraluminal ultrasound imaging during deployment of a self-expanding vascular stent and quantitated changes in arterial morphology produced by the stent. Cross-sectional images of arterial lumens (n = 50) were obtained before stenting, in-vitro (n = 35) from formalin-preserved human superficial femoral arteries and in-vivo (n = 15) from canine iliac arteries containing laser-induced eccentric stenoses. Comparison of ultrasound-derived vessel dimensions (minimum and maximum diameter and cross-sectional area) with histological morphometric analysis of corresponding vessel sites showed good correlation by linear regression analysis (r = 0.930-0.987, p = 0.001-0.005). Following stent placement, 23 intraluminal ultrasound images were obtained from the stented vessel sites (in-vitro n = 15, in-vivo n = 8) and were compared to prestented cross-sectional areas. In the in-vitro vessels there was a small increase (p = 0.023) in area, but there was no change in the in-vivo arteries (p = 0.6). To assess the effect of stenting on luminal shape (ellipticity), minimum/maximum diameter ratios were compared before and after stent deployment. There was an increase in this ratio in the in-vitro vessels (p = 0.001) but no change in the in-vivo arteries (p = 0.2). We conclude that intraluminal ultrasound produces clear and accurate images of the location, shape and degree of arterial pathology, ensuring good stent: vessel size matching and immediate quantitative assessment of the effects of arterial stent placement.

Coronary artery stenting after angioplasty with self-expanding parallel wire metallic stents

Parallel wire stents were implanted over exchange guide wires at percutaneous transluminal coronary angioplasty sites in 27 canine coronary arteries that were predilated with slightly oversized balloons. Stents were stainless steel, self-expandable, 3.5 to 4.5 mm in diameter, 9 to 12 mm in length, and were made of 10 wires that were longitudinally laser-welded in a zig-zag design. The compressible stent was delivered by the withdrawal of a Teflon outer catheter (4.2 to 4.9F) and the push of a polyethylene inner catheter. Aspirin, 80 mg per day, was given from the day before the study began, and heparin (150 U/kg) was administered during implantation. Quantitative angiography and pathologic examinations were performed at day 0 and at weeks 2, 4, 12, 26 and 52. The coronary angiographic diameter at the stent site immediately after stenting marginally increased from diameter before stenting: 3.22 ± 0.40 mm versus 3.14 ± 0.37 mm ( p = 0.03), and during a mean of 14 weeks of follow-up, remained unaltered from immediate poststenting: 3.29 ± 0.43 mm versus 3.22 ± 0.40 mm ( p = NS) with no stent displacement. Comparisons of patency and thrombosis between heparin-coated and uncoated stents, between left anterior descending and circumflex arteries, and among the three different diameters of stents showed uniformly good results. At microscopy, the wires were oriented perfectly and embedded in the arterial wall, and by 2 weeks they were covered by mucopolysaccharide ground substance, smooth muscle cells, and an almost complete monolayer of neoendothelial cells. Scanning electron microscopy showed these cells to be large, immature, ovoid, and oriented with the blood flow; by 1 month they formed a complete mature neoendothelial covering with tight intercellular junctions. The neointima reached a peak thickness of 200 ± 132 μm at 6 months. Thus this stent that was implanted after angioplasty showed good long-term patency, stability, and tolerability with low thrombogenicity; it appears promising for application to humans.

Thrombogenicity of metallic vascular stents in arteries and veins—An experimental study in pigs

Endovascular expanding metallic stents were percutaneously implanted in the iliac arteries and veins of pigs. The vessels had been stenosed by a ligature of catgut 4 weeks prior to this. Platelets were labeled with Indium 111 and the deposition onto the dilated and stented areas was dynamically registered for 240 min with a scintillation camera. All six arterial and six venous stents remained patent throughout the examination period. At the site of arterial stenting there was an increase, of deposited activity, and in the veins a decrease. These experimental findings support the use of endovascular stents after dilation, especially in venous stenoses.

Adjuvant therapy for intracoronary stents. Investigations in atherosclerotic swine.

Early thrombosis has complicated human stent implantation in several trials. To determine the best anticoagulation/antiplatelet therapy to maintain stent patency after percutaneous transluminal coronary angioplasty, we implanted the flexible balloon-expandable coil stent into the left anterior descending coronary artery of 28 atherosclerotic 8-month-old Hanford miniature swine. Animals were randomly assigned to one of three treatment groups: group A, aspirin (1 mg/kg/day) and dipyridamole (1 mg/kg three times a day); group B, aspirin and dipyridamole (same doses) plus Coumadin (dose required to prolong prothrombin time 1.3-1.5-fold that of normal); and group C, control. Adjuvant therapy was begun 3 days before stenting. Two pigs (one from group A and one from group B) died during implantation, both without thrombosis. Twenty-six animals survived until follow-up angiography and sacrifice at 1 month. No occlusive thrombosis of the stent occurred in survivors. Reduction of the stent lumen diameter was observed in every case at follow-up. Percent lumen reduction was 19% in group A, 26% in group B, and 24% in group C. Marked smooth muscle cell hyperplasia was seen by light and transmission electron microscopy at stent struts. Scanning electron microscopy of the luminal surface showed a variable morphology consisting of normal endothelium, adherent leukocytes, stellate periluminal cells, and occasional fibrin strands and red blood cells. Luminal narrowing was not affected by anticoagulation therapy, antiplatelet drugs, cholesterol level, or stent sizing. We conclude that occlusive thrombosis does not complicate stent implantation in this model but that substantial luminal narrowing due in part to smooth muscle hyperplasia does occur. The significance of luminal narrowing at the stent site requires further study.

Angiographic and Histologic Course after Implantation of Balloon Expandable Intravascular Stents in Miniswine Coronary Arteries: Short‐ and Mid‐Term Observations

Sixteen balloon expandable Medtronic Wiktor tantalum stents were implanted in the major coronary arteries of six minipigs, which were maintained on a normal diet and given 500 mg aspirin per day. Angiographic and histologic examinations were performed 6 and 26 weeks after implantation. Angiographically reviewed, stenting increased the inner diameter of the coronary arteries from 2.61 ± 0.44 to 3.02 ± 0.34 mm (n = 16, P ≤ 0.001). Six weeks later, this value was reduced from 2.98 ± 0.35 to 2.33 ± 0.46 mm (n = 9, P ≤ 0.05), and between 6 and 26 weeks, an increase from 2.17 ± 0.44 to 2.93 ± 0.40 mm occurred (n = 6, P ≤ 0.05). Histologic evaluation at 26 weeks after stent implantation revealed an increase of the cross‐sectional area of the total vessel from 4.30 ± 1.09 to 5.50 ± 1.67 mm2 (n = 9; P ≤ 0.01). This was due to widening of the total vessel and intimal proliferation, which amounted to 1.19 ± 0.46 mm2 within the stented segment, as compared to 0.03 ± 0.03 mm2 in control sections (P ≤ 0.01). The areas of free vessel lumen, media muscularis, and adventitia remained unchanged. In 15 of the 16 hislologically examined coronary arteries, the internal elastica was fractured at the site of stent implantation. Twelve stents had also penetrated through the external elastica without evidence of wall hemorrhage. Thirteen out of 16 stents were angiographically followed, of which 12 were patent at the final reangiography. In one animal, acute thrombosis of the stented vessel after guidewire induced coronary artery spasm caused chronic right heart failure due to right ventricular myocardial infarction. Sudden death occurred in another pig 2 hours after successful implantation of three grossly oversized stents (inner vessel diameter: 2.4 ± 0.2 mm, stent diameter 3.2 ± 0.5 mm). Autopsy revealed extensive dissections of the media with subsequent vessel occlusion. It is concluded that Medtronic Wiktor stents can be placed easily, even in more distal or curved coronary arteries. Despite antiaggregational medication, intimal proliferation is observed early after implantation, reaches a maximum at about 6 weeks, and is followed by a regression 26 weeks poststenting. At 26 weeks follow‐up, the free vessel lumen at the stent site was not significantly reduced as compared to control segments. Proper adjustment of internal vessel diameter and stent diameter is necessary to prevent major dissections and thrombotic occlusions.

Mechanical properties of arteries

Mechanical properties of arteries