(Circulation. 1997;95:363-370.)
© 1997 American Heart Association, Inc.
Articles |
Serial Follow-up After Optimized Ultrasound-Guided Deployment of Palmaz-Schatz Stents
In-Stent Neointimal Proliferation Without Significant Reference Segment Response
the Department of Medicine, Division of Cardiology, Klinikum Innenstadt, University of Munich, Germany.
Correspondence to Priv-Doz Dr med Harald Mudra, Medizinische Klinik, Klinikum Innenstadt, Ziemssenstrasse 1, D-80336 Muenchen, Germany.
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Abstract |
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Background The effects of ultrasound-guided high-pressure stenting on late stent and reference segment dimensions are unknown. In this study, we report about angiographic and ultrasound measurements to assess the amount and distribution of neointimal ingrowth within the stent and the changes of plaque burden and dimensions within the reference segments.
Methods and Results Sixty-eight consecutive patients with 72 lesions received single or multiple Palmaz-Schatz coronary stents with a standardized protocol for stent optimization under ultrasound guidance. The residual angiographic diameter stenosis was 3±12% (reference diameter, 3.16±0.61 mm). At follow-up 4.8±2.5 months later, angiography revealed a diameter stenosis of 27±21% with a restenosis rate of 15.3% (confidence interval: 7.8% to 25.6%). Lumen renarrowing within the stent was exclusively due to neointimal ingrowth; no stent compression was observed. The neointima covered 20±20% of the stent area and was more pronounced in the midportion of the stent. Volumetric assessment performed in 26 patients resulted in 13±14% or 65±28% of the stent volume occupied by neointimal ingrowth in patients without or with restenosis, respectively. Vessel remodeling had an impact on lumen dimensions only at reference sites but not within the stent. Plaque burden of 46±11% and 48±11% at the proximal and distal reference sites, respectively, did not show a relevant progression during the follow-up.
Conclusions Serial ultrasound analyses did not show any evidence of stent compression or relevant vessel remodeling. Restenosis was solely due to neointimal ingrowth. Despite a considerable plaque burden within the reference segments, there was no relevant progression of the disease adjacent to the stent.
Key Words: ultrasonics • stents • angioplasty • angiography • restenosis
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Introduction |
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Tissue ingrowth and possibly stent compression are discussed as predominant mechanisms for stent restenoses in the long-term follow-up.1 Little is known, however, about the effects of high-pressure stenting on the extent and spatial distribution of neointimal ingrowth within and adjacent to the stent as well as on late stent dimensions. Intravascular ultrasound (IVUS) is a relatively new clinical tool to assess the delicate interaction between the stent and the vessel wall that cannot be seen in coronary angiography, and it allows precise guidance for stent optimization.2 3 Moreover, IVUS, unlike coronary angiography, can also depict the vessel wall and therefore currently is the only tool to assess the amount and composition of plaque burden4 5 6 7 as well as changes in vessel geometry over time.8 9 10
The purpose of the present study was to compare immediate and long-term angiographic and ultrasound results after ultrasound-guided optimal stent deployment in a consecutive series of patients. We wanted to determine the mechanism of restenosis, assess the amount and distribution of neointimal ingrowth, and measure the reference segment response after IVUS-guided high-pressure stenting with respect to cross-sectional area changes of total vessel, lumen, and plaque adjacent to the stent.
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Methods |
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Patients
We prospectively studied 80 patients aged 37 to 88 years (mean age, 61 years) after successful IVUS-guided placement of Palmaz-Schatz coronary stents (Johnson and Johnson Interventional Systems) in 84 lesions between February 1994 and April 1995. All patients had given written informed consent for the implantation procedure and the follow-up investigation. The 80 patients represented a consecutive series of IVUS-guided Palmaz-Schatz stenting procedures, while 85 other patients with successful stent implantation during the same time at our institution were not eligible for the present study either because they had received a different stent type, no IVUS study was performed, or they had not yet completed the follow-up. Twelve patients were excluded from analysis because of technical shortcomings or the use of different ultrasound equipment during the follow-up investigation. Therefore, 68 patients with a total of 72 stented lesions were enrolled in the present study.
Indications, Stents, Implantation Technique, and Adjunctive Therapy
The indications for stent deployment were acute vessel closure in 5 lesions (7%), dissection and/or suboptimal result in 18 (25%), or elective in 49 (68%, with 29 restenoses). A total of 88 Palmaz-Schatz stents (mean, 1.2±0.5 stents/lesion) were used: 45 15-mm standard stents with a central articulation, 2 new 18-mm and 25 new 14-mm stents with a double-spiral articulation, 10 half (7-mm) standard stents, and 6 new 8-mm stents. Fifty-eight lesions were covered by a single stent and 14 by 2 to 3 serial overlapping stents. The stented lesion was located within one of the main native coronary arteries in 53 cases or in a venous graft in 19 (Table 1
). All target vessels allowed at least a 3.0-mm balloon diameter for stent placement. After predilation, the stents were manually crimped on the same balloon catheter and expanded until an angiographically optimal result had been achieved (ie, visual diameter stenosis <10%). IVUS was then performed to assess the diameters of both the reference segments and the stent. Redilations with higher pressure up to 22 atm and/or a larger balloon diameter were performed if necessary (Table 2) to reach an optimal stent expansion as described elsewhere.3 For vessels with a lumen area of >9 mm2, criteria for optimal stent expansion were similar to those used in the MUSIC study11 (see "Appendix"). Short (9-mm) balloons were used in 34 (47%) of the lesions. In 21 patients, the first IVUS analysis was performed before stent placement to assess lesion composition and dimensions. All patients were receiving long-term treatment with low-dose aspirin (100 mg/d) and antianginal therapy. Before stent delivery, unfractionated heparin (10 000 to 20 000 IU) was given intravenously to maintain an activated clotting time >300 seconds. Forty-four patients met the IVUS criteria of optimal stent expansion and continued taking low-dose aspirin intake as their only antithrombotic therapy. The remaining 24 patients received a combination of low-dose aspirin and either ticlopidine (500 mg/d) or coumadin for 4 to 8 weeks.
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Follow-up Protocol
All patients in the present study were seen in the outpatient department of our institution 4 to 6 weeks after stent placement and were scheduled for repeat coronary angiography at 6 months after stent placement or earlier if symptoms or exercise tolerance tests suggested restenosis. The control angiogram was performed in all 68 patients at a mean of 4.8±2.5 months after the initial procedure.
Angiography and Analysis
Initial and follow-up angiograms were performed in multiple biplane projections with the use of 8F guiding catheters after intracoronary injections of 0.25 mg nitroglycerin. All projections of the initial angiography were repeated at follow-up. From technically suitable angiograms, the optimal views of the stented lesion were digitized (MediaGrabber, RasterOps Corp) with an image resolution of 640x480 pixels. Qualitative analysis of baseline angiograms was performed with respect to lesion type and type of dissection after predilation according to AHA/ACC classifications.12 Computerized quantitative analysis was performed according to previously described and validated edge-detection algorithms, with the guiding catheter taken as reference.13 Quantitative measurements included the proximal and distal diameters of the reference, giving the mean reference diameter, the minimal lumen diameter, and the length of the lesion. Immediately after optimization of the stent and at follow-up, the minimal stent lumen diameter and the reference lumen diameters were measured and diameter stenosis was calculated with the use of the view that showed the most severe lumen narrowing. Furthermore, acute lumen gain (final minimal diameter after stent optimization minus minimal lesion diameter), late lumen loss (final minimal stent lumen diameter minus follow-up minimal lumen diameter), net lumen gain (acute lumen gain minus late lumen loss), and loss index (late lumen loss/acute lumen gain) were calculated.
IVUS Procedure and Analysis
Every IVUS investigation within a single patient was performed with the use of the same IVUS system at baseline and at follow-up. Twelve patients with 14 lesions were studied with the use of an electronic system with a 3.5F catheter operating on a frequency of 20 MHz (Endosonics Corp). In 56 patients with 58 lesions, a mechanical system (Vingmed Corp) with a 30-MHz probe mounted on a 2.9F common sheath catheter (Cardiovascular Imaging Systems Inc) was used. After the patient was given an intracoronary injection of 0.25 mg nitroglycerin, the IVUS catheter was introduced into the coronary artery distal to the stented segment. Under continuous video registration (S-VHS, Panasonic 7330-E, Matsushita Electric Inc), a slow manual pullback was performed by the same operator (H.M.) from a distinct landmark through the entire stented lesion back to the guiding catheter. All 56 IVUS studies with the mechanical system at follow-up as well as 26 baseline studies were performed with the use of a motorized pullback system (Cardiovascular Imaging Systems Inc) at a speed of 0.5 mm/s. After every procedure, the imaging catheter was tested for correct distance calibration by imaging cylindrical phantoms with an internal diameter of 2.0 to 5.0 mm.
IVUS images of optimal quality that showed a central and coaxial position of the probe from the proximal and distal references 1 to 3 mm apart from the stent ends by use of reproducible landmarks such as calcium spots or side branches and taken from three to five distinct locations within the stent (Fig 1) were digitized off-line (MediaGrabber, RasterOps Corp).
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Qualitative Analysis
Plaques were characterized according to their acoustic properties. Type A plaques showed attenuation of the ultrasound signal within at least 45° of the vessel circumference, whereas type B plaques did not show these characteristics.
Quantitative Measurements
The reproducibility of IVUS measurements within coronary stents has been previously published for use of the electronic system.3 For the mechanical system predominantly used in the present study, reproducibility between repetitive IVUS pullbacks was additionally tested for vessel area, stent area, and lumen area determination at 40 randomly chosen corresponding sites. The absolute and relative differences (mean±SD) between two consecutive measurements for vessel area, stent area, and lumen area were 1.4±1.2, 0.7±0.6, and 1.2±1.2 mm2 and 6.9±7.0%, 5.7±5.7%, and 10.2±9.7%, with correlation coefficient values of .94, .95, and .91, respectively.
The minimal lumen area, minimal stent area, and vessel area (within the medial to adventitial border) were traced in each frame and calculated by use of a commercially available software program for IVUS measurements (TapeMeasure, Indec Systems Inc). Residual plaque burden was calculated as vessel area minus lumen area. Neointimal ingrowth was defined as echogenic material within the stent at follow-up and assessed with respect to maximal thickness and absolute as well as relative area (stent area minus lumen area and stent area minus lumen areax100/stent area, respectively) at the tightest stent site and all other sites interrogated at baseline. From corresponding baseline and follow-up frames, the following parameters were determined for the stented and the reference segments: lumen loss (minimal stent or lumen area at baseline minus minimal lumen area at follow-up), stent compression (stent area at baseline minus stent area at follow-upx100/stent area at baseline), chronic vessel recoil (vessel area at baseline minus vessel area at follow-upx100/vessel area at baseline), and plaque area change [(vessel area minus lumen area at follow-up) minus (vessel area minus lumen area at baseline)]. In patients who showed a minimal lumen diameter at follow-up less than the diameter and ring-down artifact of the echo probe, the calculations of neointimal hyperplasia were based on the angiographically determined lumen diameter, assuming a circular residual lumen shape. In the 26 lesions investigated twice with a motorized pullback, an end-diastolic image was digitized every 2 seconds from the distal to the proximal reference segments throughout the stent, representing 1 mm of lesion length. In each of these sequential images, lumen and stent areas were traced and volumetric measurements of stent volume and neointimal ingrowth (stent volume minus lumen volume) were assessed by application of Simpson's rule.
Definition and Analysis of Restenosis
A stent was considered restenotic if the angiographic lumen diameter reduction at follow-up was >50% of the mean reference diameter or if the ultrasound analysis showed a minimal lumen area within the stent <25% of the mean reference segment lumen area assessed 3 to 5 mm away from the stent margins. A diffuse restenosis was defined as a lumen narrowing according to these angiographic or ultrasound criteria encompassing >50% of the stent length, while shorter restenoses were defined as focal.
Statistical Analysis
Values are reported as mean±SD. Statistical analyses were performed with a commercially available software program (StatView 4.02, Abacus Concepts Inc). Correlations between repetitive ultrasound or angiographic measurements were tested by linear regression analysis for two variables. Intraindividual comparisons were made by use of the paired t test. For unpaired variables, a Mann-Whitney U test was performed. A difference was considered significant with a two-sided probability value <.05.
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Results |
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There were no procedural complications except two side-branch occlusions during stent optimization followed by a mild enzyme elevation with no changes in the ECG. No stent thrombosis was observed.
Angiographic Analysis
The majority of the lesions were types B and C (Table 1
), and the mean lesion length was 10.6±6.2 mm. No dissections were present at the time of the final angiogram. The quantitative angiographic and procedural data are given in Table 2. At follow-up, a lumen diameter stenosis 
50% was seen in 11 of the stented lesions, resulting in a restenosis rate of 15.3% (CI, 7.8% to 25.6%).
IVUS Analysis
Qualitative Assessment at Baseline
Lesion morphology was assessed in 21 lesions (29%) before stent deployment; in the remaining cases, this was achieved during the first IVUS analysis after stent placement. The plaque type at the tightest lesion site could be assessed in 66 (92%) of the 72 lesions. In 22 (33%) of these lesions, a type A plaque was found; in 44 lesions (67%), a type B plaque was found.
The vessel area could be assessed in 113 (84%) of the 134 reference segments and in 93 (40%) of 232 analyzed sites within the stent, while in the remaining sites, distal shadowing due to stent filaments and/or calcium precluded a sufficient tracing of the inner adventitial contour.
At the final IVUS analysis, all stents were properly attached to the vessel wall over their entire length. There was no evidence of plaque prolapse within or adjacent to the stent.
Quantitative Analysis at Baseline
The lumen area at the proximal and distal reference sites was 11.4±3.7 and 9.8±3.9 mm2, respectively. Within the stent, the lumen area at the tightest site was 8.4±2.9 mm2. The average lumen area of all analyzed stent sites was 9.5±3.0 mm2. This resulted in a residual maximal and averaged area stenosis of 15±14% and 7±15%, respectively. The vessel area of the proximal and distal reference sites was 21.7±5.8 and 20.0±7.4 mm2, respectively. The corresponding mean plaque areas occupied 46±11% and 48±11% of the vessel area, respectively. The mean vessel area within the stent was 23.4±5.9 mm2 and 23.0±7.5 mm2 at the tightest in-stent site. The area encompassed by the residual plaque covered 54±8% of the vessel area on average (Table 3). At the tightest stent site, the plaque burden was significantly higher than at all other stent sites (58±10% versus 53±8%; P=.0087). Type B lesions showed a smaller residual mean plaque area within the stent than type A plaques (P=.0242) but no difference of the residual area stenosis (Table 4).
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Qualitative Assessment at Follow-up
At follow-up, echogenic material within the stent representing neointimal ingrowth could be clearly identified to various degrees within every stented lesion. In four lesions with severe diffuse in-stent restenosis, the diameter of the imaging catheter was larger than the residual lumen diameter, thus precluding a precise ultrasound measurement of the neointimal mass. The neointimal material showed a great variability with regard to its spatial distribution within the circumference of the stent and its thickness within each stent cross section.
Quantitative Analysis at Follow-up
The lumen area of the distal reference segments remained unchanged at follow-up, whereas the proximal reference showed a slight decrease (Table 4). The intraindividual changes of reference lumen area did not correlate with the corresponding plaque burden at baseline, but type B plaques demonstrated a larger lumen loss than type A plaques (P=.0430) (Table 4). The average and minimal lumen areas within the stent had significantly decreased to 7.8±3.5 and 7.1±3.6 mm2, respectively (Table 3). This corresponded to a maximal and average late lumen area loss of 1.8±2.3 and 1.6±2.0 mm2, respectively, with a trend, albeit nonsignificant, toward a larger lumen loss in type B lesions (Table 4). Nine lesions showed a restenosis according to IVUS criteria, with a diffuse pattern in six stents and a focal pattern in three stents (two mid and one proximal). The stent area at all analyzed sites was not significantly different from the baseline value. The measured differences between baseline and follow-up demonstrated a normal distribution around zero (Fig 2A). The vessel size of the reference and stent sites remained within the twofold interstudy variability of ±15% in most stented segments. In 7% of the reference sites and in 6% of the stent sites, the vessel size showed a decrease >15%. A >15% increase was present in 17% of the reference sites and in 15% of the stent sites (Fig 2B and 2C). A change in vessel size correlated with a parallel lumen area change only at the reference sites (r=.64, P<.0001) but not within the stent. The neointimal ingrowth had a maximal thickness of 0.6±0.7 mm and covered an area of 2.5±2.4 mm2, reaching up to 1.6 mm or 11.3 mm2 in patients with significant restenosis. The neointimal ingrowth covered 20±20% of the stent area on average and 26±25% at the tightest stent site (Table 5). The late lumen area loss and neointimal area were strongly correlated (y=0.56+0.88x; r=.94). The neointimal ingrowth was most pronounced in the midsection of the stent, as were the absolute and relative changes in plaque area (Table 5). Regions of stent overlap in multiple stents did not show a more pronounced neointimal ingrowth. Compared with the spiral-bridged Palmaz-Schatz stent, articulated 15-mm stents did not show a significantly smaller minimal lumen area at follow-up despite a smaller acute minimal stent area. Accordingly, late lumen loss and neointimal area were larger in the midsection of the nonarticulated stent despite comparable balloon size and inflation pressure used during stent optimization (Table 6). Restenotic stents did not show a smaller stent area than stents without restenosis (Table 7). The absolute and relative changes in plaque area did not significantly correlate with the lesion type or with the residual plaque area at baseline.
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Volumetric IVUS Results
In the 26 lesions that were assessed with motorized pullback both at baseline and at follow-up, stent volume did not decrease. In-stent lumen volume, however, decreased from 138±32 to 124±40 mm3 in patients without restenosis and to 43±31 mm3 in patients with restenosis due to neointimal ingrowth, resulting in a 65±28% reduction of lumen volume due to neointimal ingrowth (Table 8). The middle third of the stented segment showed a trend toward a more pronounced neointima formation than the proximal and distal thirds of the stent.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix References |
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This follow-up study in 68 consecutive patients undergoing IVUS-guided stenting demonstrates the mechanisms and extent of lumen renarrowing within Palmaz-Schatz stents and the late response of the adjacent reference segments. Our results show that restenosis of Palmaz-Schatz stents is exclusively due to neointimal ingrowth, which is most pronounced in the middle portion of the stent, and not to stent compression. The adjacent reference segments not covered by the stent did not show a clinically relevant change in lumen dimensions or a change in total vessel area in the majority of the lesions despite application of high balloon pressures.
Angiographic Results
IVUS guidance of stent optimization resulted in an angiographic residual lumen diameter stenosis of 3±12% and is comparable to the latest studies published by Colombo et al14 and Hall et al,15 which show a mean residual diameter stenosis of 0±14% and 1±10% achieved with comparable definition of IVUS criteria for optimal stent deployment. Although the present study includes only a relatively small number of consecutive patients, the restenosis rate of 15.3% appears remarkably low, particularly when considering the fact that 40% of all patients presented with restenosis as the primary stent indication. These data compare favorably with the results of the STRESS and BENESTENT studies16 17 and are comparable to the 19% restenosis rate in another series after IVUS-guided stenting.18 This might be the result of achieving a maximal acute lumen gain through IVUS-guided stenting. This concept was previously introduced by Kuntz and colleagues19 20 for angioplasty in general and is currently the only clinically available approach to enhance late lumen dimensions, because effective methods to reduce tissue proliferation within the stent are still under investigation. Despite the given correlation between acute gain and late loss,20 the mean late lumen loss in this series with enhanced initial gain is only slightly higher than in the STRESS and BENESTENT studies, resulting in a higher net gain and a lower loss index.
Ultrasound Assessment Within the Stent
The stent expansion achieved by the use of IVUS guidance led to a mean area stenosis of 7%, reaching up to 15% at the tightest stent site. The acutely achieved stent expansion remained unchanged during follow-up at each stent site, indicating a lack of any significant stent compression as shown in previous angiographic and ultrasound studies.1 21 22 A change in vessel area within the stent occurred in 
20% of the analyzed sites, with no correlation to the corresponding lumen area. This shows that vessel remodeling in the stented segment does not affect the lumen. Neointimal ingrowth represented the only relevant mechanism of in-stent restenosis in this series of patients. This result is in accordance with the results of animal studies showing an exaggerated intimal hyperplasia after stenting in the pig model23 24 and with previous clinical observations.1 21 22 25 Despite a large variability in the spatial distribution and amount of neointimal formation, there was a strong correlation between late lumen loss and neointimal area. The volumetric assessment showed a 20% reduction in stent lumen volume by neointimal ingrowth. This result in a nonselected consecutive series of patients compares favorably with the results of the Washington Center group, which showed a 20% reduction in patients without restenosis and 48% in patients with restenosis, and may be due to the larger relative stent expansion achieved in our series (93% versus 77%).22 Regardless of the stent type (articulated or nonarticulated), the site with the largest lumen loss due to neointimal formation was located in the midportion of the stent. This finding has been reported before for articulated Palmaz-Schatz stents.26 The articulation site, with its lack of mechanical support and more severe injury to the intima, was thought to be the main cause of excess neointima formation.26 Our results, however, suggest that other, more lesion-specific factors, such as enhanced cellular proliferation at the center of the target lesion, are responsible for this overly proportional neointimal ingrowth. The observed trend toward a lower intimal proliferation in type A lesions also suggests a relation between plaque characteristics and the degree of cellular proliferation response after stenting.
Ultrasound Assessment of the Reference Segments
The response of the adjacent reference segments not covered by the stent is of major interest because high-pressure dilation in this region may lead not only to acute dissections but also to severe barotrauma, triggering a cellular hyperplastic reaction.23 24 27 A major advantage of ultrasound guidance during stent optimization consists in the detailed knowledge it provides of the true vessel dimensions and plaque burden adjacent to the stent, which allows a precise sizing of the balloon used for high-pressure inflations.2 3 This appears to be the reason that dissections outside the stent could be avoided in this series. Moreover, the minimal late lumen loss found in this series only within the proximal reference segments, which paralleled a slight increase of plaque area, may be interpreted as the result of a less traumatic high-pressure dilation strategy. These observations have interesting clinical implications, because it is still not known to which vessel region the stent covering should ideally be extended to minimize the risk of restenosis. Despite an average plaque burden of 47% within the reference segments, without angiographic evidence of lumen narrowing reflecting the Glagov effect,28 there was no evidence for a significant progression of the disease during the follow-up period.
Limitations of the Study
The relatively small number of patients eligible for analysis in this study may render it difficult to generalize the results and to apply them to other patient populations with possibly different lesion characteristics, eg, smaller target vessels. However, this study represents a consecutive series of patients treated with a standardized protocol of IVUS guidance according to the criteria used in the MUSIC study.11 Only a limited number of cross sections within the stented segment, ie, the proximal, medial, and distal stents, could be analyzed serially because not all patients were investigated with a motorized pullback system at baseline and at follow-up. Because the volumetric assessment performed on those patients analyzed twice by means of a motorized pullback shows similar results compared with the general study population, it seems unlikely that the analysis of more in-stent sites would have led to different results. The mode of lesion classification used in this study also represents a limitation because it was performed in most patients after stent placement, which may have altered the echo reflectiveness of the compressed plaque material. For this reason, a crude classification of plaques was used that was based solely on the presence or absence of shadowing of the ultrasound beam. An a priori analysis of every lesion before stent placement would allow a better understanding of specific lesion differences during stent placement.
Conclusions
The results of this study of a consecutive series of patients undergoing IVUS-guided stenting clearly show that in-stent restenosis is exclusively due to neointimal ingrowth and not to stent compression. Furthermore, different stent designs (articulated or nonarticulated Palmaz-Schatz stents) did not cause different lumen dimensions at follow-up. Despite the application of high-pressure balloon inflations generally involving the reference segments with a plaque burden at baseline of nearly 50% of the vessel area, there was no relevant change of reference lumen dimensions at follow-up. This result may be of clinical relevance for the definition of optimal stent length.
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Appendix |
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An optimal stent expansion was defined as follows:
1. Complete apposition of the stent against the vessel wall.
2. Minimal in-stent lumen area 90% of the averaged reference lumen area or 100% of the smaller reference lumen area. In stents with a minimal lumen area 9.0 mm2, this parameter had to be 80% of the averaged reference lumen area or 90% of the smaller reference lumen area.
3. Lumen area at the proximal stent entrance 90% of the proximal reference lumen area.
Received June 25, 1996; revision received August 22, 1996; accepted August 31, 1996.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix References |
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1. Gordon PC, Gibson CM, Cohen DJ, Carozza JP, Kuntz RE, Baim DS. Mechanisms of restenosis and redilatation within coronary stents: quantitative coronary assessment. J Am Coll Cardiol. 1993;21:1166-1174.[Abstract]
2.
Nakamura S, Colombo A, Gaglione A, Almagor Y, Goldberg SL, Maiello L, Finci L, Tobis JM. Intracoronary ultrasound observations during stent implantation. Circulation. 1994;89:2026-2034.
3.
Mudra H, Klauss V, Blasini R, Kroetz M, Rieber J, Regar E, Theisen K. Ultrasound guidance of Palmaz-Schatz intracoronary stenting with a combined intravascular ultrasound balloon catheter. Circulation. 1994;90:1252-1261.
4.
Waller BF, Pinkerton CA, Slack JD. Intravascular ultrasound: a histological study of vessels during life—the new `gold standard' for vascular imaging. Circulation. 1992;85:2305-2310.
5.
Yock PG, Linker DT. Intravascular ultrasound: looking below the surface of vascular disease [comment]. Circulation. 1990;81:1715-1718.
6.
Nissen SE, Gurley JC, Grines CL, Booth DC, McClure R, Berk M, Fischer C, De Maria AN. Intravascular ultrasound assessment of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation. 1991;84:1087-1099.
7.
Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF, Chuang YC, Ditrano CJ, Leon MB. Patterns of calcification in coronary artery disease. Circulation. 1995;91:1959-1965.
8. Blasini R, Mudra H, Klauss V, Regar E, Schomig A. Remodelling of coronary arteries after balloon angioplasty: in vivo determination in patients using intravascular ultrasound. J Am Coll Cardiol. 1995;25:139A. Abstract.
9. Kimura T, Kaburagi S, Tashima Y, Nobuyoshi M, Mintz GS, Popma J. Geometric remodeling and intimal regrowth as mechanisms of restenosis: observations from Serial Ultrasound analysis of REstenosis (SURE) trial. Circulation. 1995;92(suppl I):I-76. Abstract.
10. Mintz GS, Pichard AD, Kent KM, Satler LF, Popma JJ, Wong SC, Painter JA, DeForty D, Leon MB. Endovascular stents reduce restenosis by eliminating geometric arterial remodeling: a serial intravascular ultrasound study. J Am Coll Cardiol. 1995;25:36A. Abstract.
11. DeJaegere P, Mudra H, Almagor Y, Figulla H, Penn I, Doucet S, Bartorelli A, Hamm C, for the MUSIC Investigators. In-hospital and 1-month clinical results of an international study testing the concept of IVUS guided optimized stent expansion alleviating the need of systemic anticoagulation. J Am Coll Cardiol. 1996;27:137A. Abstract.
12.
Dorros G, Cowley MJ, Simpson J. Percutaneous transluminal coronary angioplasty: report of complications from the National Heart, Lung, and Blood Institute PTCA registry. Circulation. 1983;67:723-730.
13.
Kastrati A, Schomig A, Dietz R, Neumann FJ, Richardt G. Time course of restenosis during the first year after emergency coronary stenting. Circulation. 1993;87:1498-1505.
14.
Colombo A, Hall P, Nakamura S, Almagor Y, Maiello L, Martini G, Gaglione A, Goldberg SL, Tobis JM. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation. 1995;91:1676-1688.
15. Hall P, Colombo A, Almagor Y, Maiello L, Martini G, Tobis JM. Preliminary experience with intravascular ultrasound guided Palmaz-Schatz stenting: the acute and short term results on a consecutive series of patients. J Intervent Cardiol. 1996;7:141-159.
16.
Serruys PW, De Jaegere P, Kiemeneij F, Macaya C, Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P, Belardi J, Sigwart U, Colombo A, Goy JJ, Van Den Heuvel P, Delcan J, Morel MA. A comparison of balloon-expandable stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994;331:489-495.
17.
Fishman DL, Leon MB, Baim DS, Schatz RA, Savage MP, Penn I, Detre K, Veltri S, Ricci D, Nobuyoshi M, Cleman M, Heuser R, Almond D, Teirstein PS, Fish RD, Colombo A, Brinker J, Moses J, Shaknovich A, Hirshfeld J, Bailey S, Ellis S, Rake R, Goldberg S. A randomized comparison of coronary stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331:496-501.
18. Nakamura S, Hall P, Blengino S, Maiello L, Colombo A. Does focal overstretch increase restenosis? Ultrasound evaluation after Palmaz-Schatz coronary stent deployment. Circulation. 1994;90(suppl I):I-23. Abstract.
19. Kuntz RE, Safian RD, Levine MJ, Reis GJ, Diver DJ, Baim DS. Novel approach to the analysis of restenosis after the use of three new coronary devices. J Am Coll Cardiol. 1992;19:1493-1499.[Abstract]
20. Kuntz RE, Gibson CM, Nobuyoshi M, Baim DS. Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. J Am Coll Cardiol. 1993;21:15-25.[Abstract]
21. Klauss V, Blasini R, Regar E, Rieber J, Konig A, Mudra H. Mechanism of coronary in-stent restenosis: neointimal proliferation or stent compression? Serial assessment by intravascular ultrasound. Circulation. 1993;88(suppl I):I-598. Abstract.
22. Dussaillant GR, Mintz GS, Pichard AD, Kent KM, Satler LF, Popma JJ, Wong SC, Leon MB. Small stent size and intimal hyperplasia contribute to restenosis: a volumetric intravascular ultrasound analysis. J Am Coll Cardiol. 1995;26:720-724.[Abstract]
23. Schwartz RS, Huber KC, Murphy JG, Edwards WD, Camrud AR, Vlietstra RE, Holmes DR. Restenosis and the proportional neointimal response to coronary artery injury: results in a porcine model. J Am Coll Cardiol. 1992;19:267-274.[Abstract]
24. Karas SP, Gravanis MB, Santoian EC, Robinson KA, Anderberg KA, King SB. Coronary intimal proliferation after balloon injury and stenting in swine: an animal model of restenosis. J Am Coll Cardiol. 1992;20:467-474.[Abstract]
25. Mudra H, Blasini R, Regar E, Klauss V, Rieber J, Theisen K. Intravascular ultrasound assessment of the balloon-expandable Palmaz-Schatz coronary stent. Coron Artery Dis. 1993;4:791-799.[Medline] [Order article via Infotrieve]
26. Ikari Y, Hara K, Tamura T, Saeki F, Yamaguchi T. Luminal loss and site of restenosis after Palmaz-Schatz coronary stent implantation. Am J Cardiol. 1995;76:117-120.[Medline] [Order article via Infotrieve]
27. Muller DWM, Ellis SG, Topol EJ. Experimental model of coronary artery restenosis. J Am Coll Cardiol. 1992;19:418-432.[Abstract]
28. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987;316:1371-1375.[Abstract]
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|
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