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Incomplete Stent Apposition After Implantation of Paclitaxel-Eluting Stents or Bare Metal Stents

Insights From the Randomized TAXUS II Trial
and for the TAXUS II Study Group
Originally published 2005;111:900–905


Background— The clinical impact of late incomplete stent apposition (ISA) for drug-eluting stents is unknown. We sought to prospectively investigate the incidence and extent of ISA after the procedure and at 6-month follow-up of paclitaxel-eluting stents in comparison with bare metal stents (BMS) and survey the clinical significance of ISA over a period of 12 months.

Methods and Results— TAXUS II was a randomized, double-blind study with 536 patients in 2 consecutive cohorts comparing slow-release (SR; 131 patients) and moderate-release (MR; 135 patients) paclitaxel-eluting stents with BMS (270 patients). This intravascular ultrasound (IVUS) substudy included patients who underwent serial IVUS examination after the procedure and at 6 months (BMS, 240 patients; SR, 113; MR, 116). The qualitative and quantitative analyses of ISA were performed by an independent, blinded core laboratory. More than half of the instances of ISA observed after the procedure resolved at 6 months in all groups. No difference in the incidence of late-acquired ISA was observed among the 3 groups (BMS, 5.4%; SR, 8.0%; MR, 9.5%; P=0.306), with a similar ISA volume (BMS, 11.4 mm3; SR, 21.7 mm3; MR, 8.5 mm3; P=0.18). Late-acquired ISA was the result of an increase of vessel area without change in plaque behind the stent. Predictive factors of late-acquired ISA were lesion length, unstable angina, and absence of diabetes. No stent thrombosis occurred in the patients diagnosed with ISA over a period of 12 months.

Conclusions— The incidence and extent of late-acquired ISA are comparable in paclitaxel-eluting stents and BMS. ISA is a pure IVUS finding without clinical repercussions.

Although intravascular brachytherapy has been proved to be effective in preventing recurrent in-stent restenosis,1 potential issues such as late thrombosis,2 black holes,3 and late-acquired incomplete stent apposition (ISA)4 became evident with its wide clinical application. One retrospective intravascular ultrasound (IVUS) registry suggested that ISA at the time of procedure might be associated with subsequent stent thrombosis.5 Therefore, late-acquired ISA was postulated to contribute to late stent thrombosis after brachytherapy by providing a nidus for thrombus formation.6 However, there has been no prospective analysis to elucidate the clinical significance of late-acquired ISA.

Recently, sirolimus- and paclitaxel-eluting stents have been demonstrated to dramatically reduce restenosis rates.7,8 Despite these promising results, concerns remain that these drug-eluting stents may have the same potential risks as brachytherapy, with some similarities between the 2 technologies in antiproliferative effects on vascular smooth muscle cells and endothelial cells. The aims of this prospective IVUS analysis of the TAXUS II study were as follows: (1) to investigate the incidence of ISA after implantation of paclitaxel-eluting stents and compare it with that with bare metal stents (BMS), (2) to evaluate the extent of ISA quantitatively, and (3) to survey the clinical significance of ISA once the diagnosis has been made.


Patient Selection

Between June 2001 and January 2002, the TAXUS II trial enrolled 536 patients, who were randomized into 2 consecutive and independent cohorts.8 Patients in the first cohort received either the TAXUS-NIRx slow-release (SR) paclitaxel-eluting stent or the BMS. Those in the second cohort were randomized to either the TAXUS-NIRx moderate-release (MR) paclitaxel-eluting stent or the BMS. Patients were eligible if they had a single de novo lesion of a native coronary artery with an estimated stenosis between 50% and 99%, lesion length <12 mm, and vessel diameter between 3.0 and 3.5 mm. The current IVUS substudy included patients who underwent serial IVUS examination after the procedure and at 6-month follow-up. The ethics committees of all participating centers approved the study protocol. All patients gave written informed consent before enrollment. The primary result of this study was reported elsewhere.8

Study Device and Procedure

The study stent was the NIR Conformer stent (Boston Scientific Corp and Medinol Ltd). All stents were 15 mm long and 3.0 or 3.5 mm in diameter. The paclitaxel-eluting stent (TAXUS NIRx) was identical to the BMS, except that it was coated with a total load of 1.0 μg/mm2 of paclitaxel incorporated into a proprietary polymer (Translute) that provides controlled biphasic release. For both stents, the initial burst release over the first 48 hours after implantation is followed by a low-level release phase for approximately 10 days. The difference between the 2 stents is an 8-fold higher release rate in the initial burst of the TAXUS-MR stent compared with the TAXUS-SR stent.

Balloon predilatation was performed, followed by study stent implantation. Postdilatation was performed if necessary. Use of additional stents was permitted if patency of the stented vessel was compromised. The second stents were of the same type as originally assigned. The third stents could be of any type considered appropriate by the investigator, except for the study stents. However, this IVUS study excluded the patients who received stents other than the allocated stents. There were no objective angiographic or IVUS criteria for ensuring optimal stenting. All patients received a 300-mg loading dose of clopidogrel followed by clopidogrel 75 mg/d (or ticlopidine 250 mg twice daily) for 6 months and aspirin 75 mg/d indefinitely.

Clinical Follow-Up

Clinical status was assessed at hospital discharge and 1, 6, and 12 months after the procedure. The 6-month follow-up was an office visit together with angiographic and IVUS follow-up. The 12-month follow-up was an office visit or a phone call. The 12-month clinical follow-up was completed in 99% of patients in the first cohort and 98% in the second cohort.

IVUS Imaging and Visual Evaluation of ISA

Serial IVUS procedures were performed by use of an automated pullback at 0.5 mm/s. All IVUS procedures were recorded on VHS videotapes. ISA was defined as ≥1 strut clearly separated from the vessel wall, with evidence of blood speckling behind the stent struts without overlapping side branches.5,9 The determination of ISA was based on the consensus of 2 independent analysts blinded to the type of stent. ISA was classified into the following 3 groups on the basis of serial assessment: (1) resolved, ISA present after the procedure but no longer present at follow-up; (2) persistent, ISA present both after the procedure and follow-up; and (3) late-acquired, ISA not present at baseline but present at follow-up.

Quantitative IVUS Analysis

Quantitative IVUS analysis was performed by an independent core laboratory that continues to be blinded to treatment allocation (Cardialysis, Rotterdam, the Netherlands). In the stented segment, the lumen, stent, and external elastic membrane contours were detected by use of the CURAD QCU analysis software (Curad BV), applying 3D reconstruction, as described elsewhere.10 In the segment with ISA, the lumen contour was delineated outside the stent contour (Figure 1). The QCU software detected and calculated the fraction of the lumen area that lies outside of the stent, eg, ISA area. ISA is thus conceptually considered a part of a “functional” lumen. In the segment with ISA, mean vessel area (VA), mean stent area (SA), mean lumen area (LA), mean neointimal hyperplasia area (NIHA), mean ISA area (ISAA), maximal ISA area, and ISA volume were measured. Plaque behind the stent area (PBSA) was derived by VA − SA − ISAA (Figure 1).

Figure 1. 1-1, A and B, Cross-sectional and longitudinal IVUS images of a patient who has a segment with ISA at middle of a stent. Cross-sectional view (A) corresponds to “a” section of longitudinal view (B). C and D show images after contour detection is performed in A and B. Green, blue, and red lines indicate external elastic membrane (EEM) contour, stent contour, and lumen contour, respectively. ISA is recognized as area in which lumen contour is delineated outside stent. 1-2, Schematic diagram of contours and definitions. NIHA indicates neointimal hyperplasia area; ISAA, ISA area; VA, vessel area; LA, lumen area; SA, stent area; and PBSA, plaque behind stent area.

Statistical Analysis

Pooling of the control BMS groups of the 2 cohorts was combined because the baseline and 6-month follow-up data showed no significant differences between the 2 individual BMS groups. Therefore, 3 groups are reported in this study: the combined BMS, the TAXUS-SR, and the TAXUS-MR groups. Discrete variables are displayed as percentages and tested with Fisher exact test. Continuous variables are expressed as mean±SD. Delta values (Δ) for each measurement were calculated as: follow-up − postprocedure. When 3 groups were compared, overall probability values were derived from 1-way ANOVA. Comparisons between postprocedure and 6-month follow-up were performed with a 2-tailed paired t test. A value of P<0.05 was considered statistically significant. To identify potential causative factors responsible for late-acquired ISA, multivariable modeling analyses were performed, including all the conventional preprocedural, periprocedural, and postprocedural factors recorded in the framework of this trial. All covariates were modeled univariately on each outcome, as well as multivariately by use of a stepwise procedure in an appropriate regression model (logistic regression for binary outcomes, linear regression for continuous outcomes). The significance level thresholds for entry and exit of independent variables were set at a value of P=0.1.


Baseline Characteristics

Of the 536 randomized patients, 469 with serial and visually analyzable IVUS entered this substudy (BMS, 240; SR, 113; MR, 116). The patients’ baseline clinical and procedural characteristics are shown in Table 1. Except for the older age in the SR group (P=0.044), all baseline characteristics were comparable among the 3 groups.

TABLE 1. Baseline Clinical and Procedural Characteristics

BMSTaxus SRTaxus MR
LAD indicates left anterior descending artery; RCA, right coronary artery; LCx, left circumflex artery; and MI, myocardial infarction. Values are presented as relative percentages or mean±SD.
No. of patients240113116
Age, y59.5±9.762.0±10.259.0±10.4
Male, %78.368.174.1
Current smoker, %28.321.124.1
Diabetes mellitus, %14.612.415.5
Hypertension, %60.862.859.5
Hypercholesterolemia, %72.482.376.7
Unstable angina, %35.632.728.7
Previous MI, %
Target vessel, %
Balloon-artery ratio1.1±0.21.1±0.21.1±0.2
Maximal inflation pressure, atm12.3±2.812.6±2.712.1±2.8
Stent size, mm3.26±0.253.27±0.253.24±0.25

Incidence and Predictors of ISA

The incidence of ISA is shown in Table 2 according to the classification of ISA. Postprocedural ISA was less frequent in the MR group (2.6%) than the other groups (BMS, 7.9%; SR, 11.5%; P=0.028). Of 19 instances of ISA observed after the procedure in the BMS group, 11 (58%) were resolved at 6 months. In the SR group, 8 of 13 (62%) were resolved. All instances of postprocedural ISA were resolved in the MR group. The incidence of late-acquired ISA was similar among the 3 groups, ranging from 5.4% to 9.5%. A multivariate analysis identified lesion length (P=0.0072), unstable angina (P=0.0721), and absence of diabetes (P=0.0832) as predictive factors of late-acquired ISA. The treatment allocation was not retained in the multivariate analysis, with a probability value of P=0.16 in the univariate analysis.

TABLE 2. Incidence of ISA

BMS (n=240)Taxus SR (n=113)Taxus MR (n=116)P
Values are presented as numbers and relative percentage.
Postprocedural ISA19 (7.9)13 (11.5)3 (2.6)0.028
Resolved ISA11 (4.6)8 (7.1)3 (2.6)0.285
Persistent ISA8 (3.3)5 (4.4)0 (0)0.056
Late-acquired ISA13 (5.4)9 (8.0)11 (9.5)0.306

Clinical Outcome of ISA

Table 3 summarizes the clinical outcome of patients who exhibited ISA in comparison with those without ISA. Up to 12 months after deployment of the stents, in both the BMS and TAXUS groups, no differences in adverse clinical event rates were observed between the patients who showed ISA after the procedure and those who did not (Table 3). Similarly, ISA detected at 6-month follow-up was not associated with an excess of adverse event rates at 12-month clinical follow-up in either the BMS or TAXUS group (Table 4). No stent thrombosis was reported in patients diagnosed with ISA.

TABLE 3. Adverse Clinical Events and Presence of ISA: Postprocedural ISA

BMS (n=240)TAXUS SR+MR (n=229)
No Postprocedural ISAPostprocedural ISAPNo Postprocedural ISAPostprocedural ISAP
NA indicates not applicable; MI, myocardial infarction; and TLR, target lesion revascularization. Values are presented as numbers (relative percentages).
Postprocedural ISA includes both persistent and resolved ISA.
No. of patients2211921316
Up to 6 months
    Death0 (0.0)0 (0.0)NA0 (0.0)0 (0.0)NA
    Q-wave MI1 (0.5)0 (0.0)1.0000 (0.0)0 (0.0)NA
    Non–Q-wave MI8 (3.6)0 (0.0)1.0001 (0.5)1 (6.3)0.135
    TLR27 (12.2)1 (5.3)0.7077 (3.3)0 (0.0)1.000
    Stent thrombosis0 (0.0)0 (0.0)NA0 (0.0)0 (0.0)NA
Up to 12 months
    Death1 (0.5)0 (0.0)1.0000 (0.0)0 (0.0)NA
    Q-wave MI1 (0.5)0 (0.0)1.0003 (1.4)0 (0.0)1.000
    Non–Q-wave MI8 (3.6)0 (0.0)1.0001 (0.5)1 (6.3)0.135
    TLR28 (12.7)1 (5.3)0.4847 (3.3)0 (0.0)1.000
    Stent thrombosis0 (0.0)0 (0.0)NA2 (0.9)0 (0.0)1.000

TABLE 4. Adverse Clinical Events and Presence of ISA: ISA Observed at 6 Months

BMS (n=240)TAXUS SR+MR (n=229)
No ISA at 6 MonthsISA at 6 MonthsPNo ISA at 6 MonthsISA at 6 MonthsP
NA indicates not applicable; MI, myocardial infarction; and TLR, target lesion revascularization. Values are presented as numbers (relative percentages).
ISA at 6 months includes both persistent and late-acquired ISA.
No. of patients2192120425
Up to 6 months
    Death0 (0.0)0 (0.0)NA0 (0.0)0 (0.0)NA
    Q-wave MI1 (0.5)0 (0.0)1.0000 (0.0)0 (0.0)NA
    Non–Q-wave MI8 (3.7)0 (0.0)1.0001 (0.5)1 (4.0)0.207
    TLR28 (12.8)0 (0.0)0.1457 (3.4)0 (0.0)1.000
    Stent thrombosis0 (0.0)0 (0.0)NA0 (0.0)0 (0.0)NA
Up to 12 months
    Death1 (0.5)0 (0.0)1.0000 (0.0)0 (0.0)NA
    Q-wave MI1 (0.5)0 (0.0)1.0003 (1.5)0 (0.0)1.000
    Non–Q-wave MI8 (3.7)0 (0.0)1.0001 (0.5)1 (4.0)0.207
    TLR29 (13.2)0 (0.0)0.0867 (3.4)0 (0.0)1.000
    Stent thrombosis0 (0.0)0 (0.0)NA2 (1.0)0 (0.0)1.000

Quantification of ISA

Of 33 patients with late-acquired ISA, the quantification was not possible in 4 patients. Although ISA was recognized visually on the videotapes in these patients, it was impossible to differentiate the lumen outside the stent from the plaque behind the stent on the digitized still images. Thus, 29 patients with 32 late-acquired ISA segments were assessed quantitatively. For similar reasons, the quantification was possible in 18 patients (20 segments) of 22 patients with resolved ISA. Quantification was performed in all 13 patients (15 segments) with persistent ISA. The extent of late-acquired ISA measured by length, volume, mean area, and maximal area is summarized in Table 5. All quantitative ISA parameters were similar among the 3 groups. Figure 2 shows the change of IVUS variables (VA, PBSA, and LA) in the segments with late-acquired and resolved ISA, including all groups. In the segments with late-acquired ISA, VA at follow-up increased significantly, whereas PBSA did not change. As a result, there was a significant increase in LA with occurrence of ISA at follow-up. In the segments with resolved ISA, there was no difference in VA between after the procedure and at 6 months, whereas PBSA increased significantly. As a result, LA decreased significantly, together with the disappearance of ISA at follow-up. NIHA at follow-up in the segments with late-acquired and resolved ISA was 0.36 and 1.35 mm2, respectively (P=0.0003).

TABLE 5. Quantification of Late-Acquired ISA

No. of patients12710
No. of ISA segments13811
ISA length, mm3.6±2.25.7±3.92.8±2.40.089
ISA volume, mm311.4±12.721.7±20.68.5±13.90.181
Mean ISA area, mm23.0±2.13.6±1.22.1±1.40.179
Maximal ISA area, mm24.0±2.65.1±1.83.4±2.60.342

Figure 2. Change of IVUS variables in segments with late-acquired ISA (A) and resolved ISA (B). VA indicates vessel area; LA, lumen area; SA, stent area; and PBSA, plaque behind stent area. *P<0.01.


The major findings of this study are the following: (1) More than 50% of instances of postprocedural ISA resolve at follow-up. (2) An increase of plaque behind the stent without change in vessel area results in resolved ISA at follow-up. (3) The incidence of late-acquired ISA after implantation of paclitaxel-eluting stents is similar to that of BMS. The extent (length, volume, and area) is similar between paclitaxel-eluting stents and BMS. (4) An increase of vessel area without change in plaque behind the stent is the “mechanistic” IVUS change observed in the patients with late-acquired ISA. (5) The predictive factors of late-acquired ISA are lesion length, unstable angina, and absence of diabetes. (6) The presence of ISA is not associated with adverse clinical events.

Postprocedural ISA

In the previous IVUS-guided trials, such as the STRUT (Stent Treatment Region assessed by Ultrasound Tomography), the CRUISE (Can Routine Ultrasound Influence Stent Expansion), and the AVID (Angiography-directed versus IVUS-Directed coronary stent placement) trials, the incidence of postprocedural ISA as a result of incomplete deployment was reported to range from 4% to 22%.5 Although a significant difference in the incidence of postprocedural ISA was seen among the 3 groups in our study, the incidence of 2.6% to 11.5% was similar to the previous observations.

In the previous reports, late outcome of postprocedural ISA was not documented. In our study, of 19 instances of postprocedural ISA in the BMS group, 11 (58%) disappeared at 6-month follow-up. Similarly, 8 of 13 (62%) in the SR group and 3 of 3 (100%) in the MR group were resolved at follow-up. The quantitative assessment of resolved ISA demonstrated that the disappearance of postprocedural ISA was attributable to an increase of tissue behind the stent without change in vessel area. It is apparent that paclitaxel elution from the stent did not adversely affect this spontaneous resolution of postprocedural ISA. However, it seems wise to avoid incomplete stent deployment to ensure efficient drug release from the stent struts to the vessel wall.

Late-Acquired ISA

ISA was more frequently observed at 6-month follow-up in the sirolimus-eluting stent group than in the control group in RAVEL (RAndomized study with the sirolimus-eluting VElocity balloon-expandable stent in the treatment of patients with de novo native coronary artery Lesions).9 However, the true incidence of late-acquired ISA could not be determined, because no IVUS examination was performed after the procedure. In addition, in a retrospective analysis, it has been reported recently that late-acquired ISA occurs in 4.4% after BMS implantation.11 For the first time, we prospectively investigated the incidence of late-acquired ISA after implantation of polymer-controlled paclitaxel-eluting stents in comparison with BMS. The rates of late-acquired ISA in the SR and MR groups (8.0% and 9.5%) were similar to that in the BMS group (5.4%). Furthermore, the quantitative assessment revealed no differences in the extent of ISA. In ASPECT (ASian Paclitaxel-Eluting stent Clinical Trial), which compared nonpolymeric paclitaxel-eluting stents with BMS, late-acquired ISA was observed only in 1 case in the high-dose group (3.6%, 1/28).12 The incidence in the ASPECT trial was smaller than in the present study; however, it is difficult to compare the results because of an imbalance in the number of serial IVUS examinations between the 2 studies (81 in ASPECT and 469 in TAXUS II).

Several potential underlying mechanisms of late-acquired ISA may be postulated: peristent remodeling, regression of plaque behind the stent, dissolution of thrombotic material behind the stent, cell necrosis, and cell apoptosis. The serial quantitative assessment in the present study showed that an increase in vessel area (peristent remodeling) in the absence of increase in plaque behind the stent resulted in late-acquired ISA. Our finding with 33 instances of late-acquired ISA confirms a recent report that demonstrated that regional positive remodeling was the primary cause of late-acquired ISA in 11 stents.13 Peristent remodeling has been shown to occur after BMS implantation.14,15 This suggests that the key mechanism to late-acquired ISA is an imbalance between peristent remodeling and tissue growth behind the stent. The multivariate analysis in the present study identified the absence of diabetes and unstable angina as predictive factors of late-acquired ISA. It is likely that the more proliferative nature of the healing process in diabetic patients tends to prevent the occurrence of ISA. In contrast, in patients with unstable angina, it is suspected that the culprit lesions often contain thrombotic materials, which may dissolve at follow-up and create a new empty space behind the stent.

Clinical Significance of ISA

Uren et al5 retrospectively investigated the postprocedural IVUS findings of 53 patients who developed stent thrombosis. The incidence of ISA was higher in their patient population compared with the previous reports. For the first time, we prospectively followed up the 35 patients (19 in the BMS group and 16 in the TAXUS group) with ISA after the procedure. Despite the termination of clopidogrel at 6 months, no stent thrombosis was reported up to 12 months. In addition, during the time frame of 12 months, no stent thrombosis occurred in the 46 patients (21 in the BMS, 25 in the TAXUS) in whom IVUS identified ISA at 6-month follow-up. Therefore, the clinical significance of ISA is considered to be benign and inconsequential, but larger cohorts are necessary to confirm this information. Degertekin et al16 recently reported a benign feature of ISA after sirolimus-eluting stent implantation, but the conclusion cannot be generalized to other drug-eluting stents and should be restricted to the specific dose and elution profile of polymer-controlled paclitaxel-eluting stents and sirolimus-eluting stents.

Study Limitations

First, the power to detect the incidence of ISA was not considered, because it was not the primary end point in the TAXUS II trial. Second, the analyses were limited to the patients who received only the allocated study stents with serial IVUS, raising the possibility of selection bias. However, of the 536 patients enrolled in the TAXUS II trial, as many as 469 (87.5%) entered this substudy. Third, this represents a time frame of 12 months. Therefore, longer-term follow-up with larger cohorts will be necessary to confirm our findings.


The polymer-controlled paclitaxel-eluting stents do not increase the incidence of late-acquired ISA compared with BMS. In addition, paclitaxel elution from the stent maintains the process of spontaneous resolution of postprocedural ISA. By prospectively following up the patients with ISA, we demonstrate that ISA is a pure IVUS finding without clinical repercussions.

This study was supported by a grant from Boston Scientific Corp. We thank all of the investigators, their staffs, and the study staff.


Correspondence to Prof P.W. Serruys, MD, PhD, Thoraxcentre, Bd 406, Erasmus MC, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. E-mail


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