European Heart Journal Advance Access originally published online on September 4, 2006
European Heart Journal 2006 27(19):2330-2337; doi:10.1093/eurheartj/ehl229
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Patterns of restenosis after drug-eluting stent implantation: insights from a contemporary and comparative analysis of sirolimus- and paclitaxel-eluting stents
1 EMO Centro Cuore Columbus, 48 Via M. Buonarroti, 20145 Milan, Italy
2 San Raffaele Scientific Institute, Milan, Italy
3 Institute of Medical Statistics and Biometry, Milan, Italy
4 Abano Terme Hospital, Abano Terme, Italy
Received 30 March 2006; revised 14 July 2006; accepted 17 August 2006; online publish-ahead-of-print 4 September 2006.
* Corresponding author. Tel: +39 02 4812920; fax: +39 02 48193433. E-mail address: info{at}emocolumbus.it
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Abstract |
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Aim To evaluate patterns of restenosis following implantation of sirolimus-eluting stent (SES) and paclitaxel-eluting stent (PES) in comparable unselected lesions.
Methods and results We have identified all episodes of restenosis after SES or PES implantation in our institutions between March 2003 and March 2005. Restenosis pattern was classified as focal, diffuse, proliferative, or occlusive. The position of focal restenosis was also categorized as proximal, in-stent, distal, or multi-focal. We have characterized 150 and 149 restenotic lesions in SES and PES groups, respectively. The incidence of diffuse and occlusive restenosis was significantly higher in PES than in SES (47.6 vs. 27.0%, P<0.001). Multivariable (OR 2.693, 95% CI 1.425–5.089, P=0.002) and propensity (OR 3.00, 95% CI 1.584–5.672, P<0.001) analyses confirmed the positive association of PES with non-focal restenosis. For both stents, focal-edge restenosis was significantly more likely to occur proximally than distally (61.0 vs. 16.9%, P<0.001 for PES and 45.8 vs. 16.8%, P<0.001 for SES).
Conclusion Focal restenosis remains the most common pattern with SES. In contrast, just under half of restenosis in PES is the more severe non-focal pattern. Paradoxically, the majority of focal restenosis occurs at the proximal stent margin for both platforms.
Key Words: Stent • Restenosis • Paclitaxel • Sirolimus
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Introduction |
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Current perceptions based on a limited number of restenotic lesions in sirolimus-eluting stent (SES) and paclitaxel-eluting stent (PES) have led to the concept that when restenosis occurs it is likely to be focal.1–4 This observation combined with the knowledge, that focal restenosis in bare metal stents (BMS) carries a more benign prognosis than non-focal restenosis,5 has further encouraged the widespread utilization of drug-eluting stents (DES).6 The early observations of PES and SES restenosis are based on small numbers or selected lesion cohorts. A recent report has shown that when PES are utilized in unselected lesions in the real world, a significant proportion of restenosis is non-focal.7 No similar data in unselected lesions is available for SES, indeed only 99 SES restenotic lesions have been characterized in the literature.1,2,4,8–11 Furthermore, DES restenosis, even if it remains infrequent, has the potential to become a clinically relevant entity. We have also recently demonstrated that the pattern of restenosis in DES is still related to subsequent outcome with significantly higher restenosis and repeat revascularization rates in non-focal restenotic lesions.12 Thus, we undertook an analysis of the patterns of restenosis that occurred after SES and PES were contemporaneously and consecutively implanted in our institutions over a 2 year period.
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Methods |
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From March 2003 to March 2005, all consecutive patients treated with DES implantation at our institutions were prospectively entered into a dedicated database. All patients gave prior written informed consent both for the procedure and data collection and analysis. Procedural anticoagulation and anti-platelet therapy followed standard protocols.13 Interventional approach and the choice of DES implanted were at the operators' discretion without any declared bias. It is standard practice in our institutions to alternate implantation of SES and PES from one case to the next, as we consider both stents to be equally deliverable. We analysed all restenotic lesions which occurred following DES implantation in de novo lesions, including diffuse disease, bifurcations, chronic total occlusions, bypass grafts, and left main (LM) disease. We do not implant DES in patients with acute ST-elevation myocardial infarction undergoing primary angioplasty. Patients who received a mixture of different types of DES, had a BMS was implanted, were undergoing DES implantation for either BMS or DES restenosis, or had previously had brachytherapy in the same vessel were not included in this analysis. A number of the restenotic lesions have previously been included in the studies reported by Iakovou et al.7 (62 lesions) and Cosgrave et al.12 (90 lesions).
Following DES implantation, it is our practice to perform clinical follow-up by telephone contact or office visit at 1, 6, 9, and 12 months after the index procedure. Angiographic follow-up is encouraged for all patients between 6 and 9 months; all of the patients who do not undergo angiography are recommended to undergo non-invasive assessment of inducible ischaemia.
Quantitative angiography was performed using a validated edge detection system (CMS, version 5.2, MEDIS, The Netherlands). Minimal luminal diameter (MLD), reference vessel diameter (RVD), and percent diameter stenosis were measured at baseline, post-stenting, and at follow-up. Angiographic restenosis was defined as diameter stenosis
50% by quantitative coronary angiography (QCA) within a previously stented segment (stent and 5 mm proximal and distal) at the follow-up angiogram.
All the angiograms of lesions with angiographic restenosis were reviewed and the pattern of restenosis classified according to the following scheme: focal (
10 mm in length), diffuse (restenosis >10 mm within the stent), proliferative (restenosis >10 mm in length extending outside the stent), and occlusive. This classification scheme is the same as that used in the SIRIUS4 and TAXUS IV3 studies and is based on the scheme of Mehran et al.5 Focal restenosis was further categorized according to its position as proximal edge in-stent, distal edge, or multi-focal. Edge restenosis was defined as restenosis occurring within 5 mm either side of and including the stent margin. Multi-focal restenosis was defined as more than one area of focal restenosis within the same stented segment. For stents in the side branch of a bifurcation, proximal-edge restenosis was defined as focal restenosis occurring within 5 mm of the ostium of the side branch. All other definitions of restenosis pattern and position in side branch stents were the same as for all other stents. In order to exclude potential cases of stent thrombosis, the case records of all patients were examined at the time of restenosis detection. Any lesions that re-presented as an acute ST-elevation myocardial infarction or were considered by the operator to be actual or possible stent thrombosis were excluded from subsequent analysis.
Statistical analysis
Continuous variables are presented as means ± standard deviation and categorical variables as frequencies (%). Continuous variables were compared using independent sample Student's t or Mann–Whitney U test and categorical variables with 
2 statistics. A logistic regression model was used to identify independent predictors of restenosis pattern. At this stage, the diffuse, proliferative, and occlusive restenosis patterns were combined into a single non-focal group, in order to simplify and strengthen subsequent analysis. This was done because, overall, there were lower numbers of non-focal restenotic lesions. We entered into the multivariable-model, significant (P<0.05), univariate predictors of restenosis pattern: female gender, DES type, AHA/ACC type C lesions at index, RVD at index, stent length implanted per lesion, stent diameter, and the presence of overlapping stents in the lesion. We did not include the following significant (P<0.05) factors: RVD post-stenting and MLD at baseline, as they are directly related to RVD at index; maximum balloon diameter, as it is related to stent diameter. We also included diabetes mellitus despite its non-significant association with pattern due to its established clinical significance.
In order to account for potential differences between the SES and PES cohorts, a propensity analysis was performed on a lesion-based setting for the pattern of restenosis.14 This was performed using logistic regression with DES type as fixed dummy dependent and propensity score (propensity to be treated with PES estimated by a non-parsimonious multivariable logistic regression with 31 covariates) as continuous covariate.15 The results are reported as odds ratios (OR) with associated 95% confidence interval (CI). A P-value of <0.05 was considered to be statistically significant and all reported P-values are two-sided. Lesion-based univariate, multivariable and propensity score analyses were performed using the Generalized Estimating Equation (GEE) approach with an exchangeable variance–covariance matrix in order to take into account clustered data (more lesions within the same patient). Statistical analysis was performed using SPSS 11.5 (SPSS Inc.).
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Results |
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Between March 2003 and March 2005, 1376 de novo lesions in 803 patients were treated with SES implantation and 1199 de novo lesions in 692 patients treated with PES implantation. There were no significant differences in major clinical or lesion characteristics between the SES and PES groups from which the restenotic population was derived, nor were there any differences in long-term clinical events during follow-up as shown in Table 1. The rate of angiographic follow-up was 68.3% in SES and 72.0% in PES (P=0.194). The median duration of clinical follow-up was 415 days (inter-quartile range 349–525 days) in SES patients and 408 days (inter-quartile range 340–508 days) in PES patients (P=0.35). Clinical follow-up was available for 99.4 and 99.3% of SES and PES patients, respectively (P=0.49). In the SES group, we identified 119 patients with 150 restenotic lesions, whereas in the PES group we identified 117 patients with 149 restenotic lesions. In the patients with angiographic follow-up, this represents binary restenosis rates on a per lesion basis of 15.9 and 17.4% for SES and PES, respectively (P=0.509). There was no difference in symptomatic status at the time of detection of restenosis between patients treated with PES and SES; 67 (57.3%) PES patients were symptomatic, whereas 77 (64.7%) SES patients had symptoms (P=0.299). Of those patients who did not undergo angiographic follow-up, 92.7% in the SES group were asymptomatic vs. 91.9% of the PES group (P=0.844), whereas only 5.4% of the SES group had a positive test for ischaemia as compared with 6.3% of the PES group (P=0.853), and 94.9% of the patients were still taking dual anti-platelet therapy at the time of restenosis detection with no difference between the PES and SES groups (95.7% in the PES group vs. 94.1% in the SES group, P=0.77).
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Patterns of restenosis in SES and PES
The baseline clinical, procedural, and QCA characteristics of the restenotic lesions that developed following PES and SES implantation are shown in Table 2. Figure 1 shows the patterns of restenosis in the total cohort and both stent groups. The incidence of diffuse and occlusive restenosis was significantly higher for PES than SES (47.6 vs. 27.0%, P<0.001). The incidence of proliferative restenosis was extremely low for both DES (0.7% in each).
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The results of a univariate analysis of factors associated with focal and non-focal patterns of restenosis are shown in Table 3. There was no difference in symptomatic status of patients at the time of detection of restenosis between lesions with focal and non-focal restenosis; 106 (57.6%) focal lesions were associated with symptoms, whereas 69 (60%) non-focal lesions were associated with symptoms (P=0.744). The results of a multivariable analysis undertaken to identify factors independently associated with non-focal restenosis are shown in Table 4. This revealed that stent type remained associated with the pattern of restenosis, with a positive association between PES and non-focal restenosis. Furthermore, female gender and the use of overlapping stents were also independently associated with non-focal restenosis. In order to account for possible baseline differences between the two stent groups, we performed a propensity analysis. This further confirmed the strong association between the type of stent and the pattern of restenosis: OR for association of PES with non-focal restenosis was 3.00, with 95% CI 1.584–5.672 (P<0.001).
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Distribution of focal restenosis
When only the focal restenotic lesions were considered (Figure 2), a further clear distinction between PES and SES emerged. For PES, the incidence of focal intra-stent restenosis was much lower than SES (16.9 vs. 33.6%, P=0.018). In both platforms, focal restenosis occurred much more frequently at the margins of the stent. Furthermore, the incidence of restenosis at the proximal edge was much higher than at the distal edge for both stents (61.0 vs. 16.9%, P<0.001 for PES and 45.8 vs. 16.8%, P<0.001 for SES).
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When considering the pattern of restenosis solely within the stent margins, Figure 3 demonstrates that focal is more likely than diffuse restenosis for SES, whereas the opposite is the case for PES (P<0.001).
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Discussion |
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The main findings of this report are as follows. (i) When restenosis occurs in DES, the most common pattern is focal; (ii) For PES, there is a significantly higher incidence of non-focal restenosis compared with SES; (iii) For both stents, focal-edge restenosis was significantly more likely to occur proximally than distally; (iv) PES implantation, female gender, and the presence of overlapping stents are all associated with non-focal restenosis in DES.
Non-focal restenosis in DES
Earlier reports based on low number of DES restenotic lesions have shown a high proportion of focal restenosis in DES. These initial data were mainly derived from the early experiences with DES1,2 or from selected cohorts.3,4 Our large contemporary series confirms that focal restenosis is indeed common in both SES and PES. However, our data demonstrate that in the real world, non-focal restenosis is more common than has been generally appreciated, particularly in PES.
These data are the first to our knowledge to compare the pattern of restenosis in a contemporaneous cohort of DES implantation in unselected lesions. This analysis has demonstrated significant differences in restenosis pattern between the two stent platforms. Both groups were well matched at the baseline and our finding of a greater proportion of non-focal restenosis in PES was confirmed by both multivariable and propensity analyses. We therefore feel that the differences we have seen are a true reflection of the in vivo behaviour of PES and SES when they restenose. The complexity of the disease treated seems likely to be the main reason underlying these findings. Both SIRIUS8 and TAXUS IV3 only recruited patients with single-vessel disease with no LM, ostial, bifurcation, or occluded lesions. In contrast, our population had substantial proportions of all of these lesion subsets (Table 1). We also feel this is likely to explain our higher overall restenosis rates as compared with much of the randomized trial literature. It therefore appears that one cannot necessarily extrapolate the results regarding restenosis in the available randomized trials with DES to unrestricted utilization of DES in the real world.
Intuitively, one could postulate that a greater restenotic burden may increase a patient's likelihood of developing symptoms, yet there was no difference in symptomatic status between patients with focal and non-focal restenosis. It may be that our sample sizes were too small to demonstrate a difference in symptomatic status between the two groups.
Diffuse vs. focal intra-stent restenosis in PES
The low incidence of focal intra-stent restenosis in PES compared with SES is notable, particularly if we consider that intra-stent restenosis in PES is much more likely to be diffused than focal (Figure 3). Focal restenosis in SES has been reported to reflect local problems with the stent at the affected point, such as strut fracture, non-uniform strut expansion, or incomplete lesion coverage.2,11 Although it is currently unknown whether similar mechanisms trigger restenosis in PES, at the very least it would appear that the neo-intimal response is more likely to be diffuse than focal, contrary to the response seen in SES.
Proximal-edge restenosis is much more common than distal-edge restenosis
An interesting and counter-intuitive observation from our study is the higher incidence of proximal-edge restenosis in both stent platforms. From the knowledge of factors influencing restenosis in BMS, one would expect that, edge restenosis should occur more frequently distally, where the vessel is likely to be both smaller in diameter and also subjected to greater barotrauma and injury from the balloon. However, for both PES and SES, distal-edge restenosis is infrequent and the reasons underlying this are not immediately apparent. Lemos et al.2 reported that edge restenosis occurred more frequently in the proximal than in the distal stent border in a small series of 19 lesions, although in contrast to our findings that focal intra-stent restenosis remained the predominant pattern overall. The SIRIUS investigators4 noted that focal restenosis at the margins of SES was the most common pattern in 31 restenotic lesions, although they do not comment on a difference between the proximal and distal edges. It is tempting to speculate that elution of drug into the bloodstream may be producing higher drug concentrations at the distal edge with consequently lower rates of restenosis, although from our study, we cannot discount the possible role of deployment-related factors, such as incomplete lesion coverage or vessel trauma outside the stented area, also playing a role.
Non-focal restenosis is more common in women and with overlapping stents
As well as confirming that DES type was associated with the pattern of restenosis, our multivariable logistic regression analysis also verified that female gender and the presence of overlapping stents were associated with a non-focal pattern. While we think that the association of overlapping stents with non-focal restenosis reflects the longer length of stent implanted (particularly as the length of stent implanted was associated with non-focal restenosis in univariate analysis), it is not immediately apparent why women should be more likely to have non-focal restenosis than men. A preliminary analysis of the 47 lesions from female patients in our series has shown them to be older and have a greater incidence of diabetes mellitus than male patients. In contrast, they have fewer type B2 and C lesions and there is no difference in RVD at the baseline or implanted stent length. Whether or not our finding of an association between female gender and non-focal restenosis is true, or is actually due to other confounding factors, is difficult to ascertain accurately from our small number of female patients and requires further dedicated studies. A recent report has found non-focal restenosis to be more common in BMS in women suggesting that this finding may be common to both the BMS and DES eras.16
Study limitations
There are a number of potential limitations to our data. As they are retrospective and not randomized, we cannot discount that selection bias has influenced our results, despite the lack of significant differences in major clinical and angiographic parameters in the patients treated with SES and PES.
It is likely that there were further restenotic lesions in the approximately 30% of patients that did not undergo angiographic follow-up in both groups. However, as there was no difference in the symptomatic status of patients with different patterns of restenosis and the majority of patients who did not undergo angiographic follow-up were asymptomatic, we do not believe that any unidentified restenotic lesions could significantly change our overall findings.
Finally, one should be cautious when considering obstructive restenosis. It is impossible post-hoc to ascertain angiographically whether the occlusion originated in neo-intimal proliferation or thrombosis. None of the lesions reported here came from patients who presented with clinically suspected or proven stent thrombosis. It is also important to note that in the seminal paper, by Mehran et al.5 on restenosis in BMS, a gradient of increasing intimal hyperplasia was demonstrated by intra-vascular ultrasound from proliferative to occlusive patterns, arguing strongly that occlusion is actually an extension of diffuse and proliferative restenosis and not simply the result of thrombotic occlusion. Given the controversial and unresolved issues surrounding DES stent thrombosis,17 we have deliberately refrained from further speculation about our observed difference in occlusive restenosis between PES and SES.
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Conclusions |
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From this morphological analysis of restenosis in PES and SES, we conclude that the overall pattern of restenosis has changed in the DES era with a shift towards focal restenosis and the virtual abrogation of proliferative restenosis. Nevertheless, non-focal restenosis remains a significant entity, particularly in PES. Furthermore, focal restenosis in both stents has a preponderance to occur at the proximal stent margin. Further studies are now warranted to elucidate optimal strategies for the prevention and treatment of restenosis in contemporary interventional practice.
Conflict of interest: There are no potential conflicts of interest or funding sources to disclose.
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References |
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