CLINICAL STUDIES
Propensity and mechanisms of restenosis in different coronary stent designs
Complementary value of the analysis of the luminal gain-loss relationship
Javier Escaned, MD, PhDa,
Javier Goicolea, MD, PhDa,
Fernando Alfonso, MD, PhDa,
Maria José Perez-Vizcayno, MDa,
Rosana Hernandez, MD, PhDa,
Antonio Fernandez-Ortiz, MD, PhDa,
Camino Bañuelos, MD, PhDa and
Carlos Macaya, MD, PhDa
a Interventional Cardiology Unit, San Carlos University Hospital, Madrid, Spain
Manuscript received October 5, 1998;
revised manuscript received May 18, 1999,
accepted June 29, 1999.
Reprint requests and correspondence: Dr. Javier Escaned, Unidad de Cardiología Intervencionista, Hospital Clinico Universitario San Carlos, Prof. Martin Lagos S/N, 28040 Madrid, Spain
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Abstract
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OBJECTIVES
This study sought to investigate the influence of stent design on the long-term angiographic outcome.
BACKGROUND
The proportional relationship between vessel injury and late luminal loss in percutaneous revascularization should be best appreciated in coronary stenting, where recoil and shrinkage are theoretically minimal. It is unclear whether all stent designs can counterbalance this reactive loss by achieving a large initial luminal gain (bigger is better).
METHODS
In 523 lesions successfully stented, the long-term angiographic results of slotted-tube (n = 331), coil (n = 85), multicellular (n = 70) and self-expandable mesh (n = 37) stent designs were compared using the angiographic gain-loss relationship (GLR).
RESULTS
Restenosis rate was 10% for multicellular, 20% for slotted-tube, 46% for coil and 49% for self-expandable designs (p = 0.001). At a difference with other designs, no significant GLR was found in coil stents, suggesting additional mechanisms of luminal loss (i.e., plaque protrusion, stent compression) to neointimal proliferation. Significant differences in late loss between stents were found within each quartile of luminal gain, suggesting a specific role of design in luminal loss. Multivariate analysis identified use of coil and self-expandable stents, vessel size, minimal luminal diameter preintervention, luminal gain and stent length as variables with independent predictive value for several indices of angiographic long-term outcome.
CONCLUSIONS
The analysis of GLR: 1) demonstrates that stent design influences late luminal loss; 2) challenges the applicability of the widely accepted "bigger is better" approach to all stent designs; and 3) appears as a valuable tool in assessing long-term stent performance.
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Abbreviations and Acronyms
| | MLD | = minimal luminal diameter | | PTCA | = percutaneous transluminal coronary angioplasty |
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Although the growth of stenting is in large part due to the demonstration in major randomized studies of its superior long-term results when compared with balloon angioplasty (1–3), restenosis still occurs in approximately 20% of cases. In comparison with balloon angioplasty, in which elastic recoil and vessel remodelling have been proposed as important contributors to the luminal loss in the long term, restenosis after coronary stenting is thought to be due mainly to neointimal proliferation (4,5). In this regard, the extent of the intimal proliferative response has been consistently shown in experimental (6) and angiographic (7) studies to bear a proportional relationship with the degree of damage inflicted to the vessel during its revascularization. Whether stent design might have an influence on the degree of injury and the process of vascular repair, or in facilitating other causes of luminal loss than neointimal proliferation (stent recoil, insufficient scaffolding), remains undetermined.
Based on these premises, in the present work, we study the influence that stent design may play in the long-term angiographic results, as judged by the relationship between the luminal gain obtained during the procedure and the luminal loss observed at angiographic follow-up.
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Methods
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Study population.
We included in the study all patients successfully treated at our hospital with four basic stent designs, who completed routine, prospective angiographic follow-up and full quantitative angiographic analysis (as part of a prospective, programmed angiographic follow-up of all patients treated with coronary stents), with the following exclusion criteria: 1) total coronary occlusions and lesions concomitantly treated with debulking techniques (laser or atherectomy) or other revascularization devices (radiofrequency or cutting-balloon angioplasty); and 2) segments treated with more than one stent configuration. Angiographic success was defined as postprocedural diameter stenosis <50%.
Coronary stenting.
Coronary stenting was performed with four different basic stent designs: 1) self-expandable mesh (Wallstent; Schneider, Bülach, Switzerland); 2) slotted tube (Palmaz-Schatz 153 series; Johnson and Johnson, Warren, New Jersey); 3) balloon-expandable coil (Gianturco-Roubin I and Gianturco Roubin II; Cook Inc., Bloomington, Indiana); and balloon expandable multicellular (MultiLink; Advanced Cardiovascular Systems, Santa Clara, California; and NIR; Medinol/Scimed, Tel Aviv, Israel). The classification of stents in these four categories is justified on the following grounds. 1) The largest amount of information available on the long-term outcome of coronary stenting is based on the use of the Palmaz-Schatz stent, which therefore merits an individual category as a reference when assessing the anti-restenosis effect of new stent designs (as recommended by the U.S. Food and Drug Administration stent equivalence trials). This design includes a central articulation that, as discussed later, may be detrimental in the long term. 2) Both multicellular stents have continuous stainless steel designs without articulation and similar scaffolding properties, hoopstrength and total metal area when expanded. 3) Both coil designs present similar flexibility, strut pattern and metal surface when fully expanded and have larger spacing between struts and lower collapse pressure than the slotted tube and multicellular configurations described above. 4) Alternatively, the Wallstent is a self-expanding mesh that exerts a persistent radial force. Detailed description of these stents, with extensive technical documentation supporting the above discussion, can be found elsewhere (8,9).
The procedure was performed using the femoral or brachial artery approach, using 8F or 9F guiding catheters. Patients were anticoagulated with heparin (initial bolus of 100 IU/kg body weight with additional boluses as required by activated clotting time or duration of the angioplasty). On-line quantitative angiography and intravascular ultrasound were not routinely used to guide the procedure, and the final result was left to the judgment of the operator. All stents were implanted after predilation. Angiographic success was defined as a <50% residual diameter stenosis. Postprocedural medication included a minimum of 12 h of intravenous infusion of heparin. Until 1994, treatment included oral anticoagulation with a warfarin derivative (dosage adjusted to keep the international normalized ratio in the range of 3.5 to 4.5) and a calcium antagonist. Since then, oral anticoagulation was not routinely indicated, and oral aspirin ( 150 mg/day) and ticlopidine (500 mg/day during 2 days, subsequently 250 mg/day) was given instead.
Quantitative angiography.
Cineangiography frames corresponding to basal, initial stenting and long-term follow-up results were digitized and analyzed using a commercially available automated edge detection quantitative angiography system (Artrek; Quinton Imaging, Ann Arbor, MI). The filmed catheter tip was used as a calibration device. Intracoronary administration of 200 µg of nitroglycerin was performed to ensure control of vasomotor tone. In follow-up angiograms, particular attention was paid to perform measurements at the site in which the stent was deployed, either using the radiopacity of the prosthesis (when visible) or angiographic landmarks. From the reference and minimal luminal diameters (MLDs) at each stage of the study, a number of angiographic parameters were obtained, including acute luminal gain (defined as the increase in luminal diameter documented during the procedure), late luminal loss (or the decrease in absolute dimensions at follow-up of the initially achieved lumen), net gain (or the difference between acute gain and late loss) and loss index (the ratio between luminal loss and gain). Restenosis rate was also defined as a dichotomous variable (50% diameter stenosis at follow-up).
Statistical analysis.
A lesion-based approach was followed (10,11). Univariate analysis was performed using the Student t test for comparison of mean values (with Bonferroni’s correction when required), and the chi-square for comparison of percentages (with Yates correction when required). Linear regression analysis was also performed using a least-square approach. On the grounds of the luminal gain obtained, the 523 lesions were divided into four approximately equal-sized groups, or quartiles. Within each of these quartiles, comparisons between stent designs were performed using one-way analysis of variance, with concomitant Fisher PLSD and Scheffé-F tests. Multiple linear regression analysis was used for multivariate modelling and statistical adjustment to differences in baseline characteristics between stent designs. Dummy variables were generated to input the influence of stent design into the model, using the Palmaz-Schatz design as a reference. A p < 0.05 was considered significant.
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Results
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From March 1990 to January 1997, a total of 5,609 coronary stenoses were treated at our institution in 3,508 patients. Coronary stents were implanted in 1,200 lesions. Of this population, 207 were total occlusions, 30 had concomitant atherectomy, 8 had concomitant laser percutaneous transluminal coronary angioplasty (PTCA) and 34 had concomitant radiofrequency or cutting-balloon PTCA. Of the 921 remaining lesions, 29 were excluded due to failed stenting and 8 due to subacute stent thrombosis. Twenty-two lesions could not be followed due to patient death. A total of 197 lesions receiving two different stent designs and/or stent designs not contemplated in the study were also excluded. Angiographic follow-up of 96 lesions was not performed due to patient refusal or contraindication for recatheterization. The angiographic follow-up rate in eligible lesions was, therefore, 86% (569/665 lesions) and was completed by July 1997. During subsequent QCA analysis, 46 lesions were found not suitable for adequate QCA assessment in either pre-, postprocedural or follow-up frames and were excluded. The final 523 lesions, present in 483 patients, fulfilled the inclusion criteria of the study. Demographic characteristics are shown in Table 1. Male gender was predominant (410, 85%). Age was 59.3 ± 10.2 years. In 443 (92%), one coronary segment was stented, while two or three segments were treated with stents in 34 (7%) and 4 (1%) patients, respectively. The design used was self-expandable mesh in 37 (7%) segments, slotted tube in 331 (63%), coiled wire in 85 (16%) and multicellular in 70 (14%). The angiographic characteristics of the lesions treated are shown in Table 1. Prospective angiographic follow-up was performed at 169 ± 5 days.
Figure 1 shows baseline and postprocedural quantitative angiographic data. Several statistically significant differences between stent configurations were noted in quantitative angiography variables, including vessel size, and MLD pre-, poststenting and at follow-up. Adjustment for these differences was performed later using multivariate modelling.
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Figure 1 Baseline and postprocedural quantitative angiography data in the four stent designs. *Differences between stent design with a Fisher PSLD with p < 0.05. MLD = minimal luminal diameter.
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Figure 2 shows absolute changes in luminal dimensions induced by the four different stent designs. Multicellular and self-expanding mesh designs were associated with the largest acute luminal gain, followed by the slotted-tube and coil designs. In spite of similar initial results, large differences in luminal loss, net gain and loss index between the multicellular and self-expanding configurations were noted in the long term, which favored the performance of the multicellular design. On the contrary, the coil configuration yielded significantly less acute luminal gain and presented larger luminal loss in the long term. The net gain was thus not different from that observed in the self-expanding design.
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Figure 2 Changes in luminal dimensions induced by the four stent designs, derived from data in Figure 1. *Differences between stent designs with a Fisher PSLD with p < 0.05.
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Figure 3 shows the observed percent stenosis data at follow-up for the four stent designs included in the study, displayed as cumulative frequency distribution curves. The disparate curves reflect significant variations in the restenosis rate observed with each device. Any definition of percent diameter stenosis can be used to compare the performance of the four stent designs. When defined as a 50% diameter stenosis at follow-up, restenosis rate was 10%, 20%, 46% and 49% for the multicellular, slotted tube, coil and self-expandable mesh configurations, respectively (p = 0.001). Total occlusion at follow-up occurred in 16 (3%) cases: 9 (3%) in the Palmaz-Schatz, 4 (5%) in the coil, 3 (8%) in the self-expandable and none in the multicellular designs (p = NS). Exclusion of these 16 cases did not influence the conclusions outlined in the previous paragraphs.
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Figure 3 Percent diameter stenosis at follow-up for the four stent designs studied, displayed as cumulative frequency distribution curves.
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The results of the univariate linear regression analysis of the gain-loss relationship are shown in Table 2. A proportional, statistically significant relationship between gain and loss was demonstrated in all but one stent type, the coil design, in which no statistically significant relation between both parameters was found. This difference could not be ascribed to differences in population size between groups. Within each quartile of luminal gain, significant differences in luminal loss between the four stent designs were found (Table 3 and Fig. 4). No significant differences in vessel size in the four designs within each quartile were noted.
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Table 2 Results of Univariate Linear Regression Analysis of Luminal Gain and Loss in the Four Stent Designs Studied
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Figure 4 Late luminal loss per quartile of initial luminal gain observed in the four stent designs studied. The bars indicate 95% confidence intervals.
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Table 4 shows the result of multivariate analysis used as a technique of adjustment for baseline differences between groups and modelling. In accordance with most ongoing equivalence trials on coronary stenting, the Palmaz-Schatz design was used as a reference by not being entered in the model as a dummy variable. The variables MLD, postintervention and percent diameter stenosis were not entered in the model, because the presence of the variables MLD before luminal gain and vessel diameter would make the model colinear (the only exception being loss index, in which luminal gain had no independent predictive value). Their influence in the model is, however, maintained by the remaining variables. The variables that retained statistically significant predictive value after a discriminant approach were vessel size, MLD preintervention, luminal gain, length of the stented segment and use of coil or self-expanding mesh designs. When loss index was taken as the dependent variable, luminal gain had no independent predictive value. The variable MLD post had an independent predictor value and was entered in the model instead. Other variables such as restenotic lesion, left anterior descending location, saphenous graft, eccentricity, presence of side branch, bend or calcium did not influence the statistical strength of the model or have independent predictive value on the above-mentioned variables and were therefore excluded.
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Table 4 Results of Multiple Regression Analysis for Minimal Luminal Diameter, Luminal Loss and Net Luminal Gain at Follow-up
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Discussion
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The more you gain, the more you lose.
Vascular damage caused during lesion revascularization is accepted as the initiating phenomenon of a variety of pathophysiological mechanisms that eventually lead to restenosis (4,5). As a corollary to this response-to-injury phenomenon, experimental and angiographic research first demonstrated the existence in humans and some animal models of a proportional relationship between the degree of vessel wall damage and the subsequent degree of neointimal proliferation and luminal loss (6,12). Subsequently, differences in restenosis propensity between percutaneous revascularization devices were reported, paralleling the gain-loss relationship and suggesting that, in addition to the absolute luminal gain, device-specific effects of wall injury resulted in variable neointimal proliferative responses, which were considered the main substrate of restenosis (7). It is now accepted that the angiographically determined luminal loss might result not only from neointimal proliferation but also from: 1) the phenomenon of vessel remodelling or shrinkage (13); and 2) differences in the luminal shape resulting from each device (which, as demonstrated with intracoronary imaging techniques, may cause major inaccuracies during the angiographic assessment of the acute result of the intervention)(14).
Bigger is better.
Alternatively, it has been suggested that the ability of a revascularization device to reduce restenosis is more related to its ability to provide the greatest acute luminal gain than its ability to reduce subsequent intimal hyperplasia (15). This would be the case of devices that generate a large luminal gain and concomitantly present a favorable slope of the gain-loss relationship, leading to a favorable net luminal gain. The concept has gained wide acceptance after major trials comparing PTCA and stenting demonstrated that the superiority of the latter in reducing restenosis relies on achievement of a large initial luminal gain and not on absolute reduction of luminal loss (1–3).
Bigger is not always better.
In this work, we focused our attention on the potential use of the gain-loss relationship in comparing different coronary stent designs. Theoretically, restenosis after stenting should be a direct result of neointimal proliferation (elastic recoil and vessel shrinkage should be minimal), and the reliability of the angiographic luminal gain and loss should be maximal due to the round luminal morphology achieved by stenting. Lesions concomitantly treated with other revascularization techniques (which might modify the propensity to restenosis) and total coronary occlusions, in which an increased restenosis rate after stenting has been reported (16), were excluded. The results obtained provide new insights on the apparent conflict between the two bodies of knowledge outlined above by demonstrating that, with independence of the luminal gain achieved, stent design may significantly influence long-term outcome. In this regard, the analysis of the gain-loss relationship constitutes a valuable tool in comparing the performance of several stent configurations. Taking the performance of self-expanding mesh and multicellular stents in our study, significant differences in luminal loss between both designs were documented within each quartile of luminal gain. The continuous and proportional relationship between luminal gain and loss through all the quartiles of luminal gain for both designs suggests that the leading mechanism contributing to luminal loss in these two stent configurations is the generation of neointimal hyperplasia. Although both stent designs rendered excellent and similar initial angiographic results, the disparate differences in neointimal proliferation clearly affected the long-term outcome of the self-expanding design. The approach of obtaining a large luminal gain with the sole aim to reduce restenosis is thus challenged.
Conversely, the implantation of coil stents was associated with less initial gain and significantly large luminal losses during follow-up. An intriguing observation is that, in this design, the relationship between luminal gain and loss was statistically nonexistent. Following the rationale outlined in the previous paragraph, a plausible explanation is that luminal loss in this design derives not only from neointimal proliferation but also from factors not proportionally related to the degree of vessel damage, such as the following: 1) plaque prolapse through the free space between stent struts (this design presents the largest gaps) (17); 2) more stent recoil than in other designs (as demonstrated with intravascular ultrasound imaging) (18); and 3) a higher propensity of the coil design to restenose in the lower than in the upper quartiles of luminal gain, in agreement with the results of the GR II Stent Trial (19). In this regard, the long-term performance of the coil stent in the upper quartile of luminal gain was similar to that of the multicellular and Palmaz-Schatz designs.
The Palmaz-Schatz 153 stent demonstrated a statistically significant proportional relationship between gain and loss. Per-quartile analysis suggests that the performance of this stent also improves in the upper quartile of luminal gain. In support of these findings, intracoronary ultrasound in Palmaz-Schatz stents has demonstrated a clear relationship between incomplete expansion and the volume of neointimal hyperplasia (20). Because cross-sectional metal coverage of a stent is influenced by the degree of stent expansion, it remains plausible that these designs facilitate the develop-ment of restenosis in the lower quartiles of luminal gain. Plaque prolapse between between the two stent subunits (21) may also be more relevant under those circumstances.
Keeping in mind the limitations inherent in animal models of vascular disease, there is experimental evidence supporting the concept that stent design influences restenosis (22–25). Wall injury is mainly dictated by stent configuration and not by wall stretching (22,23). Multicellular designs generate 38% less neointimal hyperplasia than slotted-tube stents (22). The delivery of pressure by each individual strut on the vessel wall may substantially vary between different designs, particularly if, like in the self-expandable stent, there is strut overlap and chronic outward expansion of the stent (26). Some strut patterns may be less favorable than others in facilitating endothelial cell confluence and reendothelialization. Finally, plaque prolapse or insufficient stent expansion may also lead to suboptimal hemorrheology.
In agreement with previous works, we also found that vessel size influences the long-term result of stenting, favoring larger vessels (1,3,27). A small MLD preintervention was associated with increased luminal loss, as recently reported after stenting (27) and previously after PTCA (10). The length of the stented segment is also a well-known predictor of restenosis (27). Balloon pressure did not significantly influence long-term angiographic outcome (27). Unlike with other studies (3,28), LAD location was not identified as an independent predictor of long-term result.
Study limitations.
The present work is representative of the practice in a large hospital with wide experience in coronary stenting, but, being nonrandomized, it may not be free from inadvertent selection bias (i.e., selection according to specific anatomic characteristics by the operator). Although there were baseline differences between groups, multivariate analysis was performed as a technique of statistical adjustment, allowing their comparison. The antithrombotic drug regimen used in the study was not constant, following the changes in worldwide stent practice during the last five years. Finally, intravascular ultrasound was not routinely used to guide stent deployment.
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Acknowledgments
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The important work of all the staff of the angiographic core lab at our Institution is acknowledged. We are grateful to Dr. Paul Phillips, San Diego, CA, for critical review and comments and to Dr. Cristina Fernandez, from the Clinical Research Unit at our Institution, for valuable statistical advice.
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References
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Abstract
Methods