CLINICAL RESEARCH
Vascular Effects of Sirolimus-Eluting Versus Bare-Metal Stents in Diabetic Patients
Three-Dimensional Ultrasound Results of the Diabetes and Sirolimus-Eluting Stent (DIABETES) Trial
Pilar Jiménez-Quevedo, MD*,
Manel Sabaté, MD, PhD*,*,
Dominick J. Angiolillo, MD ,
Marco A. Costa, MD, PhD,
Fernando Alfonso, MD, PhD*,
Joan Antoni Gómez-Hospital, MD, PhD ,
Rosana Hernández-Antolín, MD, PhD*,
Camino Bañuelos, MD*,
Javier Goicolea, MD, PhD ,
Francisco Fernández-Avilés, MD, PhD||,
Theodore Bass, MD,
Javier Escaned, MD, PhD*,
Raul Moreno, MD*,
Cristina Fernández, MD, PhD*,
Carlos Macaya, MD, PhD* for the DIABETES Investigators
* San Carlos University Hospital, Madrid, Spain
University of Florida Cardiovascular Imaging Core Laboratories, Jacksonville, Florida
"Prínceps d'Espanya" University Hospital, Barcelona, Spain
"Do Meixoeiro" University Hospital, Vigo, Spain
|| Clínico University Hospital, Valladolid, Spain
Manuscript received October 31, 2005;
revised manuscript received December 29, 2005,
accepted January 16, 2006.
* Reprint requests and correspondence: Dr. Manel Sabaté, Hospital Clínico San Carlos, Plaza Cristo Rey s/n, 28040 Madrid, Spain (Email: manelsabate1{at}telefonica.net).
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Abstract
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OBJECTIVES: A predefined intravascular ultrasound (IVUS) substudy was performed to evaluate the vascular effects of sirolimus-eluting stent (SES) versus bare-metal stent (BMS).
BACKGROUND: The Diabetes and Sirolimus-Eluting Stent (DIABETES) trial is a prospective, multicenter, randomized, controlled trial aimed at demonstrating the efficacy of the SES compared with BMS in diabetic patients.
METHODS: Serial intravascular ultrasound analyses were performed in 140 lesions (SES = 75; BMS = 65) immediately after stent implantation and at nine-month follow-up. Vessel, luminal, and stent mean areas and volumes were evaluated at both edges and within the stented segment. Qualitative assessment of residual dissections and stent apposition were also performed.
RESULTS: Baseline clinical and angiographic characteristics were similar between groups. At 9 months, in-stent neointimal hyperplasia (NIH) mean area and volume were significantly reduced in the SES group (median NIH area 0.01 mm2 [0.0 to 0.1] vs. 2.0 mm2 [1.0 to 2.9] and median NIH volume 0.11 mm3 [0 to 2.1] vs. 35.3 mm3 [16.6 to 62.6]; both p < 0.0001). In the SES group, stent edges evidenced significant increase in lumen dimensions mainly due to significant increase in vessel volume, whereas those of the BMS group presented vessel shrinkage leading to significant lumen reduction. Late acquired incomplete stent apposition was observed in 11 lesions (14.7%) in the SES group and 0 in the BMS group (p = 0.001). At one year, no stent thromboses occurred in malapposed stents.
CONCLUSIONS: The SES implantation effectively inhibits NIH in diabetic patients. The antirestenotic effect of SES is also appreciated at the stent edges. Late acquired stent malapposition is a frequent phenomenon in diabetic patients treated with SES.
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Abbreviations and Acronyms
| | BMS = bare-metal stent | | DIABETES = Diabetes and Sirolimus-Eluting Stent trial | | EEM = external elastic membrane | | ISA = incomplete stent apposition | | IVUS = intravascular ultrasound | | NIH = neointimal hyperplasia | | SES = sirolimus-eluting stent |
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Despite advances in the medical treatment and revascularization procedures, coronary artery disease remains a leading cause of morbidity and mortality in diabetic patients (1). Diabetic patients often present unfavorable coronary anatomy with small and diffusely diseased vessels (2) and exhibit different healing response after stent implantation as compared with nondiabetics (3). The sirolimus-eluting stent (SES) has been demonstrated to reduce restenosis in selected patients with de novo coronary lesions (4,5). Retrospective subgroup analyses of pivotal clinical trials have suggested that SES may be effective in diabetic patients (6,7). However, the potent antiproliferative effect of SES (8), which markedly inhibits neointimal hyperplasia (NIH) (4,5), may also induce deleterious local phenomena such as necrosis or apoptosis (9), which potentially affect the plaque behind the stent and the vessel wall (10). Volumetric intravascular ultrasound (IVUS) provides complementary information on the extent of neointimal proliferation, arterial remodeling, and collateral effects such as edge restenosis and incomplete stent apposition (ISA). To date, few data of the mechanistic effects of SES in diabetics have been reported. The Diabetes and Sirolimus-Eluting Stent (DIABETES) trial is the first randomized multicenter study to compare the outcomes of diabetic patients treated with SES versus bare-metal stents (BMS) (11).
The aim of the present study was to evaluate the vascular effects of SES compared with BMS by means of serial three-dimensional volumetric IVUS analyses as well as to report the one-year clinical results in patients enrolled in the DIABETES trial.
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Methods
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Patient selection.
Between February and December 2003, the DIABETES trial enrolled 160 diabetic patients with de novo coronary stenoses (2.25 to 4.0 mm in diameter by visual estimation) located in one, two, or three vessels to receive either SES (Cypher, Cordis, Miami, Florida) or BMS (Velocity, Cordis) implantation. A total of 221 coronary stenoses were treated in this trial (111 lesions in 80 patients with Cypher stents and 110 lesions in 80 patients with Velocity stents). There were no exclusions based on lesion length or presence of chronic total occlusions. The DIABETES study protocol has been described in detail elsewhere (11). Clopidogrel was maintained for one year in all randomized patients. The current IVUS study was prespecified in the DIABETES trial protocol, and the goal was to obtain a minimum of 60% of the implanted stents assessed by IVUS. The study was approved by the institutional review board of each participating center, and all patients signed a written informed consent.
Volumetric IVUS.
The IVUS studies were performed with a 40-MHz mechanical system (Atlantis; Boston Scientific, Natick, Massachusetts). Images were acquired during a motorized pullback of the IVUS probe at a constant speed of 0.5 mm/s, after intracoronary administration of 0.1 to 0.2 mg nitroglycerin, after the procedure, and at nine-month follow-up. All IVUS procedures were recorded on super-VHS videotapes. Qualitative and quantitative volumetric IVUS analyses were performed by an independent core laboratory (University of Florida Cardiovascular Imaging Core Laboratories, Jacksonville, Florida) using a methodology previously reported (12). The analysts were blinded to treatment allocation. The stented coronary segments and both edges (5 mm adjacent to the distal and proximal stent borders) were selected for quantitative and qualitative analysis. Quantitative three-dimensional IVUS analysis was performed using a dedicated quantitative intravascular ultrasound analysis system (QIVA, Pie Medical Imaging, Maastricht, the Netherlands) (12). Lumen, stent, and external elastic membrane (EEM) areas were measured along the entire stented and edge segments. Volumes were determined from a summation of measured cross-sectional areas in all frames of the pullback region based on Simpson's rule (12).
In-stent NIH volume was calculated as stent volume minus luminal volume at nine-month follow-up. Percent NIH volume was defined as the ratio of NIH volume to the stent volume multiplied by 100. Mean in-stent NIH area was calculated as in-stent NIH volume divided by stent length. For totally occluded vessels at follow-up, which were not associated with stent thrombosis, it was estimated that the entire length of the stent was filled with NIH (13).
Incomplete stent apposition was defined as  1 strut clearly separated from the vessel wall, with evidence of blood speckling behind the stent struts without overlapping side branches (14). To define ISA, consensus between two independent analysts blinded to treatment allocation was required. On the basis of serial intravascular analyses ISA was classified into three categories: 1) resolved: ISA present at baseline but no longer at follow-up; 2) persistent: ISA present at baseline and at nine-month follow-up; and 3) late acquired: ISA not present at baseline but present at nine-month follow-up. In the segment with ISA, the lumen contour was delineated outside the stent contour. Lumen area outside of the stent was also measured (ISA area). Further, vessel, stent, and lumen mean areas and volumes were measured in both the ISA and the non-ISA segments within the stent.
Clinical follow-up.
After discharge, clinical follow-up was obtained at 1, 9, and at 12 months. At 12 months, clopidogrel was withdrawn in all patients who did not receive additional revascularization during follow-up.
Statistical analysis.
The sample size for this prespecified IVUS substudy was calculated for a difference of 30% in the mean in-stent NIH area between the groups (estimated for a mean in-stent NIH area of 2.2 mm2 in the BMS arm vs. 1.5 mm2 in the SES arm), with a standard deviation of 1.5, alpha error of 0.05, and beta error of 0.20 (13). Thus, a minimum of 105 lesions were prespecified for enrollment to allow for 25% attrition due to noncompliance with invasive follow-up procedures, IVUS technical failures, and suboptimal IVUS quality.
Data are presented as frequencies, mean ± 1 SD, or median (interquartile range). Following evaluation of normal distribution (Kolmogorov-Smirnov test), comparisons between BMS and SES stents were performed with two-tailed, unpaired t tests for continuous parameters, paired t tests for change from post-procedure to follow-up, or median comparisons when applicable using the median test. Categoric variables were compared by means of the chi-square test or Fisher exact test when at least 25% of values showed an expected cell frequency below 5. Significance was set at alpha of 0.05.
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Results
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Baseline characteristics.
One hundred seventeen patients (140 lesions) were included in this IVUS substudy. This cohort involved 73% of patients included in the trial. We could not perform IVUS in 81 lesions. Main reasons included very small vessel size (n = 53; 66%), distal location of the target stent in tortuous vessels (n = 19; 23%), and diffuse disease distal from the target stent (n = 9; 11%).
Baseline demographic and angiographic characteristics of this subset of patients were comparable between SES and BMS groups (Tables 1 and 2). This cohort of patients assessed by IVUS presented similar baseline clinical characteristics to those not evaluated by IVUS. However, from the angiographic point of view, lesions evaluated by IVUS evidenced larger vessel size and more often were located in the right coronary artery both in the SES and in the BMS group. Besides, in the BMS group, IVUS-assessed stents were less often implanted in chronic total occlusions than in those without IVUS assessment. In terms of outcomes, stents studied by IVUS presented less frequent restenosis at follow-up. The length of restenotic segment was similar between lesions assessed or not by IVUS (18.7 ± 10 mm vs. 18.2 ± 11 mm, respectively, in the BMS group; p = 0.69; 11.8 ± 7 mm vs. 12.0 ± 8 mm, respectively, in the SES group; p = 0.76). Occlusive restenoses were not interrogated by IVUS (one in the SES group and six in the BMS group). Finally, two stents in the SES group and one in the BMS group with edge effect were not studied by IVUS.
At nine-month angiographic follow-up, 112 patients (134 lesions) were reassessed by IVUS (95.7% of the eligible patients and lesions).
Stented segment IVUS analysis.
Post-procedure IVUS parameters were similar between groups (Table 3). There was an increase in EEM area from post-procedure to follow-up in the SES group (15.8 ± 4.8 mm2 to 16.7 ± 4.3 mm2 from post-procedure to follow-up; p = 0.04). In the BMS group, mean lumen area was significantly reduced from post-procedure to follow-up (8.0 ± 2.5 mm2 to 5.3 ± 2.5 mm2; p < 0.001). The NIH median area and volume were significantly reduced in the SES group as compared to the BMS group (median NIH area 0.01 mm2 [0.0 to 0.1] vs. 2.0 mm2 [1.0 to 2.9]; median NIH volume 0.11 mm3 [0.0 to 2.1] vs. 35.3 mm3 [16.6 to 62.6]; both p < 0.0001). Figure 1 depicts the non-gaussian distribution of main IVUS volumetric outcomes between groups, with the marked difference observed between mean and median values especially in the SES group.
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Figure 1 (Top panels) Histograms of neointima hyperplasia (NIH) volume in the sirolimus-eluting stent (SES) group (left) and the bare-metal stent (BMS) group (right). A non-Gaussian distribution is demonstrated in both groups (Kolmogorov-Smirnov test: p < 0.0001 for SES group; p = 0.02 for BMS group). The median test evidenced significant differences between groups. (Bottom panels) Histograms of percent volume obstruction in the SES group (left) and the BMS group (right). A non-Gaussian distribution is demonstrated in both groups (Kolmogorov-Smirnov test: p < 0.0001 for SES group; = 0.03 for BMS group). The median test evidenced significant differences between groups.
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More than 50% of segments treated with SES evidenced virtually no NIH (Fig. 1). Neointimal hyperplasia inhibition by SES was independent of the diabetes status and stent size and length (Table 4).
Edge effect.
Volumetric analysis of the stent edges demonstrated a different pattern of vascular changes between groups (Fig. 2). In the SES group, a significant increase in EEM volume (vessel enlargement) could encompass an increase in plaque volume, resulting in discrete net luminal enlargement. Conversely, in the BMS group, negative remodeling of the EEM led to net luminal reduction despite the absence of plaque growth. This pattern of vascular behavior was similar in either edge.
ISA, coronary aneurysm, and edge tears.
Overall, the incidence of ISA was significantly higher in the SES group than in the BMS group (n = 22 [29%] vs. n = 5 [7.7%]; p = 0.001). This phenomenon occurred mainly as a result of an increased incidence of late acquired ISA in the SES group (n = 11 [14.7%] vs. n = 0 [0%]; p = 0.001). Additionally, four patients (three in the SES group and one in the BMS group) also presented ISA at follow-up. However, because their baseline studies were not available for serial comparison, they were not accounted as late acquired ISA. There were no significant differences between groups in both resolved (n = 0 [0%] in the SES group vs. n = 2 [3.1%] in the BMS group; p = 0.2) and persistent ISA (n = 8 [10.7%] in the SES group vs. n = 2 [3.2%] in the BMS group; p = 0.1). An example of late acquired ISA is depicted in the Figure 3.
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Figure 3 (Top) Intravascular imaging of a stent completely apposed immediately after the implantation. (Bottom) Same artery imaging at nine-month follow-up: Late acquired incomplete stent apposition is evidenced.
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To determine the main mechanism of the three types of ISA, a quantitative analysis of the lumen and EEM areas specifically at the malapposition sites was performed and compared with the corresponding segments of the post-procedure IVUS pullback. In addition, we compared lumen and EEM areas at the malapposition site (ISA segment) with the remaining part of the stent without malapposition (non-ISA segment). In those lesions with late acquired ISA (n = 11) a significant increase in lumen and vessel mean areas at the ISA segment were observed from post-procedure to follow-up (mean lumen area 7.5 ± 1.9 mm2 vs. 8.8 ± 1.5 mm2; p = 0.04; mean EEM area 16.6 ± 3.9 mm2 vs. 19.2 ± 2.9 mm2; p = 0.03). In addition, mean lumen and EEM areas were significantly larger at the ISA segment compared with non-ISA segments (mean lumen area 8.8 ± 1.5 mm2 vs. 7.5 ± 1.2 mm2; p = 0.02; mean EEM area 19.2 ± 2.9 mm2 vs. 16.7 ± 2.8 mm2; p = 0.03). Thus, local positive remodeling appeared to be involved in the mechanism of late acquired ISA in diabetic patients. Late acquired ISA was mainly localized at stent edges (73%).
Overall, stents with persistent malapposition (n = 10) did not evidence significant changes in EEM or lumen mean areas between post-procedure and follow-up (lumen area 8.9 ± 2.7 mm2 vs. 8.8 ± 3.7 mm2; p = 0.9; EEM area 18.4 ± 5.9 mm2 vs. 18.7 ± 5.8 mm2; p = 0.8). Finally, stents with resolved ISA (n = 2) presented an increase in mean plaque area (delta change 5.9 mm2) and virtually, no modification in mean EEM area (delta change –0.6 mm2). As a result, mean lumen area was reduced at follow-up (delta change –4.3 mm2).
None of the segments assessed by IVUS evidenced coronary aneurysm. Resolved and persistent rates of edge tears were comparable between groups (SES vs. BMS: 3.9% vs. 6.5% [p = 0.7] and 2.6% vs. 0% [p = 0.5], respectively).
Clinical outcomes at one year.
One-year clinical follow-up of the entire population included in the DIABETES trial was available in all patients (100%). Overall, the incidence of major adverse cardiac events was significantly lower in the SES group (Table 5).
At one year, all patients (100%) were on treatment with clopidogrel. The subacute (from 24 h to 30 days after the index procedure) and late (beyond 30 days after the index procedure) stent thrombosis rates were 0% in the SES group up to one-year follow-up. There were two stent thromboses in the BMS group, one subacute and one late; the first occurred while the patient was on dual antiplatelet therapy and the latter one week after transient clopidogrel withdrawal (due to gastrointestinal surgery) two months after the index procedure. Only one patient with late acquired ISA underwent nonclinically driven target lesion revascularization based on the IVUS findings. Following clopidogrel withdrawal at one year, there was no reported stent thrombosis associated with documented ISA.
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Discussion
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This is the first randomized blinded IVUS study in patients with diabetes mellitus to evaluate the antirestenotic effect of SES compared with BMS. Compared with the BMS group, diabetic patients treated with SES evidenced a marked reduction in NIH volume within the stented segment. This study also demonstrated an enhanced compensatory vessel enlargement at both proximal and distal edges and a significantly higher incidence of late acquired ISA associated with the implantation of SES. Finally, the clinical beneficial effect of SES implantation in this cohort of diabetic patients with small coronary arteries persisted up to the one-year follow-up. This is in accordance with the findings of the cohort of diabetic patients included in the Sirolimus-Eluting Stent and a Standard Stent in the Prevention of Restenosis in Small Coronary Arteries (SES-SMART) study (15,16).
The NIH was similarly inhibited in both insulin and non–insulin-dependent diabetics treated with SES. The relative reduction in NIH volume was higher in the insulin-dependent group, which was likely owing to a higher proliferative response observed in the BMS group. The subanalyses of the Sirolimus-Eluting Stent in Coronary Lesions (SIRIUS) and SES-SMART trials (7,16) suggested a reduced antiproliferative effect of SES in insulin-dependent diabetics, mainly related to restenosis at the stent edges (peri-stent). Such a hypothesis was not confirmed in the overall DIABETES trial and in the present IVUS substudy. The higher degree of NIH suppression demonstrated in insulin-dependent lesions may indicate that in the absence of peri-stent restenosis (7,16), rapamycin may be even more efficacious in this subgroup which usually presents an exacerbated proliferative response to stent implantation (3).
Opposite patterns of changes in EEM were observed at the edge segments in vessels treated with SES versus BMS (Fig. 2). As a result, lumen was preserved in the edge segments of patients treated with SES. Vessel shrinkage or lack of positive remodeling has been previously observed at the edges after BMS implantation (17,18). Whether the present IVUS findings are associated with a beneficial vascular effect of sirolimus at unstented adjacent coronary segments remains to be demonstrated. Interestingly, both groups in the present study showed minimal plaque proliferation at the edges, which may be related to stent deployment techniques used in this trial. In the DIABETES trial, judicious stent deployments with special attention to cover the entire diseased segment and avoid trauma outside the stented zone, namely, geographical miss, were performed (19,20).
The incidence of late acquired ISA was markedly increased in the SES group. This phenomenon was associated with local vessel enlargement at ISA sites. Recently, in the SIRIUS trial (21), late acquired ISA was documented in 8.7% of stents evaluated with IVUS and it was mainly located at the middle portion of the stent. Conversely, in our trial late acquired ISA was mainly located at stent edges. The positive remodeling appeared to be the main cause of ISA, which was extended beyond the boundaries of the stent, leading to a beneficial vascular effect at the edges (Fig. 2). On the other hand, trials by the use of paclitaxel-eluting stent demonstrated similar rates of ISA as compared with BMS (22). Late acquired ISA may be related to localized hypersensitivity response to the polymer that remains in situ after complete drug release (23). Eventually, diabetes mellitus as a proinflammatory disease (24) may exhibit an enhanced inflammatory reaction after drug-eluting stent implantation. However, at present no data exist regarding a higher incidence of late acquired ISA after SES implantation in diabetics than in nondiabetics. Other plausible mechanistic explanations for the ISA phenomenon include wash-out of plaque or thrombus entrapped behind the stent struts after the procedure, tissue necrosis, and positive vessel remodeling associated with the lack of NIH (10). Although no thrombotic event was associated with ISA even after withdrawal of clopidogrel, a word of caution must be given to keep these patients under clinical control given the possibility of the occurrence of very late stent thrombosis (25).
Study limitations.
The main limitation of this study is the potential selection bias inherent to any IVUS evaluation. Therefore, this data can not be extrapolated to the diabetic population with vessels not amenable for IVUS assessment. However, in this DIABETES IVUS substudy >70% of patients could be assessed by IVUS and no baseline clinical or angiographic differences were observed between SES and BMS groups. Also, IVUS assessment was performed in only three out of eight SES presenting with restenosis (Table 2). Therefore, we cannot extrapolate these findings to the entire cohort of restenotic SES. This is also an inherent limitation of any IVUS study, especially when one tries to avoid the undesirable risk of inducing a nonclinically driven target lesion revascularization.
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Footnotes
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Dr. Jiménez-Quevedo is a recipient of a Community of Madrid-European Social Funding grant.
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E. Camenzind, P. G. Steg, and W. Wijns
A Cause for Concern
Circulation,
March 20, 2007;
115(11):
1440 - 1455.
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Abstract
Methods