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CLINICAL STUDY: INTERVENTIONAL CARDIOLOGY

Clinical and quantitative coronary angiographic predictors of coronary restenosis

A comparative analysis from the balloon-to-stent era

Nestor Mercado, MD, DSc^*,1, Eric Boersma, PhD^*, William Wijns, MD, PhD, Bernard J. Gersh, MB, DPhil, ChB, FACC, Carlos A. Morillo, MD, Vincent de Valk, PhD^||, Gerrit-Anne van Es, PhD^||, Diederick E. Grobbee, MD, PhD^¶ and Patrick W. Serruys, MD, PhD, FACC^*

^* Thoraxcenter, University Hospital Dijkzigt, Rotterdam, The Netherlands
Cardiovascular Center, Onze Lieve Vrouw Ziekenhuis, Aalst, Belgium
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
Department of Cardiology, Fundacion Cardiovascular del Oriente Colombiano, Bucaramanga, Colombia
^¶ Julius Center for Patient Oriented Research, University Medical Center, Utrecht, The Netherlands
^|| Cardialysis, Rotterdam, The Netherlands

Manuscript received December 7, 2000; revised manuscript received May 7, 2001, accepted May 21, 2001.

Reprint requests and correspondence: Dr. Eric Boersma, Thoraxcenter, University Hospital Rotterdam, Room H-543, Dr Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands
boersma{at}thch.azr.nl

	Abstract

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OBJECTIVES

We sought to assess whether coronary stents have modified the predictive value of demographic, clinical and quantitative coronary angiographic (QCA) predictors of coronary restenosis.

BACKGROUND

A systematic analysis in a large cohort of registries and randomized trials of the percutaneous transluminal coronary angioplasty (PTCA) and stent era has never been performed.

METHODS

A total of 9,120 treated lesions in 8,156 patients included in nine randomized trials and 10 registries, with baseline, post-procedural and six-month follow-up QCA analyses, were included in this study. Predictors of restenosis were identified with univariate and multivariate logistic regression analyses. Interaction terms were introduced in the regression equation to evaluate whether the predictors of restenosis were common to both eras or specific for either one of the revascularization techniques.

RESULTS

The restenosis rate was 35% after PTCA and 19% after angioplasty with additional stenting. In the univariate analysis, favorable predictors were previous coronary artery bypass graft surgery (CABG), stent use, stent length and a large pre-procedural minimal lumen diameter (pre-MLD); unfavorable predictors were weight, body mass index, diabetes mellitus, multi-vessel disease, lesion length and a high residual post-procedural diameter stenosis (post-DS). Predictors specific for the PTCA population were a large post-procedural MLD (post-MLD) as favorable and a severe pre-procedural DS (pre-DS) as unfavorable. Favorable predictors specific for the stent population were a large post-MLD and a large pre-procedural reference diameter (pre-RD). In the multivariate analysis, the best model included the following favorable predictors: stent use, a large post-MLD, previous CABG and the interaction term between stent use and a large post-MLD; unfavorable predictors were lesion length and diabetes mellitus.

CONCLUSIONS

There are no major differences in demographic and clinical predictors of coronary restenosis between PTCA and stent populations. In the modern (stent) era, a severe pre-DS is no longer an unfavorable predictor of restenosis. Still important, but more so in the stent population, is a large post-MLD (optimal result). Finally, a larger pre-RD became a favorable predictor with the advent of stenting.

Abbreviations and Acronyms   CABG = coronary artery bypass graft surgery   CI = confidence interval   DS = diameter stenosis   IVUS = intravascular ultrasound   LAD = left anterior descending coronary artery   MLD = minimal lumen diameter   PTCA = percutaneous transluminal coronary angioplasty   OR = odds ratio   QCA = quantitative coronary angiography   RD = reference diameter

From the mechanistic point of view, there is a clear difference between restenosis after PTCA alone and PTCA plus stenting. As assessed by IVUS studies, the prevailing mechanism in restenosis after PTCA alone is arterial remodeling, with late vessel contraction responsible for >60% of late lumen loss (9), whereas accelerated intimal hyperplasia predominantly causes in-stent restenosis (10).

Previous reports, which are hampered by their small sample sizes, have analyzed a limited number of potential predictors of restenosis in either the stent or PTCA population analyzed separately. The aim of this study was to assess to what extent the introduction of coronary stents has modified the predictive value of previously identified demographic, clinical and QCA predictors of coronary restenosis in the balloon era. We combined two patient populations: patients treated with PTCA only (PTCA population) and patients who also had coronary stents implanted (stent population).

	Methods

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Patients were selected from 19 different studies: six randomized trials comparing the use of active medications aimed at coronary restenosis prevention after PTCA alone or PTCA plus stenting with placebo (Coronary Artery Restenosis Prevention On Repeated Thromboxane A₂-antagonism [CARPORT] study [11], Multicenter European Research trial with Cilazapril after Angioplasty to prevent Transluminal coronary Obstruction with Restenosis [MERCATOR] [12], Prevention of Angioplasty Reocclusion with Ketanserin [PARK] [13], Multicenter American Research trial with Cilazapril after Angioplasty to prevent Transluminal coronary Obstruction with Restenosis [MARCATOR] [14], FLuvastatin Angiographic REstenosis [FLARE] [15] and TRAPidil In Stent [TRAPIST] [16]); 10 stent registries (BElgian NEtherlands STENT [BENESTENT-2] pilot study [17], stent Primary Angioplasty in Myocardial Infarction [PAMI] pilot study [18], West European Stent Trial [WEST-1] [19], WEST-2 [20], Wallstent native study [21], Registry for Optimal beStent Evaluation [ROSE] [22], DUET [23], European Antiplatelet Stent Investigation [EASI] [24], Study Of PHosphorycholine coating On Stents [SOPHOS] [25] and MAGIC 5-L [26]); and finally, three randomized trials comparing PTCA plus coronary stenting with PTCA alone (BENESTENT-1 [27], BENESTENT-2 [28] and stent PAMI [29]).

These 19 studies were chosen because they are highly representative of the randomized trials and registries of PTCA and coronary stenting that have been performed in the past decade, antedating the use of intracoronary brachytherapy. In eight studies, treatment of more than one lesion per patient was allowed (CARPORT, MERCATOR, PARK, MARCATOR, BENESTENT-2, FLARE, stent PAMI, MAGIC 5-L); the remaining studies included only patients with a single lesion. For patients with multilesion PTCA or multilesion coronary stenting, all lesions were analyzed, and each was considered independently.

Patients were included in this analysis if they had three adequate angiograms—one immediately before the intervention, one immediately after and one at six-month follow-up. Patients with an unsuccessful procedure or with a lesion in a saphenous vein graft were excluded.

Off-line analysis of angiographic outcomes was done using identical and standardized methods of data acquisition and analysis and definitions of the variables in the same core laboratory (Cardialysis, Rotterdam, The Netherlands) using the Cardiovascular Angiography Analysis System II (CAAS II) (Pie Medical, Maastricht, The Netherlands) (30).

Definitions.   Procedural success was defined as a post-procedural diameter stenosis (post-DS) <50% on visual inspection in the early trials (CARPORT, MERCATOR, PARK, MARCATOR and FLARE). Subsequently (BENESTENT-1, BENESTENT-2 pilot, EASI, BENESTENT-2, stent PAMI pilot, WEST-1, WEST-2, Wallstent native, stent PAMI, ROSE, DUET, TRAPIST and SOPHOS), procedural success was defined as <50% post-DS by on-line QCA and no occurrence of an in-hospital major adverse cardiac event (death, acute myocardial infarction, coronary artery bypass graft surgery [CABG] or repeat PTCA), and finally, in the latest trial (MAGIC 5-L), procedural success was reset to <20% post-DS by on-line QCA in the absence of an in-hospital major adverse cardiac event. Coronary restenosis was defined uniformly in all but one randomized trial according to the binary criteria with a cut-off point 50% DS at follow-up (31). In this randomized trial (CARPORT), a noncategorical approach was used, and restenosis was defined as a loss of 0.72 mm in the MLD from post-PTCA to six-month follow-up. For standardization purposes, we computed the binary restenosis rate of this trial based on the DS on the follow-up angiogram. The standard definitions for proximal and distal segments of the right coronary artery, left anterior descending coronary artery (LAD) and left circumflex coronary coronary artery have been described elsewhere (32). The pre-procedural reference diameter (pre-RD) was obtained by the interpolation method, and the lesion length was defined by curvature analysis (33).

Statistical analysis.   Statistical analysis was performed using the SAS version 8.0 software package (SAS Institute, Cary, North Carolina). To test for differences in baseline variables across the studies, the Kruskal-Wallis test (continuous data) and the chi-square test (categorical data) were applied. Univariate and multivariate logistic regression analyses were used to evaluate the relationships between demographic data, clinical characteristics, stent use, QCA variables and the six-month outcome of angiographic occurrence of restenosis, which was coded as a binary variable according to the partial method. The stent length was 15 mm (with a minimal length of 8 mm) in 68% of patients with stents. In the remaining patients, the stent length varied from 18 mm (DUET study) to 48 mm (MAGIC 5-L study). For restenosis assessment, these two different subsets of the stent population (15 and >15 mm) were compared with the PTCA population.

Interaction terms between demographic data, clinical characteristics, QCA variables and stent use were introduced to evaluate the influence of coronary stents on the predictors of coronary restenosis. To prevent associations by chance, p < 0.001 was considered significant for these interaction terms. All variables were entered into the multivariate model, irrespective of the results of the univariate analysis (excluding the interaction terms in which the specified level of significance was not reached). The final multivariate model was constructed by backward deletion of the least significant variables, while the Akaike criterion was applied—that is, the applied threshold of significance depended on the degrees of freedom (df) associated with the variable at hand; if df = 1, then p = 0.157 (34). The predictive accuracy of the final multivariate model was evaluated using the C-index (35) and the goodness of fit of the model was tested with the Hosmer-Lemeshow goodness-of-fit test (36).

	Results

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A total of 9,120 treated lesions in 8,156 patients were considered for this study. Sixty-four percent of the patients were treated with PTCA only (PTCA population: n = 5,230; 6,110 lesions), and coronary stents were implanted in 36% of patients (stent population: n = 2,926; 3,010 lesions).

The restenosis rate at six-month QCA follow-up was 35% after PTCA, compared with 19% after stenting. The baseline characteristics of the PTCA and stent populations are described in Table 1.

The pre- and post-procedural and six-month follow-up QCA variables are described in Table 2. It is important to note that the restenosis rate decreased from 38% in PARK (1993, PTCA) to 12.8% in WEST-2 (1998, PTCA plus stenting). This decrease in the restenosis rate was observed despite a parallel increase in the length of treated lesions, from a median of 5.8 mm in MERCATOR (1992, PTCA) up to 14.3 mm in MAGIC 5-L (1999, PTCA plus stenting). The post-procedural minimal lumen diameter (post-MLD) increased as well, with median values ranked between 1.67 mm in PARK (1993, PTCA) to 2.89 mm in EASI (1997, PTCA plus stenting).

View larger version (22K): [in this window] [in a new window]   Figure 1 Univariate analysis of demographic, clinical and quantitative coronary angiography (QCA) predictors of coronary restenosis. When a common odds ratio (OR) is presented, the interaction term between stent use and each of the variables was not significant (p 0.001), and then this is the OR (and its corresponding 95% confidence interval [CI]) for the percutaneous transluminal coronary angioplasty (PTCA) and stent populations (solid circles). The interaction term between stent use and each of the variables was significant (p < 0.001) if the PTCA (solid triangles) and stent (solid squares) populations each had two ORs (with 95% CIs) presented. AMI = acute myocardial infarction; BMI = body mass index; CABG = coronary artery bypass graft surgery; CSA = chronic stable angina; DM = diabetes mellitus; DS = diameter stenosis; HTA = hypertension; LAD = left anterior descending coronary artery; LCx = left circumflex coronary artery; MI = myocardial infarction; MLD = minimal lumen diameter; MVD = multi-vessel disease; PVD = peripheral vascular disease; RCA = right coronary artery; RD = reference diameter; UA = unstable angina.

In the multivariate analysis, the model with the best predictive accuracy and that best fit the entire population (Table 3) was composed of the following favorable predictors: stent use (OR 0.83, 95% CI 0.72 to 0.97), a large post-MLD (OR 0.53, 95% CI 0.46 to 0.61), previous CABG (OR 0.69, 95% CI 0.53 to 0.9) and the interaction term between stent use and a large post-MLD (OR 0.34, 95% CI 0.31 to 0.39); unfavorable predictors were lesion length (OR 1.05, 95% CI 1.04 to 1.06) and diabetes mellitus (OR 1.33, 95% CI 1.16 to 1.54). The Hosmer-Lemeshow goodness-of-fit test indicated that the model fit well with the data (goodness-of-fit statistic 2.81, p = 0.94).

	Discussion

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In this study, several clinical and QCA predictors of coronary restenosis were identified in a large number of patients in two distinct populations. Significant demographic and clinical predictors of restenosis did not differ between patients treated with PTCA alone and those with stents. In contrast, three QCA variables were differentially associated with restenosis. A large post-MLD was a favorable predictor in both the PTCA and stent populations, but the protective effect was more marked in the stent population. A severe pre-DS was an unfavorable predictor in the PTCA population only, and a large pre-RD was a favorable predictor in the stent population.

Clinical predictors.   Diabetes mellitus
Patients with diabetes mellitus have been repeatedly shown to have an increased risk of developing restenosis, as compared with nondiabetics (37,38). The mechanisms responsible for the increased proclivity for restenosis in the diabetic patient are not completely understood. In an IVUS analysis, it was concluded that the main reason for increased restenosis in diabetic patients was exaggerated intimal hyperplasia in both stented and nonstented lesions (38). However, data from Van Belle et al. (39) do not support this hypothesis, but rather favor vessel remodeling (i.e., vessel constriction) as the main mechanism.

Alterations in the expression of components of the fibrinolytic system within the lesions of diabetic patients may also be an important determinant of restenosis. Sobel et al. (40) demonstrated, in a detailed immunohistochemical analysis of coronary atherectomy samples, a disproportionate elevation of concentrations of the prothrombotic plasminogen activator inhibitor type 1, which may induce restenosis by clot-associated mitogens. More recently, atherectomy specimens from restenotic lesions after PTCA showed a reduced intimal hypercellular tissue content in patients with diabetes (41). Collagen-rich sclerotic content is increased, suggesting an accelerated fibrotic rather than a proliferative response in diabetics with restenosis after PTCA, putting into context again the fundamental importance of vessel remodeling in diabetics.

Previous CABG
In the present study, restenosis was less likely to occur in the subgroup of patients with previous CABG. Vein graft intervention was excluded from our analysis. We can only speculate about possible mechanisms leading to less restenosis in patients with previous CABG. Some baseline characteristics differed between patients with and those without previous CABG, such as a lower percentage of current smokers (14% vs. 26%) and a higher proportion of patients with chronic stable angina (85% vs. 75%). However, these variables did not independently predict restenosis by univariate analysis. The association is weak, and residual confounding factors may have played a role.

Weight
Overweightness was positively associated with restenosis by univariate, but not by multivariate analysis. It may be argued that a potential relationship between obesity and restenosis is mediated through increased lipid levels. However, we found no association between total cholesterol, cholesterol subfractions and restenosis after successful PTCA by either a categorical or continuous approach (42).

Clinical diagnosis
We did not find the clinical diagnosis at the time of enrollment to be a predictor of restenosis in either the PTCA or stent populations. However, in patients treated with directional coronary atherectomy, clinical instability was associated with signs of plaque inflammation, which may promote restenosis (43).

Angiographic predictors.   Coronary stenting
The protective effect of coronary stenting against restenosis was demonstrated unequivocally by two major randomized trials (27,44). Further improvements in the technique of stent deployment and new stent designs have also contributed to decreasing the restenosis rate (45).

Pre-RD
The pre-RD is a predictor of restenosis in the stent population, but not in the PTCA population. Because the implantation of stainless-steel stents invariably results in neointimal regrowth, >50% stenosis is more likely to occur in vessels of small diameter. Supporting this concept, Bauters et al. (3) showed that stenting in vessels with a small RD was not associated with a greater lumen loss.

Post-MLD
The post-MLD clearly influences restenosis development. The "bigger is better" paradigm proposed by Kuntz et al. (46) means that for every millimeter of increase in the post-MLD, there is an OR of 0.56 (95% CI 0.49 to 0.64) for restenosis in the PTCA population and an OR of 0.33 (95% CI 0.27 to 0.42) in the stent population. Our findings indicate that the additional gain in post-MLD for restenosis prevention is more relevant after stent deployment than after plain balloon angioplasty.

Lesion length
Previous reports (5,47) have shown that lesion length was positively related with restenosis in PTCA alone and stented lesions. In these studies, lesion length was dichotomized with cut-off values 6.8 mm for patients treated with balloons and >15 mm for those treated with stents. In this study, we used a continuous approach for lesion length and for each millimeter of increase in length, we found an OR of 1.04 (95% CI 1.03 to 1.05) for lesions treated with both PTCA and stents.

Stent length
Our dichotomous approach for stent lengths 15 mm and stent lengths >15 mm, each compared to PTCA, indicated that the protective effect of stenting against coronary restenosis is reduced by 12% when longer stents are used. Kobayashi et al. (48) similarly demonstrated, in an analysis of 1,090 lesions in 725 patients, that a progressively longer stented segment is associated with an increased risk of restenosis, with six-month restenosis rates of 24%, 35% and 47% for stented segment lengths 20, >20 to 35 and 35 mm, respectively. In a recent pooled analysis of four MULTI-LINK stent trials (49), stent length was found to be a significant predictor of restenosis both by univariate and multivariate analyses, and for each millimeter of increase in stent length, there was an OR of 1.04 for restenosis development.

Location of treated lesion
The impact of the location of the treated lesion on restenosis has been described in previous PTCA (1) and stent (2) studies. Evidence is conflicting, but most often, it is claimed that LAD lesions are more prone to restenosis. In one study (1), an OR of 1.7 (95% CI 1.5 to 2.1) was found for proximal, as compared with nonproximal LAD lesions treated with PTCA alone in a sample of 2,500 patients. Another analysis of binary restenosis at follow-up in 1,399 lesions reported an OR of 1.31 for stented lesions in the LAD (2). In these two previous studies, a positive association was found, whereas others noted that the location of the stented lesion had no impact on restenosis after coronary stenting (3). After a detailed analysis, our results indicate that there is no evidence to support the idea that a given treatment location plays a role in the restenotic process.

Study limitations.   Short- and long-term clinical and angiographic outcomes after PTCA and stenting certainly have improved over the past decade as a result of better stent deployment strategies and more effective antithrombotic regimens. Both balloon-expandable stents (Palmaz-Schatz [PS]-153: 8.7%; heparin-coated PS-153: 33%; MULTI-LINK: 9%; beStent: 4%; MULTI-LINK DUET: 5.2%; Crossflex: 9.2%; and BiodivYsio: 6.7%) and self-expanding stents (Magic Wallstent: 10.4%; Wallstent: 13.8%) were used, and we did not stratify for the potential influence of different stent types on restenosis.

New techniques, such as vascular brachytherapy (50) and drug-eluting stents (51), have become available recently. Patients treated with these modalities represent a distinctive population in which the results of our analyses should not be applied.

Conclusions.   There are no major differences in demographic and clinical predictors of coronary restenosis between PTCA and stent populations. In the modern (stent) era, a severe pre-DS is no longer an unfavorable predictor of restenosis. Still important, but more so in the stent population, is a large post-MLD (optimal result). Finally, a larger pre-RD became a favorable predictor with the advent of stenting.

	Footnotes

 
¹ Dr. Mercado was funded in part by the Euro Heart Survey program of the European Society of Cardiology.

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