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J Am Coll Cardiol, 2000; 35:1580-1589
© 2000 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Longitudinal straightening effect of stents is an additional predictor for major adverse cardiac events

Mariann Gyöngyösi, MD, PhDa, Paul Yang, MDa, Aliasghar Khorsand, MSa, Dietmar Glogar, MD, FESCa on behalf of the Austrian Wiktor Stent Study Group* European Paragon Stent Investigators

a Division of Cardiology, 2nd Department of Internal Medicine, University Medical School of Vienna, Vienna, Austria

Manuscript received June 21, 1999; revised manuscript received November 11, 1999, accepted January 7, 2000.

Reprint requests and correspondence: Dr. Mariann Gyöngyösi, Division of Cardiology, Second Department of Internal Medicine, University Medical School of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria
gyongyosi{at}pop3.kard.akh-wien.ac.at


    Abstract
 Top
 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
OBJECTIVES

The aim of this study was to perform an investigation of the effects of the longitudinal straightening of coronary arteries by stents and the possible association with major adverse cardiac events (MACE) (primary end point) and angiographic restenosis (secondary end point).

BACKGROUND

Stent deployment straightens a tortuous artery, and any consequent arterial longitudinal stretch may contribute to MACE and stent restenosis severity.

METHODS

Clinical, qualitative and quantitative angiographic data on 404 patients with single stent implantation were subjected to multivariate nominal logistic regression analysis for the prediction of MACE. The predictive accuracy, sensitivity and specificity values and cut-off points of the continuous variables were determined via receiver operating characteristics curves. The longitudinal straightening effect of stents was characterized through the changes in vessel angle (defined by the tangents to the proximal and distal parts of the stenoses/stents).

RESULTS

Follow-up angiography on 354 patients revealed 73 cases of stent restenosis (≥50% diameter stenosis). Coronary bypass surgery was performed in 4 patients and repeated percutaneous transluminal coronary angioplasty in 56 patients; acute myocardial infarction (AMI) occurred in 2 patients, and 4 patients died during the follow-up. The overall incidence of MACE (death, AMI and revascularization) was 16.3% (66 patients). The best predictive accuracies and sensitivities/specificities of factors indicative of MACE were found for the minimal lumen diameter (MLD) at follow-up (predictive accuracy: 0.9305, sensitivity/specificity: 86.6%), the post-stent MLD (0.773, 77.2%), the percent diameter stenosis (%DS) at follow-up (0.9432, 87.1%), the prestent vessel angulation (0.6797, 68.2%) and the poststent changes in vessel angulation (0.6279, 62.2%). Multivariate nominal logistic regression analysis demonstrated that a poststent MLD ≤2.63 mm (p = 0.0017, odds ratio [OR] = 17.961, 95% confidence interval [CI] = 17.45–20.428), an MLD at follow-up ≤1.7 mm (p = 0.0059, OR = 11.880, 95% CI = 11.490–14.093), a %DS at follow-up ≥42.2% (p = 0.0000, OR = 49.553, 95% CI = 48.024–53.507), a prestent vessel angulation ≥33.5° (p = 0.0477, OR = 5.404, 95% CI = 5.382–7.142) and poststent changes in vessel angulation ≥9.1° (p = 0.0026, OR = 19.161, 95% CI = 18.562–21.750) were significant predictors for MACE. Multiple linear regression revealed that the poststent MLD (multivariate p = 0.0001), the MLD at follow-up (p = 0.0000), the prestent vessel angulation (p = 0.0431) and the changes in vessel angulation after stent implantation (p = 0.0316) were significant independent variables predicting angiographic stent restenosis severity.

CONCLUSIONS

The longitudinal straightening effect of coronary artery stents contributes significantly to the occurrence of MACE and angiographic restenosis, and this finding may have an impact on future stent design.

Abbreviations and Acronyms
  CI = confidence interval
  %DS = percent diameter stenosis
  LAD = left anterior descending coronary artery
  MACE = major adverse cardiac events
  MLD = minimal lumen diameter
  OR = odds ratio
  PTCA = percutaneous transluminal coronary angioplasty
  QCA = quantitative coronary angiography
  RD = reference diameter
  ROC = receiver operating characteristic


The two most important features of a coronary stent are basic to its use: the radial force with which it supports the vessel and its longitudinal flexibility, one of the major determinants of its trackability into the target lesion before deployment (1). Accordingly, the ideal coronary stent would be very flexible and should have high radial strength to avoid collapse due to the pressure exerted on it by a diseased artery wall, but it should adapt easily to changes in diameter and tortuosity due to coronary vasomotion and heartbeats. These opposing demands on stents have led to a multiplicity of designs, each of them being a compromise.

Numerous studies have examined the roles of various clinical, angiographic and procedural factors influencing the patient’s outcome after stent deployment (2–4). Several predictors of stent restenosis have been identified in recent studies, including patient-related factors such as diabetes mellitus (5,6), restenotic lesion (7), lesion length (8), smaller vessel size (9–11) and procedural variables such as the final minimal lumen diameter (MLD) (10,12), stenting of the total occlusion (13), multiple stent implantation (10,14) and bail-out conditions (11).

The starting point of this study was the angiographic observation that, apart from the radial arterial wall stretch, stent implantation straightens the coronary artery and particularly a tortuous vessel. We defined two geometric effects of stents on the vessel wall (Fig. 1): (a) the radial stretch, which increases the lumen diameter but does not change the angles between the lumen axis and the tangents, and (b) longitudinal straightening, which decreases the angles between the lumen axis and the tangents, i.e., it decreases the curvature of the vessel but does not necessarily affect the lumen diameter. In contrast with the beneficial effect of the radial stretching effect of a stent (e.g., inhibition of constrictive remodeling), the longitudinal straightening effect of a stent on an artery may theoretically provoke neointimal hyperplasia and contribute to restenosis.



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Figure 1 Schematic outline of the radial stretching (left) and longitudinal straightening (right) effect of the stent.

 
The aim of our study, therefore, was to investigate the longitudinal straightening effect of stent implantation on the coronary artery, as a possible additional risk factor for major adverse cardiac events (MACE) and angiographic restenosis, and the correlation between MACE, restenosis and the changes in vessel curves due to stent implantation in concordance with the other predictors for MACE and restenosis in a group of consecutive unselected patients with stent implantation.


    Method
 Top
 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
Study patients.   Between June 1997 and September 1998, coronary artery stents were implanted in 520 of 922 (56.4%) consecutive coronary angioplasties performed in our catheterization laboratory. Additionally, 151 patients participating in two prospective multicenter studies involving stent implantation were also included in the present retrospective data analysis, because there were no differences in the standard circumstances of stent placement and patient management, no differences in patient outcome were demonstrated (15,16), and the quantitative angiographic data were all analyzed in our angiographic core laboratory. Thus, for the purposes of this study, all 671 patients were pooled and regarded as one group. The indications for stenting were elective suboptimal results (≥20% residual diameter stenosis) after percutaneous transluminal coronary angioplasty (PTCA), either with or without dissection, and bail-out conditions. Of the total of 671 consecutive candidates, the following criteria led to the exclusion of 267 patients: 104 patients with multiple stent implantation, 61 patients with stent deployment on a coronary bypass graft, 23 patients with stent delivery failure, 15 patients in whom measurements of quantitative coronary angiographic data were impossible and 64 patients with missing clinical data during the planned six-month follow-up period. The data on the 404 patients with single stent implantation (404 lesions in 404 patients) were then entered for the further retrospective analysis. Follow-up angiography at a mean of 10.1 ± 5.6 months was carried out in 354 patients (87.6%). The clinical variables included the presence of coronary risk factors such as hypertension (medication-dependent only), diabetes mellitus (medication-dependent only), hypercholesterolemia (medication-dependent or serum cholesterol ≥240 mg/dl), smoking, a familial history of coronary artery disease, a history of previous myocardial infarction, the angina pattern, age, gender, native or restenotic lesion, lesion localization (left anterior descending coronary artery [LAD] or non-LAD and proximal lesions), type C lesion, stent balloon diameter, maximal balloon inflation pressure and the occurrence of MACE; the angiographic data, including the MLD, the reference segment diameter (RD), percent diameter stenosis (%DS), the vessel angulation before and after stent implantation, the changes in vessel angulation after stent implantation and the acute lumen gain (difference between post- and preangioplastic MLD) were recorded for all patients. Follow-up coronary angiographic data on the 354 patients undergoing control angiography were also analyzed.

Stent implantation procedures and poststenting treatment.   Lesion-specific stenting was applied in all cases, with the majority of the stents being AVE Micro (10.5%), AVE GFX (12.1%), Palmaz-Schatz (17.6%), Wiktor (38.1%) or Paragon (19.1%). Smaller numbers of Multilink, ACT-1, NIR and Bestent stents were implanted in 3.6% of the cases. Coronary angiography and stent placement were performed in a routine manner. Patients received intracoronary nitroglycerine before the initial, final and follow-up angiograms in order to achieve maximal vasodilation. All patients were given aspirin (100 mg once daily) and ticlodipin (250 mg twice daily) after stenting. All procedures were carried out in accordance with the institutional guidelines.

Angiographic analysis.   Angiograms were obtained in multiple projections at baseline, immediately after stent placement and at the planned six-month follow-up. Quantitative angiography (QCA) was performed with the use of a computer-assisted coronary angiographic measurement system (CMS Version 2.3D, MEDIS, Leiden, the Netherlands) which has undergone extensive validation studies and has been described in detail elsewhere (17). The diameters of the proximal and distal reference segments were averaged to yield MLD, RD and %DS. Each QCA variable was taken as the mean value from multiple matched views.

Vessel angulations were determined as the angles defined by the tangents to the proximal and distal parts of the stenoses/stents at the end-diastolic angiographic frames (Fig. 2). Vessel angulations before and after stent implantation and at follow-up were measured in each available angiographic view, and the greatest angulation of the lesion was entered in the further statistical procedures. Vessel angulations were measured by two independent observers, and the mean values of two measurements were taken for further consideration.



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Figure 2 Different effects of stent implantation on vessel angulation. Upper right and left: coronary artery before and after stent implantation; lower right and left: vessel curve measurements at the level of the stenosis/stent.

 
Study end points.   Major adverse cardiac events (primary end point of the study) were defined as death, nonfatal acute myocardial infarction or revascularization by PTCA or coronary artery bypass grafting.

Restenosis severity (secondary end point of the study) was determined as the %DS measured at the narrowest segment within the stent at follow-up angiography.

Changes in vessel angulation after stent implantation and at follow-up were calculated as the differences between pre- and poststent vessel angulations and between poststent and follow-up vessel angulations, respectively.

Data analysis and statistical methods.   MACE as primary end point.

For the statistical analysis, all continuous variables (age, stent diameter, maximal stent-balloon inflation pressure, balloon/artery ratio, stenosis length, pre- and poststent and follow-up MLDs, RDs and %DSs) were transformed to binary data, with 1 for the presence and 0 for the absence of risk factors for MACE. The cut-off point of this division was established on the basis of receiver operating characteristic (ROC) curves, which presented not only the best cut-off point of each continuous variable for predicting MACE, but also the predictive accuracy and the sensitivity and specificity values for each variable for the prediction of MACE. In the cases where there was an inverse association between the parameter and the occurrence of MACE (e.g., MLD, a smaller MLD with more MACE), the reciprocal values of these parameters (MLD and RD) were used, while in the other cases (i.e., the %DS, a higher %DS with more MACE), the original values were entered in the ROC analyses. The predictive accuracy of each parameter was calculated as the area under the ROC curve. The best cut-off points of the parameters were determined on the basis of the same sensitivity and specificity values. We used the points of intersection of the sensitivity and specificity curves as cut-off points (MACE yes or MACE no) because the availability of a better sensitivity through increase of the cut-off point would result in a worse specificity.

Uni- and multivariate stepwise logistic regression analysis was then carried out to identify independent correlates for MACE. First, all potential risk factors were tested in a univariate regression analysis. The interactions between multiple collinear variables were tested by using the Pearson correlation. In order to avoid collinearity and to correct the multiple comparison, the acute lumen gain (difference between pre- and poststent MLD), late lumen loss (difference between poststent MLD and MLD at follow-up), vessel angulation after stent implantation and vessel angulation at follow-up exhibiting a strong correlation (p < 0.01) with at least one other parameter were excluded from the further analysis. In the second step, all remaining variables with alpha ≤0.10 were entered into the multivariate logistic regression analysis. The relative risks of the significant predictors for the occurrence of MACE were expressed by using the odds ratio (OR) with 95% confidence intervals (CI).

Angiographic restenosis severity as secondary end point
To study the relation between angiographic restenosis severity (continuous outcome variable) and multiple categoric and continuous determinants, multiple linear regression was performed. All possible risk factors were correlated with the follow-up angiographic %DS, and variables presenting alpha <0.1 were included in the multiple regression analysis.

Data are expressed as means ± SD for continuous variables and percentages for categoric variables. The Student t test was used for data comparison within groups (vessel angulation prestent, poststent and at follow-up). Statistical significance was considered present if p < 0.05. The statistical analyses were performed with the standard SAS package and CLABROC and LABROC computer software designed by Metz (18,19).

Assessment of reproducibility of the vessel angulation measurements
Vessel angulation of 54 different stented vessels were measured by two independent observers in separate sessions, and the interobserver variability was calculated by using regression analysis. For determination of the intraobserver variability, 68 vessel angulations of stented vessels were measured three times by one observer. The intraobserver variability and the reproducibility of vessel angulation measurements were determined by using one-way analysis of variance with repeated measurements. The methodological error was calculated for the standard error of the analysis of variance. The different analyses included the error involved in the repeatedly selected arterial segment and the error involved in the repeated measurements on the vessel angulation.

The coefficient of correlation of the interobserver variability was r = 0.9352 (p < 0.001). The coefficient of variation of the repeated measurements of the vessel angulation was 8.6%. The methodological error in the vessel angulation measurements was 2.1°. Thus, a two-fold methodological error (4.2°) can be regarded as a statistically significant difference between two vessel angulation measurements.


    Results
 Top
 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
MACE as primary end point.   Table 1 presents the baseline clinical and angiographic data. During the 10.2 ± 5.9 month clinical follow-up period, the overall incidence of MACE was 16.3% (n = 66). Acute myocardial infarction due to stent restenosis/occlusion occurred in 2 patients, and death in 4 patients; 73 lesions displayed target lesion restenosis at follow-up angiography. Coronary artery bypass grafting was performed in 4 patients and repeat PTCA in 56 patients.


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Table 1 Clinical and Angiographic Baseline Characteristics for Study Patients (n = 404)

 
Table 2 summarizes the cut-off points, predictive accuracies and sensitivity/specificity values of each continuous variable for predicting MACE. The best predictive accuracy was found for the %DS at follow-up (cut-off point: 42.2%), the MLD at follow-up (cut-off point: 1.7 mm), the poststent MLD (cut-off point: 2.63 mm), the prestent vessel angulation (cut-off point: 33.5°) (Fig. 3) and the changes in vessel angulation after stent implantation (cut-off point: 9.1°).


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Table 2 Cut-off Points, Predictive Accuracy, Sensitivity and Specificity Values for All Continuous Parameters

 


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Figure 3 Predictive accuracy (ROC curve) of the prestent vessel angulation for predicting MACE (left). The closer the ROC curve is to the upper left-hand corner of the graph, the more accurate it is, because the true-positive rate is 1 and the false-positive rate is zero. Additional delineation of sensitivity and specificity curves relating to each prestent vessel angulation value and the determination of a cut-off point for the same sensitivity and specificity for predicting MACE (right). MACE = major adverse cardiac events; ROC = receiver operating curve.

 
The association of all nominal factors with MACE is detailed in Tables 3 and 4, which contain the results of uni - and multivariate nominal logistic regression analysis. Multivariate nominal logistic regression analyses demonstrated that a poststent MLD ≤ 2.63 mm, an MLD at follow-up ≤1.70 mm, a %DS at follow-up ≥42.2%, a prestent vessel angulation ≥33.5° and changes in vessel angulation after stent implantation ≥9.1° were independent predictors for MACE and represented an increased risk of MACE, with the OR ranging from 5.404 to 49.553 (Table 5).


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Table 3 Results of Uni- and Multivariate Analysis for Predicting MACE

 

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Table 4 Results of Uni- and Multivariate Analysis for Predicting MACE

 

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Table 5 Odds Ratio and 95% Confidence Intervals of Parameters Included Multivariate Nominal Regression Analysis for Predicting MACE

 
The occurrence of MACE was associated with more pronounced straightening in the stented artery (36.5 ± 20° before stent implantation, 23.4 ± 19.3° after stent implantation and 20.0 ± 15.3° at follow-up in patients with MACE, 32.8 ± 22.8° before stent implantation, 25.7 ± 18.9° after stent implantation and 25.3 ± 19.5° at follow-up in patients without MACE; Fig. 4).



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Figure 4 Vessel angulation prestent, poststent and at follow-up in patients with or without MACE. Gray bar = prestent; black bar = poststent; striped bar = follow-up.

 
Angiographic restenosis severity as secondary end point.   Multiple regression analyses revealed significant correlations between the stenosis severity at follow-up and the poststent MLD (p = 0.0001), the MLD at follow-up (p = 0.000), the prestent vessel angulation (p = 0.0431) and the changes in vessel angulation after stent implantation (p = 0.0316).


    Discussion
 Top
 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
The major finding of this study was that, besides the known predictors of MACE and restenosis severity after stent implantation (final angiographic results in terms of MLD after stent implantation, and at follow-up, %DS at follow-up), a prestent vessel angulation of more than 33.5° and changes in vessel angulation after stent implantation of more than 9.1° are additional independent predictors for MACE and restenosis.

Predictors for MACE.   As has been described for native coronary lesions by Lehmann et al. (20) and for stented lesions by Schömig et al. (21), the frequency-distribution curves of angiographic measures of restenosis display a bimodal pattern, suggesting the existence of two distinct populations with normal Gaussian distribution with different propensities to restenosis. For this reason, in our study ROC analyses were used to determine the predictive accuracy with sensitivity and specificity values for all continuous clinical and angiographic variables with the possibility of predicting MACE. As expected from the characters of the parameters, MLD and %DS at follow-up indicated the best predictive accuracy, sensitivity and specificity values for the occurrence of MACE. Prestent vessel angulation and changes in vessel angulation after stent implantation showed a similarly acceptable predictive accuracy but slightly worse sensitivity and specificity values. On the basis of the ROC curves, the other parameters were not suitable for predicting MACE. As could be anticipated from the ROC analyses, the poststent and follow-up MLD, the %DS at follow-up, the prestent vessel angulation and the changes in vessel angulation after stent implantation proved to be significant predictors for the occurrence of MACE, and these parameters present a high risk of an adverse outcome after coronary stent placement.

Relation to other studies.   Since there are numerous literature data on the limitations of the angiographic assessment of the physiologic significance of lesion severity, we chose MACE (clinical restenosis) as primary end point, from a clinical point of view (22). The clinical outcome is generally of greater interest to patients and the society than the angiographic assessment, and, thus, the clinical recurrence may be a better factor in the patient management than angiographic restenosis (22).

Our results are mostly concordant with the findings of other studies in terms of predictors of restenosis, even if we chose MACE as primary end point (23–25). The postinterventional and follow-up angiographic results have been shown to be correlated with the likelihood of restenosis (10,24,26). In contrast with other studies, where age, gender, small vessel diameter, diabetes mellitus, type C and LAD lesions, restenotic lesions and %DS after stent implantation were significant predictors for restenosis, none of these clinical or angiographic variables tested in our study were associated with MACE (3,11,26–28). The lack of concordance of the findings between our own and the above mentioned studies may result from the different patient-selection criteria: we chose only patients with single stent implantation who had angiographic follow-up or well-documented clinical follow-up data. Finally, different cut-off points for continuous variables (to transform the continuous variables to binary data) may also cause different end results; mostly the median of the variables or the intersection point between the two theoretical normal distribution components (restenosis yes or no) was used in the other studies (29).

Predictors for angiographic restenosis.   From a statistical perspective, significant power may be lost in the assay by dichotomizing all continuous parameters according to arbitrary cutoff points, even if those cutoff points were selected to maximize sensitivity and specificity. In order to surmount this statistical conflict, we analyzed all continuous data in their raw form via uni- and multiple regression analyses. However, there were no differences between the outcome results with regard to the two different (clinical and angiographic) end points, as the same parameters correlated significantly with the angiographic restenosis severity and MACE. These results were expected on the basis of the occurrence of a few deaths and nonfatal AMI cases.

Alteration in vessel geometry in relation to restenosis and MACE.   Although it has been shown that, through mild overstretch of the stented segment, the radial stretch of the stented artery reduces clinical events, the longitudinal straightening effect of stents seems to be injurious to the arterial patency. Although the average vessel angulation was decreased significantly immediately after stent implantation in both patients with and patients without MACE, it was further decreased at follow-up in patients with MACE, while in patients without MACE, there was no further decrease in the curve of the stented arterial segment. These results confirm our hypothesis that the change in arterial path due to stent implantation is a trigger for the progression of coronary vascular atherosclerosis and the occurrence of MACE. Although the exact mechanism by which this occurs is unknown, several factors related to arterial longitudinal straightening may be responsible for the development of restenosis and MACE. The alteration in vessel geometry after stent implantation provokes mechanical longitudinal stretching of the smooth muscle cells and intimal cells, leading to a series of cellular and subcellular biochemical pathways and cascades, such as the secretion of different growth factors (e.g., platelet-derived growth factor), cytokines and mitogens, which has been shown to stimulate the proliferative response to vascular injury (30–33). Moreover, in addition to stretch of the wall on one side of the stent, there is folding and redundancy on the opposite wall. It may be that both the folded and stretched sides of the stent induce biochemical changes leading to stent restenosis.

It should be noted that a wide range of stents, including relatively rigid Palmaz-Schatz and flexible coil stents (Wiktor), were analyzed without separation in this study. We have started to examine the effects of vessel angulation (alone and together with other parameters) of different stents on the occurrence of MACE and angiographic restenosis, and partial results have already been published (34).

Study limitations.   There is no objective tool for the determination of vessel angulation, and an attempt was, therefore, made to avoid subjectivity in the measurement of vessel curves before and after stent implantation and at follow-up through measurements made by two independent angiographic experts and through determination of inter- and intraobserver variabilities. The appearance of the vessel angulation depends on the angiographic view, and it may happen that the standard angiographic record is not able to reveal the maximal vessel angulation. However, despite all the limitations of the curve measurements, determination of the vessel angulation proved to be a suitable parameter for the prediction of MACE with acceptable predictive accuracy, sensitivity and specificity and inter- and intraobserver variability. Many of the stents used in this study have potentially widened gaps between adjacent coils when placed in highly angulated lesions, which might result in significantly smaller MLDs than thought. This would be evident only on intravascular ultrasonography, perhaps being totally undetectable by QCA. A further limitation of the study is the selection of the patients. Although the selected population appears to be representative of most angioplasty candidates with single stent implantation, the findings obtained in patients with multiple stent implantation may differ; however, the implantation of multiple stenting, possibly involving different stent types, affects the vessel angulation in a more complex way. We excluded patients on whom clinical follow-up data were not available, but this exclusion criterion concerned only 9.5% of all study candidates.

Conclusions.   In our study including patients with single stent implantation, a poststent MLD ≤ 2.63 mm, an MLD at follow-up ≤1.7 mm, a %DS at follow-up ≥42.2%, a prestent vessel angulation ≥33.5° and changes in vessel angulation after stent implantation ≥9.1° indicated a significant risk of the occurrence of MACE (primary end point). The ROC analyses revealed that the poststent MLD, the MLD at follow-up and the %DS at follow-up furnished the best predictive accuracy, sensitivity and specificity values for the prediction of MACE. Although the average vessel angulation after stent implantation had decreased significantly in both patients with and without MACE, the further decrease in vessel curve at follow-up was significantly associated with MACE. Multiple regression analyses demonstrated that the poststent and follow-up MLD, the prestent vessel angulation and the changes in vessel angulation after stent implantation were significant independent variables for predicting target lesion restenosis (secondary end point) at follow-up. Our results indicate that the prestent vessel angulation and the changes in vessel angulation after stent implantation should be regarded as predictive parameters in the clinical practice of coronary stenting; moreover, these findings may have an impact on future stent design.


    Appendix
 Top
 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
Austrian wiktor stent study group.   Division of Cardiology, Second Department of Internal Medicine, University Medical School of Vienna, Vienna, Austria (Dietmar Glogar, MD, FESC), University Clinic of Second Department of Internal Medicine, Landeskrankenanstalten Salzburg, Salzburg (Guenter Heyer, MD), Department of Internal Medicine, Karl Franzens University, Graz (Werner Klein, MD, Olef Luha, MD), Department of Internal Medicine, University Hospital of Innsbruck, Innsbruck (Volker Muehlberger, MD), Department of Cardiology, Medical Hospital Wels, Wels (Edwin Maurer, MD, Othmar Pachinger, MD), Second Medical Department, Landeskrankenhaus Klagenfurt, Klagenfurt (Josef Sykora, MD), Fifth Department of Internal Medicine, Kaiser-Franz-Josef-Hospital, Vienna, Austria (Heinrich Weber, MD).

European Paragon Stent Investigators: Division of Cardiology, Second Department of Internal Medicine, University Medical School of Vienna, Vienna, Austria (Dietmar Glogar, MD, FESC), King’s College Hospital, London, United Kingdom (Martyn R. Thomas), Second Department of Internal Medicine, Landeskrankenanstalten Salzburg, Salzburg (Guenter Heyer, MD), University Clinics of Zurich, Switzerland (Wolfgang Amann), CHUV, Lausanne, Switzerland (Eric Eeckhout), Second Medical Department, Landeskrankenhaus Klagenfurt, Klagenfurt (Josef Sykora, MD).


    Footnotes
 
* A list of the participating institutions and investigators of the Austrian Wiktor Stent Study Group and European Paragon Stent Investigators is given in the Appendix. Back


    References
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 Abstract
 Method
 Results
 Discussion
 Appendix
 References
 
1. Kutryk MJB, Serruys PW, on behalf of van den Brand M, de Feyter PJ, Foley D, et al. Currently available stents. In: Kutryk MJB, Serruys PW, editors. Current State of Coronary Stenting. 1997:34–51.

2. Kastrati A, Schomig A, Elezi S, et al. Predictive factors of restenosis after coronary stent placement. J Am Coll Cardiol. 1997;30:1428–1436[Abstract]

3. Schuhlen H, Kastrati A, Dirschinger J, et al. Intracoronary stenting and risk for major adverse cardiac events during the first month. Circulation. 1998;98:104–111[Abstract/Free Full Text]

4. Hirshfeld JW Jr, Schwartz JS, Jugo R, et al. Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. The M-HEART Investigators. J Am Coll Cardiol. 1991;18:647–656[Abstract]

5. Van Belle E, Bauters C, Hubert E, et al. Restenosis rates in diabetic patients. A comparison of coronary stenting and balloon angioplasty in native coronary vessels. Circulation. 1997;96:1454–1460[Abstract/Free Full Text]

6. Kornowski R, Mintz GS, Kent KM, et al. Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study. Circulation. 1997;95:1366–1369[Abstract/Free Full Text]

7. Moscucci M, Piana RN, Kuntz RE, et al. Effect of prior coronary stenosis on the risk of subsequent restenosis after stent placement or directional atherectomy. Am J Cardiol. 1994;73:1147–1153[CrossRef][Medline]

8. Schömig A, Kastrati A, Dietz R, et al. Emergency coronary stenting for dissection during PTCA: angiographic follow-up after stenting and repeat angioplasty of the stented segment. J Am Cardiol. 1994;23:1053–1060

9. Mintz GS, Hoffmann R, Mehran R, et al. Instent restenosis: The Washington Hospital Center experience. Am J Cardiol. 1998;81:7E–13E[CrossRef][Medline]

10. Ellis SG, Savage M, Fischman D, et al. Restenosis after placement of Palmaz-Schatz stents in native coronary arteries. Initial results of a multicenter experience. Circulation. 1992;86:1836–1844[Abstract/Free Full Text]

11. Clarkson PBM, Halim M, Ray KK, et al. Coronary artery stenting in unstable angina pectoris: a comparison with stable angina pectoris. Heart. 1999;81:393–397[Abstract/Free Full Text]

12. Mintz GS, Popma JJ, Pichard AD, et al. Intravascular ultrasound predictors of restenosis after percutaneous transcatheter coronary revascularization. J Am Coll Cardiol. 1996;27:1678–1687[Abstract]

13. Goldberg SL, Colombo A, Maiello L, et al. Intracoronary stent insertion after balloon angioplasty of chronic total occlusions. Am J Cardiol. 1995;26:713–719

14. Haude M, Erbel R, Straub U, et al. Short- and long-term results after intracoronary stenting in human coronary arteries: monocenter experience with the balloon expandable Palmaz-Schatz stent. Br Heart J. 1991;66:337–345[Abstract/Free Full Text]

15. Yang P, Gyöngyösi M, Hassan A, et al. Short- and long-term outcomes of Wiktor stent implantation at low versus high pressure. Am J Cardiol. 1999;84:644–649[CrossRef][Medline]

16. Yang P, Palisek-Kiss K, Thomas MR, et al. Coronary stenting with the Parargon nitinol stent: preliminary report from the European Multicenter Trial. Am J Cardiol. 1998;82:63S[CrossRef][Medline]

17. Reiber JHC. An overview of coronary quantification techniques as of 1989. Reiber JHC, Serruys PW. Quantitative Coronary Arteriography. Dortrecht: Kluwer Academic Publishers; 1991. p. 55–132

18. Metz C. Basic principles of ROC analysis. Semin Nucl Med. 1978;8:238–298

19. Metz CE, Herman BA, Roe CA. Statistical comparison of two ROC curve estimates obtained from partially-paired datasets. Med Decis Making. 1998;18:110–121[Abstract/Free Full Text]

20. Lehmann KG, Melkert R, Serruys PW. Contributions of frequency distribution analysis to the understanding of coronary restenosis. A reappraisal of the gaussian curve. Circulation. 1996;93:1123–1132[Abstract/Free Full Text]

21. Schömig A, Kastrati A, Elezi S, et al. Bimodal distribution of angiographic measures of restenosis six months after coronary stent placement. Circulation. 1997;96:3880–3887[Abstract/Free Full Text]

22. Weintraub WS, Ghazzal ZMB, Douglas JS Jr, et al. Usefulness of the substitution of nonangiographic end points (death, acute myocardial infarction, coronary bypass and/or repeat angioplasty) for follow-up coronary angiography in evaluating the success of coronary angioplasty in patients with angina pectoris. Am J Cardiol. 1998;81:382–386[CrossRef][Medline]

23. Moussa I, DiMario C, Reimers B, et al. Subacute stent thrombosis in the era of intravascular ultrasound-guided coronary stenting without anticoagulation: frequency, predictors and clinical outcome. Am J Cardiol. 1997;29:6–12[Abstract]

24. Bauters C, Hubert E, Prat A, et al. Predictors of restenosis after coronary stent implantation. J Am Coll Cardiol. 1998;31:1291–1298[Abstract/Free Full Text]

25. Goldberg SL, DiMario C, Hall P, et al. Comparison of agressive versus nonagressive balloon dilatation for stent deployment on late loss and restenosis in native coronary arteries. Am J Cardiol. 1998;81:708–712[CrossRef][Medline]

26. Bauters C, Lablanche JM, Van Belle E, et al. Effects of coronary stenting on restenosis and occlusion after angioplasty of the culprit vessel in patients with recent myocardial infarction. Circulation. 1997;96:2854–2858[Abstract/Free Full Text]

27. Elezi S, Kastrati A, Neumann FJ, et al. Vessel size and long-term outcome after coronary stent placement. Circulation. 1998;98:1875–1880[Abstract/Free Full Text]

28. Faxon DP. Identifying the predictors of restenosis. Do we need new glasses? Circulation. 1997;95:2244–2246[Free Full Text]

29. Schüchlen H, Hadamitzky M, Walter H, et al. Major benefit from antiplatelet therapy for patients at high risk for adverse cardiac events after coronary Palmaz-Schatz stent placement. Analysis of a prospective risk stratification protocol in the ISAR trial. Circulation. 1997;95:2015–2021[Abstract/Free Full Text]

30. Fontaine AB, Spigos DG, Eaton G, et al. Stent-induced intimal hyperplasia: Are there fundamental differences between flexible and rigid stent designs? J Vasc Interv Radiol. 1994;5:739–744[Medline]

31. Barth KH, Virmani R, Froelich J, et al. Paired comparison of vascular wall reactions to Palmaz stents, Strecker tantalum stents and Wallstents in canin iliac and femoral arteries. Circulation. 1996;93:2161–2169[Abstract/Free Full Text]

32. Liu MW, Roubin GS, King SB. Restenosis after coronary angioplasty. Potential biologic determinants and role of intimal hyperplasia. Circulation. 1989;79:1374–1387[Abstract/Free Full Text]

33. Gerszten RE, Lim YC, Ding HT, et al. Adhesion of monocytes to vascular cell adhesion molecule-1-transduced human endothelial cells: implications for atherogenesis. Circ Res. 1998;82:871–878[Abstract/Free Full Text]

34. Gyöngyösi M, Yang P, Hassan A, Glogar D. Arterial wall stretch due to stent implantation is an additional factor predicting major adverse cardiac events. Am J Cardiol. 1998;82:69S[CrossRef]




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