(Circulation. 1997;95:2254-2261.)
© 1997 American Heart Association, Inc.
Articles |
Prediction of Restenosis After Coronary Balloon Angioplasty
Results of PICTURE (Post–IntraCoronary Treatment Ultrasound Result Evaluation), a Prospective Multicenter Intracoronary Ultrasound Imaging Study
Interuniversity Cardiology Institute of the Netherlands, Utrecht.
Correspondence to Ron J.G. Peters, MD, Department of Cardiology, Room G3-228, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionAppendixReferences |
|---|
Background Intracoronary ultrasound (ICUS) imaging is potentially suitable to identify lesions at high risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA), but it has not been studied systematically.
Methods and Results We recruited 200 patients in whom ICUS studies were performed after successful PTCA and related their ICUS parameters to 6-month follow-up quantitative coronary angiography. This was performed in 164 patients (82%), yielding 170 lesions for analysis. The overall incidence of a 
50% diameter stenosis at follow-up (categorical restenosis) was 29.4%. Quantitative ICUS parameters were weakly but significantly related to follow-up minimal luminal diameter on quantitative coronary angiography (lumen area: R2=.36, P=.0001; vessel area: R2=.29, P=.0002; plaque area: R2=-.18, P=.021; percent obstruction: R2=-.15, P=.05), but categorical restenosis was not significantly related to these parameters (P=.63, .77, .38, and .08, respectively). There were no significant predictors of restenosis in ICUS parameters of plaque morphology: eccentric versus concentric (P=1.0), plaque type (hard, soft, or calcific, P=.98), or the number of calcified quadrants (P=.41). There were no significant predictors of restenosis in two predefined types of vessel-wall disruptions: (1) rupture: presence (P=.79), depth (partial versus complete, P=.85), or extent in quadrants (P=.6), and (2) dissection: presence (P=.31), depth (P=.82), or extent (P=.38).
Conclusions Qualitative ICUS parameters after PTCA did not predict restenosis. A larger lumen and vessel area and a smaller plaque area by ICUS were associated with a larger angiographic minimal lumen diameter at follow-up, but these parameters were not significantly related to categorical restenosis.
Key Words: restenosis • angioplasty • ultrasonics
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
Coronary artery restenosis remains a major limitation of PTCA, and a method to identify lesions at high risk for this complication immediately after the procedure is urgently needed. Patient-related predictors of restenosis have been described, such as age, diabetes mellitus, duration of anginal complaints, and unstable angina pectoris.1 2 3 4 5 A number of angiographic lesion-related predictors have also been reported. However, these findings have not been consistent in various reports,4 5 6 7 and their predictive power is very limited.
Because angiography provides information on the lumen only, information on vessel-wall morphology is very limited,8 and this technique therefore may not be sufficiently sensitive to detect morphological predictors of restenosis after PTCA. ICUS provides direct in vivo morphological and quantitative information on the vessel wall and atherosclerotic plaque9 10 11 12 and on the presence and extent of the disruptions resulting from the intervention.13 14 15 It was therefore thought to be very suitable for the study of lesion-related predictors of restenosis. However, the study of restenosis after PTCA by ICUS has been limited to a number of relatively small series with inconclusive results.14 16 We conducted a prospective multicenter study in 200 patients to establish whether morphological features of the dilated segment, as assessed by ICUS after the procedure, are predictive of subsequent restenosis.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
Patients
Patients were included in the study if they met the following criteria: (1) successful PTCA of a single coronary artery, defined as a decrease of
30% in angiographic diameter stenosis after PTCA, a residual diameter stenosis <50% (by visual assessment), and normal blood flow in the dilated artery (TIMI grade 3); and (2) reference diameter of the target vessel 2.5 mm. Exclusion criteria included the following: (1) prior PTCA at the same site; (2) acute myocardial infarction <2 weeks before PTCA; (3) prominent coronary spasm; and (4) sharp bends and curves proximal to the segment of interest, precluding the passage of the ICUS catheter. Informed consent was obtained from all patients, and the protocol was approved by the local ethics committees of all participating centers. The centers and investigators participating in the study are listed in the "Appendix."
Procedure
Standard PTCA was performed from the femoral artery approach. Balloon size was chosen with a nominal diameter to match the angiographic lumen diameter of an adjacent segment that appeared normal on the angiogram. The number of balloons and the number and pressure of the inflations were left to the discretion of the operator and were based on angiography only. After completion of the procedure, when the angiographic result met the inclusion criteria, the dilated artery was studied by ICUS (see below). If, in spite of a satisfactory initial result, the operator could not accept the angiographic appearance of the lesion after completion of the ICUS study (because of deterioration that had occurred during the time required for the ICUS study), by protocol a second ICUS study was performed after additional balloon inflations, and only this second study was used for analysis. After the ICUS study, QCA was performed. Follow-up coronary angiography was performed after 6 months. If symptoms recurred within 6 months, coronary angiography was performed earlier. If angiography was performed within 4 months but the index lesion was not redilated, the protocol required that angiography be repeated at 6 months.
QCA
The angiograms after the ICUS study and at 6-month follow-up were recorded after intracoronary injection of isosorbide dinitrate or nitroglycerin. At least two orthogonal projections were selected for analysis, and these projections were repeated at follow-up. To standardize the method of data acquisition and to ensure exact reproducibility of the angiographic studies, measurements were taken as described previously.17 18 For calibration purposes, the catheter tip was cut off for later measurement with a microcaliper. All angiograms were analyzed by a central core laboratory (Cardialysis, Rotterdam, Netherlands) using the computer-assisted CAAS-II technique, which has been described and validated previously.19 20 Restenosis, the primary end point of the study, was analyzed in two ways: as a binary definition of 50% diameter stenosis in the dilated lesion at follow-up and as a continuous variable, both as absolute MLD and as reduction in absolute luminal diameter in the dilated lesion at follow-up ("late loss").
ICUS Imaging Protocol
All ICUS studies were performed with three mechanical, single-element, 30-MHz systems: (1) the Insight system (Cardiovascular Imaging Systems Inc) using 4.3F catheters, (2) the Intrasound system (Du-MED) using 4.1F catheters; and (3) the Boston Scientific system using 3.5F catheters with a Hewlett-Packard ICUS console.
After completion of the PTCA procedure, if the patient fulfilled the criteria mentioned above, intracoronary nitroglycerin or isosorbide dinitrate was administered and an ICUS catheter was introduced over the guidewire left in place after PTCA. Settings for gain and filters were adjusted to result in an optimal visual image. The entire procedure was stored on VHS or super VHS videotape, including annotations and audio recordings. The ICUS catheter was advanced to the dilated segment for close examination of vessel morphology and disruptions. At the narrowest site, 10 mL of saline and x-ray contrast flushes through the guiding catheter were performed to facilitate the recognition of disruptions and to confirm that the narrowest point on angiography was being examined. Additional flushing at other sites was left to the discretion of the operator. The timing of this flushing and of all other relevant events during the ICUS study was marked by voice recordings on the videotape. After the morphology was carefully explored, the transducer was advanced to a site distal to the lesion, and a slow, manual pullback maneuver was performed until the transducer reached the guiding catheter.
After the ICUS study, both the catheter and the guidewire were removed and a final angiogram (for quantitative analysis) was made.
Ultrasound Image Analysis
All images were analyzed by a committee of five observers (see "Appendix") unaware of the results of angiography and follow-up examinations. Qualitative analysis of the images was performed independently by each member of the committee on a dedicated form, and all cases were reviewed in a panel discussion to reach consensus on all diagnostic parameters. The analysis consisted of two parts. First, the entire dilated segment was analyzed qualitatively (see below). Second, a single video frame in the cross section with the smallest lumen area (visually) was indicated as the narrowest site of the dilated lesion. This cross section was used for quantitative analysis (see below).
Qualitative Analysis
The following parameters (with definitions where appropriate) were assessed: image quality, classified as either acceptable or not acceptable; lesion morphology, classified as either eccentric or concentric (maximal plaque thickness/minimal plaque thickness 2 or <2, respectively) (this was performed subjectively because in the complex post-PTCA ultrasound images of dilated lesions, the accepted criteria for eccentricity cannot be applied); lesion type, classified as soft (less echogenic than adventitia), hard (as echogenic as adventitia), or calcific (at least one quadrant of calcium present)12 21 ; calcium (defined as dense reflections with acoustic shadowing9 11 ), with the number of deposits, their location relative to the narrowest point, their cumulative arc (in hours) in the dilated segment, and their depth (superficial, defined as no tissue between the deposit and the lumen; deep, all other depths; or both); rupture of the vessel wall, defined as a radial tear, ie, perpendicular to the vessel-wall layers; and dissection of the vessel wall, defined as a tear parallel to the vessel-wall layers. Regarding these disruptions, the following characteristics were noted: (1) location relative to the narrowest point; (2) the total circumferential arc in hours (with a minimum of 1); (3) maximal depth, classified as either partial (some plaque remaining intact between the rupture and the underlying media) or complete (extending through the plaque completely); and (4) the presence of calcium adjacent to the tear. Thrombus was not diagnosed by ICUS because the investigators did not feel confident making this diagnosis with existing criteria.22 23
Quantitative Analysis
Measurements on the cross section designated as the narrowest point in the panel discussion were performed independently by two observers (W.E.M.K. and G.P.). After calibration by use of the markers in the ICUS image, the circumference of the lumen (including extensions created by ruptures or dissections) and of the media/adventitia border were traced manually by use of computer-assisted planimetry24 (Fig 1
). If part of the media-adventitia interface was invisible owing to shadowing behind calcium deposits, the tracing was extrapolated from the adjacent sectors of the circumference. In cross sections with more than one quadrant of acoustic shadowing, the tracing was extrapolated from neighboring cross sections, as described by others.25 All tracings were performed according to the consensus interpretation of the image. From this, the following parameters were derived: lumen area, vessel area (area encompassed by the media-adventitia border), plaque area (defined as Vessel Area-Lumen Area), and percent obstruction (defined as [Plaque Area/Vessel Area]x100). The mean value of the two independent measurements for each parameter was entered in the database.
|
Interobserver variation of the measurements (199 baseline ICUS studies) was as follows: minimal lumen area, SD=0.66 mm2, CV=12.6%; plaque area, SD=1.34 mm2, CV=15.7%; vessel area, SD=1.43 mm2, CV=10.4%; and percent obstruction, SD=5.22%, CV=8.6%. Consistent errors were 0.02 mm2 for lumen area, -0.20 mm2 for vessel area, -0.22 mm2 for plaque area, and -0.89% for percent obstruction. Exclusion of lesions with more than one quadrant of calcium did not significantly alter the reproducibility.
Statistical Analysis
All variables were related to measures of restenosis in univariate analysis by use of the unpaired Student's t test, ANOVA, and 
2 tests where appropriate. Variables significantly related to restenosis in univariate analysis were analyzed in multivariate analysis. For late loss, stepwise linear regression analysis was performed. For categorical restenosis, stepwise logistic regression analysis was performed.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
ICUS imaging was performed after PTCA in 200 patients. The PTCA operator did not accept the angiographic appearance of the lesion after completion of the ICUS study in 46 patients because early loss of initial result (<30 minutes) occurred during the ICUS study. In 35 of these cases, a second ICUS study was performed after additional balloon inflations. The remaining 11 were excluded from the analysis because of stenting, refusal of a repeat ICUS study by the patient or physician, or incomplete data. Of the 200 patients included, 164 returned for repeat angiography (82%) within 6 months, with a total of 178 lesions. In 170 lesions (96%) in 154 patients, an acceptable ICUS examination was available, and these lesions were used in the analysis.
Baseline characteristics and procedural results of the patients included in the analysis are summarized in Table 1. These characteristics did not differ from those of the entire study group (n=200). Tables 2 and 3 summarize the angiographic findings after PTCA and at follow-up. There was little late loss at follow-up (average of 0.17±0.51 mm), but otherwise the results were as expected for balloon angioplasty. Clinical parameters, such as age, sex, diabetes, or the duration of anginal complaints, had no predictive value for angiographic restenosis in univariate analysis. The MLD after intervention was significantly greater in lesions that did not develop a 50% diameter stenosis than in those that did, and similarly, percent diameter stenosis was greatest in the group with restenosis (Table 3). Qualitative ICUS parameters and their relation with angiography are summarized in Table 4. No significant relations with restenosis were found. The relation between ruptures and dissections on ICUS imaging and the MLD as a continuous variable at follow-up angiography is presented in Figs 2 and 3. The presence of these disruptions in the dilated segment did not significantly influence the MLD at follow-up. Fig 4 presents the relation between quantitative ICUS parameters and categorical angiographic restenosis. No significant differences were found between the groups with and without categorical restenosis. In univariate analysis, quantitative ICUS parameters showed significant relations with the angiographic MLD and late luminal loss at follow-up (Table 5). In logistic regression analysis, no parameter was significantly related to categorical restenosis. Five parameters (Table 6) showed a statistically significant relation in multivariate analysis with late luminal loss on angiography. Of these, dissection at the narrowest point of the dilated segment was the only ICUS parameter with a significant relation. It was the strongest predictor of late loss (P=.009), but the predictive value was low (partial R2=.041). On the basis of observations by Honye et al,14 we compared concentric lesions without disruptions to all others. Restenosis rates were similar (2 [20%] of 10 versus 48 [30%] of 160, respectively; P=.72). Exclusion of the 35 patients in whom a second ICUS study was performed after additional balloon inflations did not alter the results of any of the comparisons. Similarly, exclusion of lesions with more than one quadrant of calcium (n=97) did not alter any of the results.
|
|
|
|
|
|
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
This study was designed to identify ICUS characteristics of dilated coronary arterial wall segments that would predict the development of restenosis after successful PTCA. This study represents the largest series of patients specifically studied for this purpose. The type and extent of vessel-wall disruption were not related to angiographic dimensions, either directly after the procedure or at follow-up, with the exception of dissection diagnosed at the narrowest cross section, which was associated with a larger MLD at follow-up. However, this was not associated with a statistically significant difference in the incidence of a
50% diameter stenosis at follow-up.
Quantitative ICUS parameters were not significantly associated with 50% diameter stenosis at follow-up, although there was a trend toward a greater extent of percent obstruction in the restenosis group, consistent with other reports.28 29 30 However, there were significant relations in univariate analysis between quantitative ICUS parameters and MLD at follow-up and late luminal loss. These relations were weak, but they are consistent with the angiographic findings of the present study and other angiographic restenosis studies6 31 and with the previously mentioned ICUS studies.28 29 30 They support the concept that residual stenosis is a significant component of the restenosis problem and that strategies aimed at reducing restenosis should include the achievement of a maximal initial result.
Until recently, the prevailing hypothesis on the mechanism of restenosis was that neointima formation is the predominant factor leading to a decrease of luminal dimensions. It has been suggested that the response of neointimal formation is related to the severity of the damage inflicted on the vessel wall during PTCA,32 33 34 and therefore the demonstration of such disruptions by ICUS could provide prognostic information. As outlined above, we did not find such a relationship.
The lack of success of trials aimed at limiting neointimal growth35 suggests that neointima formation may not be the most important factor. There is now evidence that other mechanisms dominate the development of restenosis. In particular, ICUS studies have shown that geometric remodeling is responsible for 
60% to 80% of late luminal loss after transcatheter intracoronary interventions.36 37 38 Our study could not confirm these findings because no follow-up ultrasound studies were performed. It is presently unknown which factors determine the magnitude and direction of geometric remodeling.
Considering the proposed mechanisms of restenosis outlined above, the absence of a relationship between ICUS-determined disruptions and restenosis is unexpected. However, our results confirm previous preliminary studies.13 16 As described above, we could not confirm the conclusion of Honye et al14 that concentric lesions without disruptions are predisposed to restenosis.
ICUS parameters appear to be more predictive of restenosis in studies of mixed interventional devices (balloon angioplasty, rotational and directional atherectomy, laser angioplasty).31 39 40 41 In these series, a larger lumen and smaller plaque burden at the end of the intervention were consistently associated with lower restenosis rates. However, it is difficult to compare studies with mixed interventional devices with those concerning PTCA only, such as the present study. First, it is conceivable that plaque removal (and mechanical scaffolding of the vessel wall) results in different mechanisms of vessel-wall remodeling and different degrees of intimal hyperplasia compared with PTCA. Second, the coronary arteries studied in these series were generally larger than those in PICTURE, presumably because of the inclusion of cases selected for directional atherectomy. This may affect the restenosis rates, because vessel size is one of the determinants of restenosis in multivariate analysis.7 42 Third, in most of the series with mixed devices described above, the selection of the therapeutic modality was based on preintervention ICUS studies, which results in selection of lesion types for the different devices. This selection makes a comparison with our results difficult. Consequently, ICUS may yield useful predictors in patients treated with other transcatheter devices, and this should be explored further.
Limitations
There are several limitations to this study. We included nontortuous coronary arteries, and a satisfactory angiographic result was required. These criteria may have resulted in the selection of favorable cases.
The late loss in MLD observed by QCA (0.17 mm) is low compared with other reports. With an average reference-segment diameter of 2.95 mm, a mean late loss of 0.26 mm is expected.42 Several factors may contribute to this discrepancy. First, although percent diameter stenosis was <50% visually in all lesions (inclusion criterion), there was in fact a >50% diameter stenosis on off-line QCA in 17 lesions (10%). In these cases, late loss is expected to be lower, and categorical 6-month restenosis (>50%) is actually pseudorestenosis. This may explain why a normal incidence (29.4%) of categorical restenosis was found in spite of the limited late loss. Second, it is possible that in the lesions with additional balloon dilations after the initial ICUS study, the early component of MLD loss was abolished, thereby lowering total 6-month loss.
We found a trend toward a greater percent area obstruction on ICUS in the restenosis group. With a greater number of observations, this relation would possibly reach statistical significance, consistent with the findings of others.28 29 30 It is doubtful, however, if the difference could reach clinical significance.
The use of an early generation of ICUS catheters may have influenced the results in two ways. First, image quality was not yet optimal. Second, the relatively large diameter of the catheters may have resulted in false-negative observations on vessel-wall dissections because the catheters may have "tacked" intimal flaps during the ICUS study. However, with a rupture incidence of 89% on ICUS, it is not likely that we have underestimated the degree of vessel-wall damage.Potentially, the patients who had additional dilations after the ICUS examination were a specific subgroup at high risk. By using the second, final ICUS examination for analysis, predictors present in the first ICUS examination may have remained undetected. However, it is unlikely that plaque composition is altered by additional dilations, and the incidence of disruptions remained high. In addition, we repeated the analysis of the relation of vessel-wall disruptions and restenosis after exclusion of this subgroup of patients, and this did not alter the findings.
We conclude that after angiographically and clinically successful balloon angioplasty, a larger lumen and vessel area and a smaller plaque area as determined by ICUS were associated with a larger angiographic MLD at follow-up. However, these relations were weak, and the study did not identify ICUS parameters predictive of restenosis after PTCA.
|
Appendix |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
Participating Centers
Interuniversity Cardiology Institute of the Netherlands: Klaas Bom, PhD; Elma J. Gussenhoven, MD; Hans Rijsterborgh, PhD (
deceased). Academic Hospital Free University, Amsterdam, Netherlands: Otto Kamp, MD (center coordinator); Jean G.F. Bronswaer, MD; Carel C. de Cock, MD; Cees A. Visser, MD.
Academic Hospital, University of Leiden, Netherlands: Lucas Savalle, MD (center coordinator); Bert Buys, MD (deceased).
Academic Hospital, University of Maastricht, Netherlands: Frits W.H.M. Bär, MD (center coordinator); H. Quint.
Academic Hospital, University of Amsterdam, Netherlands: George K. David, MD; Karel T. Koch, MD; Wouter E.M. Kok, MD (center coordinator); Ron J.G. Peters, MD (principal investigator); Jan J. Piek, MD.
Academic Hospital, University of Utrecht, Netherlands: Piet W. Westerhof, MD; Cornelius Borst, MD; Gerard Pasterkamp, MD (center coordinator).
Sint Antonius Hospital, Nieuwegein, Netherlands: W. Jaarsma, MD (center coordinator); H.W. Thijs Plokker, MD; V. Radjan N. Panday, MD.
Thoraxcenter, Academic Hospital Dijkzigt, Erasmus University, Rotterdam, Netherlands: Pim J. de Feyter, MD; David T. Linker, MD; Carlo di Mario, MD (center coordinator); Patrick W. Serruys, MD.
Data Management
Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, Netherlands: Martin H. Prins, MD.
Angiographic Core Laboratory
Cardialysis, Rotterdam, Netherlands: Eline Montauban van Swijndrecht, Edwin Mibbering, Patrick W. Serruys.
ICUS Analysis Committee
Otto Kamp, MD; Wouter E.M. Kok, MD; Carlo di Mario, MD; Gerard Pasterkamp, MD; Ron J.G. Peters, MD.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was supported by a grant from the Netherlands Heart Foundation, and the protocol was approved by The Netherlands Organisation for Scientific Research (0706/900-574-003).
Received September 5, 1996; revision received November 25, 1996; accepted December 16, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendixReferences |
|---|
1. Leimgruber PP, Roubin GS, Hollman J, Cotsonis GA, Meier B, Douglas JS, King SB, Gruentzig AR. Restenosis after successful coronary angioplasty in patients with single-vessel disease. Circulation. 1986;73:710-717.
2. Lambert M, Bonan R, Côté G, Crépeau J, de Guise P, Lespérance J, David PR, Waters DD. Multiple coronary angioplasty: a model to discriminate systemic and procedural factors related to restenosis. J Am Coll Cardiol. 1988;12:310-314.[Abstract]
3.
Rapold HJ, David PR, Guiteras Val P, Mata AL, Crean PA, Bourassa MG. Restenosis and its determinants in first and repeat coronary angioplasty. Eur Heart J. 1987;8:575-586.
4. Bourassa MG, Lespérance J, Eastwood C, Schwartz L, Côté G, Kazim F, Hudon G. Clinical, physiologic, anatomic and procedural factors predictive of restenosis after percutaneous transluminal coronary angioplasty. J Am Coll Cardiol. 1991;18:368-376.[Abstract]
5.
Rensing BJ, Hermans WRM, Vos J, Tijssen JGP, Rutch W, Danchin N, Heyndrickx GR, Mast G, Wijns W, Serruys PW, on behalf of the Coronary Artery Restenosis Prevention on Repeated Thromboxane Antagonism (CARPORT) Study Group. Luminal narrowing after percutaneous transluminal coronary angioplasty: a study of clinical, procedural, and lesional factors related to long-term angiographic outcome. Circulation. 1993;88:975-985.
6. Serruys PW, Foley DP, Kirkeeide RL, King SB. Restenosis revisited: insights provided by quantitative coronary angiography. Am Heart J. 1993;126:1243-1267.[Medline] [Order article via Infotrieve]
7. Hirschfeld JW, Schwartz JS, Jugo R, Macdonald RG, Goldberg S, Savage MP, Bass TA, Vetrovec G, Cowley M, Taussig AS, Whitworth HB, Margolis JR, Hill JA, Pepine CJ, and the M-Heart Investigators. Restenosis after coronary angioplasty: a multivariate statistical model to relate lesion and procedure variables to restenosis. J Am Coll Cardiol. 1991;18:647-656.[Abstract]
8. Naruko T, Ueda M, Becker AE, Tojo O, Teragaki M, Takeuchi K, Takeda T. Angiographic-pathologic correlations after elective percutaneous transluminal coronary angioplasty. Circulation. 1993;88(pt 1):1558-1568.
9. Gussenhoven EJ, Essed CE, Lancee CT, Mastik F, Frietman P, Van Egmond FC, Reiber J, Bosch H, Van Urk H, Roelandt J, Bom N. Arterial wall characteristics determined by intravascular ultrasound imaging: an in vitro study. J Am Coll Cardiol. 1989;14:947-952.[Abstract]
10.
Tobis JM, Mallery J, Mahon D, Lehmann K, Zalesky P, Griffith J, Gessert J, Moriuchi M, McRae M, Dwyer ML, Greep N, Henry WL. Intravascular ultrasound imaging of human coronary arteries in vivo: analysis of tissue characterizations with comparison to in vitro histological specimens. Circulation. 1991;83:913-926.
11. Peters RJG, Kok WEM, Havenith MG, Rijsterborgh H, van der Wall AC, Visser CA. Histopathologic validation of intracoronary ultrasound imaging. J Am Soc Echocardiogr. 1994;7:230-241.[Medline] [Order article via Infotrieve]
12. Di Mario C, The SHK, Madretsma S, van Suylen RJ, Wilson RA, Bom N, Serruys PW, Gussenhoven EJ, Roelandt JRTC. Detection and characterization of vascular lesions by intravascular ultrasound: an in vitro study correlated with histology. J Am Soc Echocardiogr. 1992;5:135-146.[Medline] [Order article via Infotrieve]
13.
Tobis JM, Mallery JA, Gessert J, Griffith J, Mahon D, Bessen M, Moriuchi M, McLeay L, McRae M, Henry WL. Intravascular ultrasound cross-sectional arterial imaging before and after balloon angioplasty in vitro. Circulation. 1989;80:873-882.
14.
Honye J, Mahon D, Jain A, White CJ, Ramee SR, Wallis JB, Al-Zarka A, Tobis JM. Morphological effects of coronary balloon angioplasty in vivo assessed by intravascular ultrasound. Circulation. 1992;85:1012-1025.
15. Gerber T, Erbel R, Görge G, Ge J, Rupprecht HG, Meyer J. A classification of morphologic effects of coronary balloon angioplasty assessed by intravascular ultrasound. Am J Cardiol. 1992;70:1546-1554.[Medline] [Order article via Infotrieve]
16. Sechtem U, Rudolph D, Klass O, Deutsch HJ, Höpp HW. Restenosis after balloon angioplasty: influence of post-interventional vessel morphology as assessed by intracoronary ultrasound. Eur Heart J. 1994;15:259. Abstract.
17.
Serruys PW, Luijten HE, Beatt KJ, Geuskens R, de Feyter PJ, van den Brabd M, Reiber JHC, ten Katen HJ, van Es GA, Hugenholtz PG. Incidence of restenosis after successful coronary angioplasty: a time related phenomenon—a quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. Circulation. 1988;77:361-371.
18. Reiber JHC, Serruys PW, Kooyman CJ, Slager CJ, Schuurbiers JHC, den Boer A. Approaches toward standardization in acquisition and quantitation of arterial dimensions from cineangiograms. In: Reiber JHC, Serruys PW, eds. State of the Art in Quantitative Coronary Angiography. Dordrecht, Netherlands: Martinus-Nijhoff; 1986:145-155.
19. Strauss BH, Escaned J, Di Mario C, Haase J, Keane D, Hermans WR, de Feyter PJ, Serruys PW. Technical considerations and practical limitations in the use of quantitative angiography during percutaneous coronary recanalization. Prog Cardiovasc Dis. 1994;36:343-363.[Medline] [Order article via Infotrieve]
20. Haase J, Di Mario C, Slager CJ, van der Giessen WJ, den Boer A, de Feyter PJ, Reiber JHC, Verdouw PD, Serruys PW. In-vivo validation of on-line and off-line geometric coronary measurements using insertion of stenosis phantoms in porcine coronary arteries. Cathet Cardiovasc Diagn. 1992;27:16-27.[Medline] [Order article via Infotrieve]
21. Hodgson JM, Reddy KG, Suneja R, Nair RN, Lesnefsky EJ, Sheehan HM. Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. J Am Coll Cardiol. 1993;21:35-44.[Abstract]
22.
Siegel RJ, Ariani M, Fishbein MC, Chae J, Park JC, Maurer G, Forrester JS. Histopathologic validation of angioscopy and intravascular ultrasound. Circulation. 1991;84:109-117.
23. Pandian NG, Kreis A, Brockway B. Detection of intraarterial thrombus by intravascular high frequency two dimensional ultrasound imaging in vitro and in vivo studies. Am J Cardiol. 1990;65:1280-1283.[Medline] [Order article via Infotrieve]
24. Wenguang L, Gussenhoven WJ, Bosch JG, Mastik F, Reiber JHC, Bom N. A computer-aided analysis system for the quantitative assessment of intravascular ultrasound images. Comput Cardiol. 1990:333-336.
25. Popma JJ, Mintz GS, Satler LF, Pichard AD, Kent KM, Chuang YC, Matar F, Bucher TA, Merritt AJ, Leon MB. Clinical and angiographic outcome after directional coronary atherectomy. Am J Cardiol. 1993;72:55E-64E.[Medline] [Order article via Infotrieve]
26. Ryan TJ, Faxon DP, Gunnar RM, Kennedy JW, King SB, Loop FD, Peterson KL, Reeves TJ, Williams DO, Winters WL. Guidelines for percutaneous transluminal coronary angioplasty: a report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty). J Am Coll Cardiol. 1988;12:529-545.[Medline] [Order article via Infotrieve]
27.
Dorros G, Cowley MJ, Simpson J, Bentifoglio LG, Block PC, Bourassa M, Detre K, Gosselin AJ, Grüntzig AR, Kelsey SF, Kent KM, Mock MB, Mullins SM, Myler RK, Passamani ER, Stertzer SH, Williams DO. Percutaneous transluminal coronary angioplasty: report of complications from the National Heart, Lung, and Blood Institute PTCA Registry. Circulation. 1983;67:723-730.
28. Fitzgerald PJ, Yock PG. Mechanisms and outcomes of angioplasty and atherectomy assessed by intravascular ultrasound imaging. J Clin Ultrasound. 1993;21:579-588.[Medline] [Order article via Infotrieve]
29. Tenaglia AN, Buller CE, Kisslo KB, Phillips HR, Stack RS, Davidson CJ. Intracoronary ultrasound predictors of adverse outcomes after coronary artery interventions. J Am Coll Cardiol. 1992;20:1385-1390.[Abstract]
30. Mintz GS, Chuang YC, Popma JJ, Pichard AD, Kent KM, Satler LF, Bucher TA, Griffin J, Leon MB. The final % cross-sectional narrowing (residual plaque burden) is the strongest intravascular ultrasound predictor of angiographic restenosis. J Am Coll Cardiol. 1995;25:35A. Abstract.
31.
Kuntz RE, Baim DS. Defining coronary restenosis: newer clinical and angiographic paradigms. Circulation. 1993;88:1310-1323.
32.
Wilentz JR, Sanborn TA, Haudenschild CC, Valeri CR, Ryand TJ, Faxon DP. Platelet accumulation in experimental angioplasty: time course and relation to vascular injury. Circulation. 1987;75:636-642.
33. Schwartz RS, Huber KC, Murphy JG, Edwards WD, Camrud AR, Vlietstra RE, Holmes DR. Restenosis and the proportional neointimal response to coronary artery injury: results in a porcine model. J Am Coll Cardiol. 1992;19:267-274.[Abstract]
34. Ellis SG, Muller DWM. Arterial injury and the enigma of coronary restenosis. Circulation. 1992;19:275-277.
35. Hillegass WB, Ohman EM, Califf RM. Restenosis: the clinical issues. In: Topol EJ, ed. Textbook of Interventional Cardiology. Philadelphia, Pa: WB Saunders; 1994:415-435.
36. Mintz GS, Pichard AD, Kent KM, Satler LF, Popma JJ, Leon MB. Intravascular ultrasound comparison of restenotic and de novo coronary artery narrowings. Am J Cardiol. 1994;74:1278-1280.[Medline] [Order article via Infotrieve]
37. Blasini R, Mudra H, Klauss V, Regar E, Schömig A. Remodeling of coronary arteries after balloon angioplasty: in vivo documentation in patients using consecutive intravascular ultrasound. J Am Coll Cardiol. 1995;25:139A. Abstract.
38. Di Mario C, Gil R, Camenzind E, Ozaki Y, von Birgelen C, Umans V, de Jaegere P, de Feyter PJ, Roelandt JRTC, Serruys PW. Quantitative assessment with intracoronary ultrasound of the mechanisms of restenosis after percutaneous transluminal coronary angioplasty and directional atherectomy. Am J Cardiol. 1995;75:772-777.[Medline] [Order article via Infotrieve]
39. Jain SP, Jain A, Collins TJ, Ramee SR, White CJ. Predictors of restenosis: a morphometric and quantitative evaluation by intravascular ultrasound. Am Heart J. 1994;128:664-673.[Medline] [Order article via Infotrieve]
40. The Guide Trial Investigators. IVUS-determined predictors of restenosis in PTCA and DCA: an interim report from the GUIDE-II trial, phase II. Circulation. 1994;90(suppl I):I-23. Abstract.
41. Hodgson JM, Suneja RR, Sheehan H, Lesnefsky E, Nair R. Can intracoronary ultrasound determined plaque morphology predict restenosis following intervention? Eur Heart J. 1992;13:309. Abstract.
42.
Foley DP, Melkert R, Serruys PW, on behalf of the CARPORT, MERCATOR, and PARK Investigators. Influence of coronary vessel size on renarrowing process and late angiographic outcome after successful balloon angioplasty. Circulation. 1994;90:1239-1251.
This article has been cited by other articles:
 |
|
 |
|
  C. Di Mario, G. R. Heyndrickx, F. Prati, and N. H.J. Pijls CHAPTER 8 Invasive Imaging and Haemodynamics ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kettelkamp, J. House, M. Garg, R. S. Stuart, A. Grantham, and J. Spertus Using the Risk of Restenosis as a Guide to Triaging Patients Between Surgical and Percutaneous Coronary Revascularization Circulation, September 14, 2004; 110(11_suppl_1): II-50 - II-54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Liu, M. Fisher, and P. Groves Down-regulation of the ERK1 and ERK2 mitogen-activated protein kinases using antisense oligonucleotides inhibits intimal hyperplasia in a porcine model of coronary balloon angioplasty Cardiovasc Res, June 1, 2002; 54(3): 640 - 648. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Alfke, J. J. Froelich, S. Nowak, and H.-J. Wagner Cardiovascular Risk Factors Do Not Predict Clinically Defined Restenosis After Percutaneous Transluminal Angioplasty for Lower Limb Ischemia Angiology, January 1, 2002; 53(1): 15 - 20. [Abstract] [PDF]
|
|
|
|
 |
|
 N. Mercado, E. Boersma, W. Wijns, B. J. Gersh, C. A. Morillo, V. de Valk, G.-A. van Es, D. E. Grobbee, and P. W. Serruys Clinical and quantitative coronary angiographic predictors of coronary restenosis: A comparative analysis from the balloon-to-stent era J. Am. Coll. Cardiol., September 1, 2001; 38(3): 645 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Okura, Y. Morino, A. Oshima, M. Hayase, M. R. Ward, J. J. Popma, R. E. Kuntz, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Preintervention arterial remodeling affects clinical outcome following stenting: an intravascular ultrasound study J. Am. Coll. Cardiol., March 15, 2001; 37(4): 1031 - 1035. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Nissen and P. Yock Intravascular Ultrasound : Novel Pathophysiological Insights and Current Clinical Applications Circulation, January 30, 2001; 103(4): 604 - 616. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Hibi, A. Takagi, X. Zhang, T.-J. Teo, H. N. Bonneau, P. G. Yock, and P. J. Fitzgerald Feasibility of a Novel Blood Noise Reduction Algorithm to Enhance Reproducibility of Ultra-High-Frequency Intravascular Ultrasound Images Circulation, October 3, 2000; 102(14): 1657 - 1663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. J. Cantor, E. D. Peterson, J. J. Popma, J. P. Zidar, M. H. Sketch Jr., J. E. Tcheng, and E. M. Ohman Provisional stenting strategies: systematic overview and implications for clinical decision-making J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1142 - 1151. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Alfonso Videodensitometric vs edge-detection quantitative angiography. Insights from intravascular ultrasound imaging Eur. Heart J., April 2, 2000; 21(8): 604 - 607. [PDF]
|
|
|
|
|
|
R.J.G Peters, W.E.M Kok, G Pasterkamp, C Von Birgelen, M Prins, and P.W Serruys Videodensitometric quantitative angiography after coronary balloon angioplasty, compared to edge-detection quantitative angiography and intracoronary ultrasound imaging Eur. Heart J., April 2, 2000; 21(8): 654 - 661. [Abstract] [PDF]
|
|
|
|
|
|
D. P. Faxon Predicting Restenosis : Bigger Is Better but Not Best Circulation, March 7, 2000; 101(9): 946 - 947. [Full Text] [PDF]
|
|
|
|
|
|
W. E. M. Kok, R. J. G. Peters, G. Pasterkamp, C. Di Mario, P. W. Serruys, M. Prins, C. A. Visser, and for the PICTURE study group Greater late lumen loss after successful coronary balloon angioplasty in the proximal left anterior descending coronary artery is not explained by extent of vessel wall damage or plaque burden J. Am. Coll. Cardiol., February 1, 2000; 35(2): 382 - 388. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C von Birgelen, G S Mintz, E A de Vrey, P W Serruys, T Kimura, M Nobuyoshi, J J Popma, M B Leon, R Erbel, and P J de Feyter Preintervention lesion remodelling affects operative mechanisms of balloon optimised directional coronary atherectomy procedures: a volumetric study with three dimensional intravascular ultrasound Heart, February 1, 2000; 83(2): 192 - 197. [Abstract] [Full Text]
|
|
|
|
|
|
P. H. Grewe, T. Deneke, A. Machraoui, J.u. Barmeyer, and K.-M. Muller Acute and chronic tissue response to coronary stent implantation: pathologic findings in human specimen J. Am. Coll. Cardiol., January 1, 2000; 35(1): 157 - 163. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Magdy, M. Al-Abbady, A. Ghoga, K. Heib, and C. Ozbek Restenosis After Angioplasty in Patients with Left Ventricular Dysfunction Asian Cardiovasc Thorac Ann, September 1, 1999; 7(3): 209 - 213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Scanlon, D. P. Faxon, A.-M. Audet, B. Carabello, G. J. Dehmer, K. A. Eagle, R. D. Legako, D. F. Leon, J. A. Murray, S. E. Nissen, et al. ACC/AHA guidelines for coronary angiography: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Coronary Angiography) developed in collaboration with the Society for Cardiac Angiography and Interventions J. Am. Coll. Cardiol., May 1, 1999; 33(6): 1756 - 1824. [Full Text] [PDF]
|
|
|
|
|
|
G. J. W. Bech, N. H. J. Pijls, B. De Bruyne, K. H. Peels, H. R. Michels, H. J. R. M. Bonnier, and J. J. Koolen Usefulness of Fractional Flow Reserve to Predict Clinical Outcome After Balloon Angioplasty Circulation, February 23, 1999; 99(7): 883 - 888. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Nishimoto, Y. Miyazaki, Y. Toki, R. Murakami, M. Shinoda, A. Fukushima, and H. Kanayama Enhanced secretion of insulin plays a role in the development of atherosclerosis and restenosis of coronary arteries: elective percutaneous transluminal coronary angioplasty in patients with effort angina J. Am. Coll. Cardiol., November 15, 1998; 32(6): 1624 - 1629. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Oshima, D. Itchhaporia, and P. Fitzgerald New developments in intravascular ultrasound Vascular Medicine, November 1, 1998; 3(4): 281 - 290. [Abstract] [PDF]
|
|
|
|
|
|
C. R. Narins, D. R. Holmes Jr, and E. J. Topol A Call for Provisional Stenting : The Balloon Is Back! Circulation, April 7, 1998; 97(13): 1298 - 1305. [Full Text] [PDF]
|
|
|
|
|
|
C von Birgelen, G S Mintz, E A de Vrey, T Kimura, J J Popma, S G Airiian, M B Leon, M Nobuyoshi, P W Serruys, and P J de Feyter Atherosclerotic coronary lesions with inadequate compensatory enlargement have smaller plaque and vessel volumes: observations with three dimensional intravascular ultrasound in vivo Heart, February 1, 1998; 79(2): 137 - 142. [Abstract] [Full Text]
|
|
|
|
|
|
D. P. Faxon Identifying the Predictors of Restenosis: Do We Need New Glasses? Circulation, May 6, 1997; 95(9): 2244 - 2246. [Full Text]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||