Published online before print April 16, 2007, doi: 10.1161/CIRCULATIONAHA.107.693739
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(Circulation. 2007;115:2435-2441.)
© 2007 American Heart Association, Inc.
Interventional Cardiology |
Pathological Correlates of Late Drug-Eluting Stent Thrombosis
Strut Coverage as a Marker of Endothelialization
From CVPath, International Registry of Pathology, Gaithersburg, Md (M.J., G.N., F.K., R.V.); Cardiac Unit, Department of Internal Medicine, Massachusetts General Hospital, Boston (A.V.F., M.C.J., H.K.G.); and Partners Healthcare Systems, Boston, Mass (J.N.).
Correspondence to Renu Virmani, MD, Medical Director, CVPath, International Registry of Pathology, 19 Firstfield Rd, Gaithersburg, MD 20878. E-mail rvirmani{at}cvpath.org
Received October 4, 2006; accepted February 22, 2007.
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Abstract |
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Background— Late stent thrombosis (LST) after Cypher and Taxus drug-eluting stent placement has emerged as a major concern. Although the clinical predictors of LST have been reported, specific morphological and histological correlates of LST remain unknown.
Methods and Results— From a registry totaling 81 human autopsies of drug-eluting stents, 46 (62 lesions) had a drug-eluting stent implanted >30 days. We identified 28 lesions with thrombus and compared those with 34 of similar duration without thrombosis using computer-guided morphometric and histological analyses. LST was defined as an acute thrombus within a coronary artery stent in place >30 days. Multiple logistic generalized estimating equations modeling demonstrated that endothelialization was the best predictor of thrombosis. The morphometric parameter that best correlated with endothelialization was the ratio of uncovered to total stent struts per section. A univariable logistic generalized estimating equations model of occurrence of thrombus in a stent section versus ratio of uncovered to total stent struts per section demonstrated a marked increase in risk for LST as the number of uncovered struts increased. The odds ratio for thrombus in a stent with a ratio of uncovered to total stent struts per section >30% is 9.0 (95% CI, 3.5 to 22).
Conclusions— The most powerful histological predictor of stent thrombosis was endothelial coverage. The best morphometric predictor of LST was the ratio of uncovered to total stent struts. Heterogeneity of healing is a common finding in drug-eluting stents with evidence of LST and demonstrates the importance of incomplete healing of the stented segment in the pathophysiology of LST.
Key Words: complications • stents • thrombus • pathology • endothelium
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Introduction |
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Polymer-based sirolimus- (Cypher) and paclitaxel-eluting (Taxus) drug-eluting stents (DES) have become the treatment of choice for patients with symptomatic coronary artery disease undergoing percutaneous coronary revascularization. Although these stents have reduced rates of restenosis and late lumen loss compared with bare metal stents, late thrombosis, a life-threatening complication of this technology, has emerged as a major concern.1,2 Although its incidence remains low, the sheer number of DES implanted worldwide, combined with the often dire consequences of late thrombotic events, makes this a significant public health issue. We have previously demonstrated in pathological specimens from patients dying of late DES thrombosis that delayed arterial healing characterized by incomplete reendothelialization and persistence of fibrin is an important underlying substrate.3–6 Although clinical predictors such as withdrawal of antiplatelet therapy are known to play a role in determining the probability of late stent thrombosis (LST), the specific morphometric and histological parameters that significantly correlate with late thrombosis remain unknown.1,2,7
Clinical Perspective p 2441
Using our database of all patients dying 
30 days after Cypher or Taxus DES implantation, this study sought to determine the most powerful pathological risk factors for late thrombosis and to identify the high-risk features of DES that might be clinically evaluable.
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Methods |
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From a registry totaling 81 human autopsies of Cypher and Taxus DES, all cases with evidence of
1 DES in place >30 days were examined (46 cases in total, 23 of which have been previously reported3–6). In cases of multiple stent deployment, overlapping and consecutively implanted DES were treated as 1 lesion, whereas DES including a gap of >5 mm were treated as separate lesions. The length of each stent was recorded and expressed as total treated length in case of overlapping stent deployment. Clinical histories and cardiac catheterization reports were reviewed when available. DES-related death was determined after a complete autopsy, including examination of the myocardium. The presence of an occlusive luminal thrombus or nonocclusive thrombus with distal embolization was considered stent-related cardiac death. None of the other major coronary arteries had evidence of severe stenosis or luminal thrombus.
Non–stent-related cardiac death was defined as a patent DES without evidence of thrombus or restenosis (luminal stenosis <75% cross sectional area) in association with 1 nonstented major coronary artery segments with evidence of severe narrowing (>75% cross-sectional area stenosis).
Stented arteries were fixed in 10% buffered formalin, dissected off the heart, radiographed, and submitted for plastic embedding. Arteries were serially sectioned 2 to 3 mm apart and stained with hematoxylin and eosin and Movat pentachrome as previously described.8 Movat pentachrome stains nuclei black, elastic fibers dark purple to black, collagen and reticulum fibers yellow, proteoglycans blue to bluish green, fibrin red, and smooth muscle cells red. Immunohistochemistry for identification of endothelial cells was performed in randomly selected cases using a CD31/CD34 antibody cocktail. (This approach has recently been shown to be superior in labeling endothelial cells compared with the conventional method of using a single monoclonal antibody to CD31.9) Resin sections (8 µm) were deplastized in warm xylenes, 2-methoxyethyl acetate, and acetone, followed by incubation in a graded series of alcohols to deionized water. Antigen retrieval was performed using steam heat with the sections in EDTA buffer (pH 8.0). The slides were then placed in 3.0% H2O2 for 20 minutes, followed by immunostaining using a cocktail of endothelial markers CD31 (dilution, 1:100; Dako, Carpenteria, Calif) and CD34 (dilution, 1:4000; MONOSAN, Uden, the Netherlands) diluted in PBS (pH 7.5) at 4°C overnight. The primary antibodies were labeled with an LSAB kit (Dako); positive staining was visualized by a 3-amino-9-ethylcarbazole substrate-chromogen system; and the sections were counterstained with Gill’s hematoxylin.
Stent thrombosis was defined as occlusive or nonocclusive thrombus, with the thrombus being composed predominantly of platelets. A nonocclusive thrombus was defined as a platelet-rich thrombus that occupied >30% of the cross-sectional area of the lumen. The requirement for a platelet component to the thrombus differentiates stent thrombosis from fibrin deposition, which is uniformly observed around DES struts that have been implanted for >30 days and occupies <25% of the lumen (unpublished data, R.V.).
Morphological and Morphometric Measurements
Computer-guided morphometric measurements were performed with IPLab software (IPLab Spectrum software, Scanalytics Inc, Vienna, Va) on sections from stents implanted >30 days. Digital images were captured (x20 magnification), and area and thickness measurements, including the external elastic lamina area, plaque burden area, stent area, lumen area, and neointimal thickness above each strut, were determined. For comparison of DES with and without mural thrombi, the percentage of fibrin surrounding stent struts and surface endothelialization was assessed on hematoxylin and eosin– and Movat pentachrome–stained sections at a magnification of x200 to overcome biased measurements. This was further confirmed in selected cases to be endothelium by immunohistochemical staining. The number of stent struts without neointimal coverage and/or surface endothelium was counted for each consecutive section, and the total number of sections, including uncovered stent struts, was recorded. The cumulative stent length lacking neointimal coverage was calculated with the following formula: stent length divided by the number of sections times the sum of uncovered sections per stent. Neointimal thickness distribution in cases with and without LST was plotted as histograms and analyzed for heterogeneity of variance.
To further examine the relationship between uncovered stent struts and/or luminal fibrin thrombus (over a strut lacking neointima) to luminal platelet-rich thrombus, the number of such struts with luminal thrombus was plotted against total number of uncovered and/or struts with mural fibrin.
To evaluate the relationship between cross-sectional strut distribution and the risk for LST, the number of stent struts per section was counted, and the distances between individual stent struts were digitally measured.
To identify the exact location of sites at risk for stent thrombosis, consecutively cut sections were separated into proximal, middle, and distal segments of the stented arteries and analyzed for the presence of uncovered stent struts and platelet-rich thrombi.
Statistical Analysis
Continuous variables are expressed as mean±SD. Nonnormally distributed variables were either log transformed to normal or compared between groups with the Wilcoxon rank-sum test. Normality of distribution was tested with the Wilk-Shapiro test. A value of P<0.05 was considered statistically significant. Differences between patients with and without thrombosed lesions were tested by Fisher exact test.
Both neointimal thickness and duration of stent implantation were log transformed to normalize the distributions of these variables and to stabilize their variances, as confirmed by the Wilk-Shapiro test and the Levene robust test for variances, respectively. Subsequently, the logarithmic form of these variables was entered into parametric tests.
Multiple logistic generalized estimating equations (GEE) modeling10,11 was performed on all morphometric and histological parameters as independent variables versus presence of thrombus as the binary dependent variable using the STATA xtgee program (STATA Corp, College Station, Tex) with an assumed binomial family distribution, a logistic link function, and an exchangeable structure in the correlation matrix. GEE was necessary because of the clustered nature of >1 individual lesion measured from some patients—resulting in unknown correlations among measurements within these lesion clusters. An optimum cut point in the variable ratio of uncovered to total struts per section (RUTSS) was derived by receiver-operating characteristic curve analysis, selecting a cut point that produced approximately equal sensitivity and specificity of the observed resulting classifications with respect to thrombus.
Multiple linear GEE estimation was used to find the best morphometric correlates of stent endothelialization as the dependent variable using xtgee with an assumed gaussian family distribution, an identity link function, and an assumed exchangeable structure for the within cluster correlation matrix. This linear model of endothelialization was important because endothelialization generally is not directly accessible to in vivo measurement, whereas other morphometric variables potentially are accessible in vivo. The result of this linear model was used to select the best morphometric explanatory variable for use in the logistic model of stent thrombus formation. The GEE approach to linear regression was required for the same reason as the logistic model of lesion thrombus. All analyses were performed with STATA statistics software (release 9).
All authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Lesion Characteristics
Within these 81 cases (109 lesions), 62 lesions (46 patients) had DES implanted >30 days and were included in the DES study group. We identified 28 lesions (23 patients) with thrombus formation and compared those with 34 lesions (23 patients) of similar duration without evidence of in-stent thrombosis (254±235 days for lesions with LST versus 244±289 days for those without; P= NS). In cases with mural thrombus formation, 13 occlusive and 15 nonocclusive thrombi were detected. In these lesions with thrombus formation, 16 Cypher (14 lesions) and 22 Taxus (14 lesions) DES were implanted; those without mural thrombi included 23 Cypher (18 lesions) and 17 Taxus (16 lesions) DES. Bifurcation stenting was reported in 6 of 23 LST cases (26%) and in 1 of 23 patients with patent DES (4%).
Patient Characteristics, Indications for Stenting, and Causes of Death
Patient characteristics were known for most of the cases with and without evidence of late thrombosis and are listed in Table 1. Antiplatelet therapy status was known for 18 of 23 patients (78%) in the LST group and for 14 of 23 patients (61%) in the patent DES group (Table 1). Of these, dual antiplatelet therapy was confirmed in 11 of 18 patients (61%) with LST and 5 of 14 patients (36%) with patent DES. Four of 18 patients (22%) with LST and 2 of 14 patients (14%) with patent DES were on aspirin monotherapy; 1 of 18 patients (6%) with LST and 1 of 14 patients (7%) with patent DES were on clopidogrel monotherapy; and 2 of 18 patients (11%) in the LST group and 6 of 14 patients (43%) in the patent DES group were not on antiplatelet therapy at the time of death. None of the differences shown in Table 1 were statistically significant by Fisher exact test.
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Indications for stent implantation were stable angina in 13 patients with LST and in 19 patients with patent DES. Acute coronary syndromes were the indication in 10 patients with LST and in 4 patients with patent DES.
A cardiac cause of death was documented in 20 patients with LST (10 sudden cardiac deaths, 10 acute myocardial infarctions), and all cardiac deaths were considered stent related. In the LST group, 3 patients died of noncardiac causes. Two suffered cerebrovascular accidents, which were the cause of death, and 1 received a heart transplant for end-stage ischemic heart disease. In 15 patients with patent DES, 2 patients died suddenly and were found to have severe in-stent restenosis. The other 13 died of sudden cardiac death with evidence of severe narrowing (ie, >75% cross-sectional area stenosis) of at least 1 major nonstented coronary artery segment. Eight patients with patent DES were diagnosed as having noncardiac deaths (pneumonia, 1; stroke, 2; trauma, 1; pulmonary embolism, 2; gastrointestinal bleeding, 2).
Morphometric and Histological Comparisons of Thrombosed and Patent DES Lesions
The external elastic lamina, plaque area, and stent area were significantly greater in lesions with mural thrombus compared with patent DES lesions (Table 2). Neointimal thickness was greater in patent DES lesions, whereas the percentage of endothelialization was significantly greater in patent DES lesions. Fibrin score was significantly greater in DES lesions with thrombus. We compared the neointimal thickness in thrombosed and patent DES lesions and found a marked shift toward less neointimal growth in DES with mural thrombus formation.
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Average total stent length was 25.9±11.5 in thrombosed stents versus 20.3±9.6 mm in nonthrombosed stents (P=0.04). We examined whether the cumulative stent length without neointimal coverage also was different in lesions with DES thrombosis versus those without thrombus. Patent DES had an average stent length without neointimal coverage of 9.9±10.1 versus 20.1±11.5 mm for lesions with thrombus (P<0.0004). The mean number of stent struts per section without neointimal coverage (ie, number of uncovered struts per section) also was significantly greater in DES lesions with thrombosis compared with those without thrombosis (Table 2).
Moreover, the average distance between individual stent struts was significantly shorter in DES lesions with mural thrombus formation compared with patent DES lesions (Table 2). There also was a good correlation between the mean number of uncovered struts per section and the average distance between stent struts (r=–0.41, P=0.001), with most uncovered stent struts showing less interstrut distance than covered stent struts.
Next, we explored the interrelationship of stent struts lacking neointimal coverage and the number of struts surrounded by platelet-rich thrombi and found a significant correlation between these parameters (r=0.43, P<0.001). On further examination, we found heterogeneity of coverage of stent struts, both within individual cross sections and between sections from the same stent. Within the same DES, although some struts show healing as demonstrated by neointimal growth, others remain bare and serve as a nidus for mural thrombus formation (Figure 1). Within a DES, the middle section of the stent (versus the proximal and distal ends) was the most common location of stent struts lacking neointimal coverage and was the most common site of thrombus formation (Figure 2).
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Pathological Correlates of LST in Lesions
Among the morphological and histological parameters listed in Table 2, multivariable GEE logistic modeling demonstrated that endothelialization was the best classifier of thrombosis. The 2 complete patient variables included as candidate predictors of thrombus in this model of lesions were age and gender. In addition, the use of bifurcation stenting per lesion was included as a candidate predictor, along with all the morphometric measurements.
Multiple linear GEE analysis was performed to find significant correlations between endothelialization and various morphometric parameters. Significant joint explanatory variables detected by the multiple linear analysis were the following: RUTSS, uncovered struts per section, stent length, total length without neointima, and log (neointimal thickness). Of these, the RUTSS was the single most significant correlate of endothelialization (Z=–13; P<0.00005).
Because the most powerful morphometric predictor of endothelialization was the RUTSS, we used univariable GEE logistic regression to analyze the probability of thrombus as classified by this ratio. The odds ratio estimated for LST in lesions having an RUTSS >30% is 9.0 (95% CI, 3.5 to 22.0). This cut point was determined by estimating classifications of thrombus versus patent DES via use of the RUTSS variable in a receiver-operating characteristic curve analysis and balancing sensitivity and specificity at 75% and 76%, respectively. To generate the RUTSS, we examined an average of 5.3±2.7 sections per stent.
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Discussion |
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Although clinical predictors of late DES thrombosis have been identified, the specific morphometric and histological parameters that best correlate with risk for this event remain unknown. Using human pathological data, we have shown for the current generation of polymeric DES that endothelialization is the best classifier of LST. Of the various morphometric parameters we examined, multiple linear GEE analysis demonstrated that the RUTSS best correlated with endothelialization. Within the same DES, although some struts show healing as demonstrated by neointimal growth, others remain bare and serve as a nidus for mural thrombus formation. A univariable logistic GEE model of occurrence of thrombus in a stent section versus RUTSS shows that there is a considerable elevation of risk of thrombus as the RUTSS increases.
Mechanisms of Heterogeneity of Stent Strut Coverage
Our data demonstrate that nonuniform healing with DES (as indicated by the number of uncovered struts per cross section) greatly increased thrombotic risk. Previous pathological studies have shown an association between lack of neointimal strut coverage and thrombus formation.12 Although the mechanisms by which the current-generation DES induce nonuniform incomplete healing are not fully understood, lesion characteristics; drug properties, dose, and distribution; and polymer biocompatibility together play important roles. Underlying plaque morphology may affect the rate of healing when stent struts penetrate deeply into a necrotic core and are not in contact with cellular areas.12 Eccentric plaques may prevent uniform strut deployment, thereby increasing local toxicity resulting from higher concentrations of drug and polymer. Indeed, sections with evidence of thrombosis showed significantly lower interstrut distances, which correlated with less neointimal growth. Local concentrations of drug are ultimately highly spacing dependent, and the variance in distance between struts will amplify differences in concentrations, leading to biological effects.13 Heterogeneity in loaded dose of drug varies from strut to strut, and greater retention of lipophilic drugs in different regions of plaque affects arterial drug concentration and results in nonuniform healing.14 The relationship between local drug concentration and cellular repair is underscored by data from overlapping versus nonoverlapping Cypher and Taxus stents in the rabbit iliac model.15
It also has been reported in a small number of patients that the nonabsorbable polymers in Cypher and Taxus provoke chronic eosinophilic infiltration of the arterial wall, suggesting hypersensitivity reactions in a small number of cases.6 To what extent polymer-induced inflammation also plays a role in retarding healing is unknown, but in some cases, it clearly is causal in inducing thrombosis.3
Restenosis Versus Thrombosis
The severe decrease in late loss and neointimal formation generated by the current-generation Food and Drug Administration–approved DES may not be required to produce major reductions in restenosis and the need for target lesion revascularization. Ellis et al16 demonstrated that the relationship between late loss and target lesion revascularization is curvilinear, with a late loss of 0 to 0.75 mm residing on a relatively flat portion of the curve for revascularization and larger degrees of late loss on a much steeper part of the curve. Reductions in in-stent late loss <0.75 mm only incrementally lower the risk of target lesion revascularization. The Taxus stent had a reported late loss of more than double that of the Cypher stent (0.39 versus 0.17 mm), but rates of revascularization do not differ significantly in their respective pivotal trials.17,18
Our data raise the possibility that a more liberal approach to reductions in late loss and suppression of neointimal growth may be able to reduce the risk of thrombosis by encouraging a higher percentage of strut-related neointimal coverage without significantly increasing target lesion revascularization. However, this hypothesis requires validation in prospective randomized clinical trials.
Evaluation of DES in Clinical Trials
Among the morphometric parameters examined, the RUTSS rather than the average volume of neointimal growth most powerfully estimates risk for LST because it is an excellent surrogate indicator of endothelialization and therefore a marker of delayed healing. This has important implications for predicting the thrombotic risk of DES in clinical trials. Uneven coverage of stent struts by neointima cannot be determined by calculating late loss from follow-up angiography. Other modalities are needed to determine strut distribution and the number of uncovered struts over the entire stent length at follow-up.
On the basis of our analysis, there is a continuum of risk for individuals that increases with the RUTSS per cross section. Our univariable logistic GEE model of occurrence of thrombus in a stent section versus RUTSS shows that in a stent with 30% uncovered struts, the odds ratio for thrombus is 9.0 (95% CI, 3.5 to 22.0) compared with a stent with complete coverage.
Study Limitations
Because this is an autopsy study, the results may not be representative of all patients who receive Cypher and Taxus DES for approved indications and survive. Moreover, the small number of patients in this autopsy study and the fact that we could not obtain complete clinical data on all subjects did not allow us to explore the relative contribution of previously reported clinical risk factors for DES LST (such as clopidogrel withdrawal) to the pathological risk factors identified in our study. Moreover, although our data demonstrate a strong correlation between lack of coverage of stent struts and LST, validating the predictive value of this correlation requires testing in larger prospective clinical trials.
Conclusion
The underlying pathology in cases of LST indicates incomplete neointimal coverage of stent struts as the most important morphometric predictor of LST because it is the most powerful surrogate indicator of endothelialization. Both plaque- and device-related issues likely play a role in promoting uneven healing.
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Acknowledgments |
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Source of Funding
This work was supported by CVPath Institute Inc, a private nonprofit organization.
Disclosures
Dr Virmani reports receiving company-sponsored research support from Medtronic AVE, Guidant, Abbott, W.L. Gore, Atrium Medical Corp, Boston Scientific, NDC Cordis Corp, Novartis, Orbus Medical Technologies, Biotronik, BioSensors, Alchimer, and Terumo. She has served as a consultant for Medtronic AVE, Guidant, Abbott Laboratories, W.L. Gore, Terumo, and Volcano Therapeutics Inc. The other authors report no conflicts.
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Footnotes |
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*The first 2 authors contributed equally to this work.
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G. S. Mintz and S.-Y. Choi Optimal Stent Expansion and Complete Neointimal Coverage: Does This Association Make Sense? J. Am. Coll. Cardiol. Intv., October 1, 2009; 2(10): 995 - 996. [Full Text] [PDF]
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J. A. Ormiston, M. W.I. Webster, R. S. Schwartz, P. Gladding, J. T. Stewart, I. P. Kay, P. N. Ruygrok, and R. Hatrick Feasibility, Safety, and Efficacy of a Novel Polymeric Pimecrolimus-Eluting Stent: Traditional Pre-Clinical Safety End Points Failed to Predict 6-Month Clinical Angiographic Results J. Am. Coll. Cardiol. Intv., October 1, 2009; 2(10): 1017 - 1024. [Abstract] [Full Text] [PDF]
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R A Byrne, S Kufner, K Tiroch, S Massberg, K-L Laugwitz, A Birkmeier, S Schulz, J Mehilli, and for the Intracoronary Stenting and Angiographic Re Randomised trial of three rapamycin-eluting stents with different coating strategies for the reduction of coronary restenosis: 2-year follow-up results Heart, September 15, 2009; 95(18): 1489 - 1494. [Abstract] [Full Text] [PDF]
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 S. Cook, E. Ladich, G. Nakazawa, P. Eshtehardi, M. Neidhart, R. Vogel, M. Togni, P. Wenaweser, M. Billinger, C. Seiler, et al. Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis Circulation, August 4, 2009; 120(5): 391 - 399. [Abstract] [Full Text] [PDF]
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S. Cook and P. Wenaweser Off-Label Use and the Spectre of Drug-Eluting Stent Thrombosis Circ Cardiovasc Interv, August 1, 2009; 2(4): 273 - 276. [Full Text] [PDF]
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Y. Onuma, N. Kukreja, N. Piazza, J. Eindhoven, C. Girasis, L. Schenkeveld, R. van Domburg, P. W. Serruys, and Interventional Cardiologists of the Thoraxcenter ( The Everolimus-Eluting Stent in Real-World Patients: 6-Month Follow-Up of the X-SEARCH (Xience V Stent Evaluated at Rotterdam Cardiac Hospital) Registry J. Am. Coll. Cardiol., July 14, 2009; 54(3): 269 - 276. [Abstract] [Full Text] [PDF]
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G. J. Wilson, G. Nakazawa, R. S. Schwartz, B. Huibregtse, B. Poff, T. J. Herbst, D. S. Baim, and R. Virmani Comparison of Inflammatory Response After Implantation of Sirolimus- and Paclitaxel-Eluting Stents in Porcine Coronary Arteries Circulation, July 14, 2009; 120(2): 141 - 149. [Abstract] [Full Text] [PDF]
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D. E. Drachman Drug-Eluting Stents in Animals and Patients: Where Do We Stand Today? Circulation, July 14, 2009; 120(2): 101 - 103. [Full Text] [PDF]
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Y. Onuma, P. Serruys, P. den Heijer, K. S. Joesoef, H. Duckers, E. Regar, N. Kukreja, S. Tanimoto, H. M. Garcia-Garcia, H. van Beusekom, et al. MAHOROBA, first-in-man study: 6-month results of a biodegradable polymer sustained release tacrolimus-eluting stent in de novo coronary stenoses Eur. Heart J., June 2, 2009; 30(12): 1477 - 1485. [Abstract] [Full Text] [PDF]
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G. Niccoli, D. Schiavino, F. Belloni, G. Ferrante, G. La Torre, M. Conte, N. Cosentino, R. A. Montone, V. Sabato, F. Burzotta, et al. Pre-intervention eosinophil cationic protein serum levels predict clinical outcomes following implantation of drug-eluting stents Eur. Heart J., June 1, 2009; 30(11): 1340 - 1347. [Abstract] [Full Text] [PDF]
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M. B. Leon, D. J. Allocco, K. D. Dawkins, and D. S. Baim Late Clinical Events After Drug-Eluting Stents: The Interplay Between Stent-Related and Natural History-Driven Events J. Am. Coll. Cardiol. Intv., June 1, 2009; 2(6): 504 - 512. [Abstract] [Full Text] [PDF]
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N. Kukreja, Y. Onuma, H. M. Garcia-Garcia, J. Daemen, R. van Domburg, P. W. Serruys, and on behalf of the Interventional cardiologists of t The Risk of Stent Thrombosis in Patients With Acute Coronary Syndromes Treated With Bare-Metal and Drug-Eluting Stents J. Am. Coll. Cardiol. Intv., June 1, 2009; 2(6): 534 - 541. [Abstract] [Full Text] [PDF]
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J. W. Kim, H. S. Seo, J. H. Park, J. O. Na, C. U. Choi, H. E. Lim, E. J. Kim, S.-W. Rha, C. G. Park, and D. J. Oh A prospective, randomized, 6-month comparison of the coronary vasomotor response associated with a zotarolimus- versus a sirolimus-eluting stent: differential recovery of coronary endothelial dysfunction. J. Am. Coll. Cardiol., May 5, 2009; 53(18): 1653 - 1659. [Abstract] [Full Text] [PDF]
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 T. Higo, Y. Ueda, J. Oyabu, K. Okada, M. Nishio, A. Hirata, K. Kashiwase, N. Ogasawara, S. Hirotani, and K. Kodama Atherosclerotic and thrombogenic neointima formed over sirolimus drug-eluting stent an angioscopic study. J. Am. Coll. Cardiol. Img., May 1, 2009; 2(5): 616 - 624. [Abstract] [Full Text] [PDF]
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G. Nakazawa, M. Vorpahl, A. V. Finn, J. Narula, and R. Virmani One step forward and two steps back with drug-eluting-stents from preventing restenosis to causing late thrombosis and nouveau atherosclerosis. J. Am. Coll. Cardiol. Img., May 1, 2009; 2(5): 625 - 628. [Full Text] [PDF]
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P. Moore, P. Barlis, J. Spiro, G. Ghimire, M. Roughton, C. Di Mario, W. Wallis, C. Ilsley, A. Mitchell, M. Mason, et al. A Randomized Optical Coherence Tomography Study of Coronary Stent Strut Coverage and Luminal Protrusion With Rapamycin-Eluting Stents J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 437 - 444. [Abstract] [Full Text] [PDF]
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N. Gonzalo, P. Barlis, P. W. Serruys, H. M. Garcia-Garcia, Y. Onuma, J. Ligthart, and E. Regar Incomplete Stent Apposition and Delayed Tissue Coverage Are More Frequent in Drug-Eluting Stents Implanted During Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction Than in Drug-Eluting Stents Implanted for Stable/Unstable Angina: Insights From Optical Coherence Tomography J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 445 - 452. [Abstract] [Full Text] [PDF]
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M. Awata, S. Nanto, M. Uematsu, T. Morozumi, T. Watanabe, T. Onishi, O. Iida, F. Sera, H. Minamiguchi, J.-i. Kotani, et al. Heterogeneous Arterial Healing in Patients Following Paclitaxel-Eluting Stent Implantation: Comparison With Sirolimus-Eluting Stents J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 453 - 458. [Abstract] [Full Text] [PDF]
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H. Otake, J. Shite, J. Ako, T. Shinke, Y. Tanino, D. Ogasawara, T. Sawada, N. Miyoshi, H. Kato, B.-K. Koo, et al. Local Determinants of Thrombus Formation Following Sirolimus-Eluting Stent Implantation Assessed by Optical Coherence Tomography J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 459 - 466. [Abstract] [Full Text] [PDF]
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G. Guagliumi and M. Costa From a Foggy Sight to a Clear Vision J. Am. Coll. Cardiol. Intv., May 1, 2009; 2(5): 467 - 469. [Full Text] [PDF]
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 P. A. Calvert and M. R. Bennett Restenosis Revisited Circ. Res., April 10, 2009; 104(7): 823 - 825. [Full Text] [PDF]
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K. Nakano, K. Egashira, S. Masuda, K. Funakoshi, G. Zhao, S. Kimura, T. Matoba, K. Sueishi, Y. Endo, Y. Kawashima, et al. Formulation of Nanoparticle-Eluting Stents by a Cationic Electrodeposition Coating Technology: Efficient Nano-Drug Delivery via Bioabsorbable Polymeric Nanoparticle-Eluting Stents in Porcine Coronary Arteries J. Am. Coll. Cardiol. Intv., April 1, 2009; 2(4): 277 - 283. [Abstract] [Full Text] [PDF]
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J. R. Margolis The Excel Stent: A Good DES, But Can We Really Stop Clopidogrel After 6 Months? J. Am. Coll. Cardiol. Intv., April 1, 2009; 2(4): 310 - 311. [Full Text] [PDF]
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H. Samady, M. McDaniel, E. Veledar, B. De Bruyne, N. H. Pijls, W. F. Fearon, and V. Vaccarino Baseline Fractional Flow Reserve and Stent Diameter Predict Optimal Post-Stent Fractional Flow Reserve and Major Adverse Cardiac Events After Bare-Metal Stent Deployment J. Am. Coll. Cardiol. Intv., April 1, 2009; 2(4): 357 - 363. [Abstract] [Full Text] [PDF]
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 M. Mutsuga, Y. Narita, A. Yamawaki, M. Satake, H. Kaneko, Y. Suematsu, A. Usui, and Y. Ueda A new strategy for prevention of anastomotic stricture using tacrolimus-eluting biodegradable nanofiber. J. Thorac. Cardiovasc. Surg., March 1, 2009; 137(3): 703 - 709. [Abstract] [Full Text] [PDF]
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M. Hamilos, J. Sarma, M. Ostojic, T. Cuisset, G. Sarno, N. Melikian, A. Ntalianis, O. Muller, E. Barbato, B. Beleslin, et al. Interference of Drug-Eluting Stents With Endothelium-Dependent Coronary Vasomotion: Evidence for Device-Specific Responses Circ Cardiovasc Interv, December 1, 2008; 1(3): 193 - 200. [Abstract] [Full Text] [PDF]
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G. J. Tearney, S. Waxman, M. Shishkov, B. J. Vakoc, M. J. Suter, M. I. Freilich, A. E. Desjardins, W.-Y. Oh, L. A. Bartlett, M. Rosenberg, et al. Three-dimensional coronary artery microscopy by intracoronary optical frequency domain imaging. J. Am. Coll. Cardiol. Img., November 1, 2008; 1(6): 752 - 761. [Abstract] [Full Text] [PDF]
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P. Wenaweser, J. Daemen, M. Zwahlen, R. van Domburg, P. Juni, S. Vaina, G. Hellige, K. Tsuchida, C. Morger, E. Boersma, et al. Incidence and Correlates of Drug-Eluting Stent Thrombosis in Routine Clinical Practice: 4-Year Results From a Large 2-Institutional Cohort Study J. Am. Coll. Cardiol., September 30, 2008; 52(14): 1134 - 1140. [Abstract] [Full Text] [PDF]
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G. Nakazawa, A. V. Finn, M. Joner, E. Ladich, R. Kutys, E. K. Mont, H. K. Gold, A. P. Burke, F. D. Kolodgie, and R. Virmani Delayed Arterial Healing and Increased Late Stent Thrombosis at Culprit Sites After Drug-Eluting Stent Placement for Acute Myocardial Infarction Patients: An Autopsy Study Circulation, September 9, 2008; 118(11): 1138 - 1145. [Abstract] [Full Text] [PDF]
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A. Schober and C. Weber Leptin and EPCs in Arterial Injury: Yes, We Can! Circ. Res., August 29, 2008; 103(5): 447 - 449. [Full Text] [PDF]
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M. Awata, S. Nanto, M. Uematsu, T. Morozumi, T. Watanabe, T. Onishi, O. Iida, F. Sera, J.-i. Kotani, M. Hori, et al. Angioscopic Comparison of Neointimal Coverage Between Zotarolimus- and Sirolimus-Eluting Stents J. Am. Coll. Cardiol., August 26, 2008; 52(9): 789 - 790. [Full Text] [PDF]
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J. D. Abbott Revealing the Silver and Red Lining in Drug-Eluting Stents With Angioscopy Circ Cardiovasc Interv, August 1, 2008; 1(1): 7 - 9. [Full Text] [PDF]
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M. Takano, M. Yamamoto, D. Murakami, S. Inami, K. Okamatsu, K. Seimiya, T. Ohba, Y. Seino, and K. Mizuno Lack of Association Between Large Angiographic Late Loss and Low Risk of In-Stent Thrombus: Angioscopic Comparison Between Paclitaxel- and Sirolimus-Eluting Stents Circ Cardiovasc Interv, August 1, 2008; 1(1): 20 - 27. [Abstract] [Full Text] [PDF]
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T. Shinke, J. Li, J. P. Chen, L. Pendyala, T. Goodchild, R. Jabara, S. Geva, T. Ueno, N. Chronos, K. Robinson, et al. High Incidence of Intramural Thrombus After Overlapping Paclitaxel-Eluting Stent Implantation: Angioscopic and Histopathologic Analysis in Porcine Coronary Arteries Circ Cardiovasc Interv, August 1, 2008; 1(1): 28 - 35. [Abstract] [Full Text] [PDF]
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D. R. Holmes Jr and D. O. Williams Catheter-Based Treatment of Coronary Artery Disease: Past, Present, and Future Circ Cardiovasc Interv, August 1, 2008; 1(1): 60 - 73. [Abstract] [Full Text] [PDF]
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 L. T. Newsome, M. A. Kutcher, and R. L. Royster Coronary Artery Stents: Part I. Evolution of Percutaneous Coronary Intervention Anesth. Analg., August 1, 2008; 107(2): 552 - 569. [Abstract] [Full Text] [PDF]
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L. T. Newsome, R. S. Weller, J. C. Gerancher, M. A. Kutcher, and R. L. Royster Coronary Artery Stents: II. Perioperative Considerations and Management Anesth. Analg., August 1, 2008; 107(2): 570 - 590. [Abstract] [Full Text] [PDF]
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M. Joner, G. Nakazawa, A. V. Finn, S. C. Quee, L. Coleman, E. Acampado, P. S. Wilson, K. Skorija, Q. Cheng, X. Xu, et al. Endothelial Cell Recovery Between Comparator Polymer-Based Drug-Eluting Stents J. Am. Coll. Cardiol., July 29, 2008; 52(5): 333 - 342. [Abstract] [Full Text] [PDF]
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A. V. Finn, G. Nakazawa, E. Ladich, F. D. Kolodgie, and R. Virmani Does underlying plaque morphology play a role in vessel healing after drug-eluting stent implantation? J. Am. Coll. Cardiol. Img., July 1, 2008; 1(4): 485 - 488. [Full Text] [PDF]
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M. J. Kern and J. Narula Looking into the vessel: the more you see, the more you want to see. J. Am. Coll. Cardiol. Img., July 1, 2008; 1(4): 556 - 559. [Full Text] [PDF]
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S. R. Dixon, C. L. Grines, and W. W. O'Neill The year in interventional cardiology. J. Am. Coll. Cardiol., June 17, 2008; 51(24): 2355 - 2369. [Full Text] [PDF]
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M. I. Hamilos, M. Ostojic, B. Beleslin, D. Sagic, L. Mangovski, S. Stojkovic, M. Nedeljkovic, D. Orlic, B. Milosavljevic, D. Topic, et al. Differential effects of drug-eluting stents on local endothelium-dependent coronary vasomotion. J. Am. Coll. Cardiol., June 3, 2008; 51(22): 2123 - 2129. [Abstract] [Full Text] [PDF]
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 G. W. Stone, M. Midei, W. Newman, M. Sanz, J. B. Hermiller, J. Williams, N. Farhat, K. W. Mahaffey, D. E. Cutlip, P. J. Fitzgerald, et al. Comparison of an Everolimus-Eluting Stent and a Paclitaxel-Eluting Stent in Patients With Coronary Artery Disease: A Randomized Trial JAMA, April 23, 2008; 299(16): 1903 - 1913. [Abstract] [Full Text] [PDF]
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J. Aoki, G. S. Mintz, N. J. Weissman, J. T. Mann, L. Cannon, J. Greenberg, E. Grube, A.R. Z. Masud, J. Koglin, L. Mandinov, et al. Chronic Arterial Responses to Overlapping Paclitaxel-Eluting Stents: Insights From Serial Intravascular Ultrasound Analyses in the TAXUS-V and -VI Trials J. Am. Coll. Cardiol. Intv., April 1, 2008; 1(2): 161 - 167. [Abstract] [Full Text] [PDF]
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Y. Suzuki, F. Ikeno, T. Koizumi, F. Tio, A. C. Yeung, P. G. Yock, P. J. Fitzgerald, and W. F. Fearon In Vivo Comparison Between Optical Coherence Tomography and Intravascular Ultrasound for Detecting Small Degrees of In-Stent Neointima After Stent Implantation J. Am. Coll. Cardiol. Intv., April 1, 2008; 1(2): 168 - 173. [Abstract] [Full Text] [PDF]
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M. Takano, M. Yamamoto, S. Inami, D. Murakami, K. Seimiya, T. Ohba, Y. Seino, and K. Mizuno Long-term follow-up evaluation after sirolimus-eluting stent implantation by optical coherence tomography: do uncovered struts persist? J. Am. Coll. Cardiol., March 4, 2008; 51(9): 968 - 969. [Full Text] [PDF]
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J. Aoki, A. Kirtane, M. B. Leon, and G. Dangas Coronary artery aneurysms after drug-eluting stent implantation. J. Am. Coll. Cardiol. Intv., February 1, 2008; 1(1): 14 - 21. [Abstract] [Full Text] [PDF]
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M. Takano, M. Yamamoto, Y. Xie, D. Murakami, S. Inami, K. Okamatsu, K. Seimiya, T. Ohba, Y. Seino, and K. Mizuno Serial long-term evaluation of neointimal stent coverage and thrombus after sirolimus-eluting stent implantation by use of coronary angioscopy Heart, December 1, 2007; 93(12): 1533 - 1536. [Abstract] [Full Text] [PDF]
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L. Testa, W. J. van Gaal, and R. Bhindi Letter by Testa et al Regarding Article, "Pathological Correlates of Late Drug-Eluting Stent Thrombosis: Strut Coverage as a Marker of Endothelialization" Circulation, November 27, 2007; 116(22): e549 - e549. [Full Text] [PDF]
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A. V. Finn, M. C. John, H. K. Gold, J. Newell, G. Nakazawa, M. Joner, F. D. Kolodgie, and R. Virmani Response to Letter Regarding Article, "Pathological Correlates of Late Drug-Eluting Stent Thrombosis: Strut Coverage as a Marker of Endothelialization" Circulation, November 27, 2007; 116(22): e550 - e550. [Full Text] [PDF]
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M. Takano, M. Yamamoto, Y. Xie, D. Murakami, S. Inami, K. Okamatsu, K. Seimiya, T. Ohba, Y. Seino, and K. Mizuno Serial long-term evaluation of neointimal stent coverage and thrombus after sirolimus-eluting stent implantation by use of coronary angioscopy Heart, November 1, 2007; 93(11): 1353 - 1356. [Abstract] [Full Text] [PDF]
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 G. J. Wilson, J. E. Polovick, B. A. Huibregtse, and B. C. Poff Overlapping paclitaxel-eluting stents: Long-term effects in a porcine coronary artery model Cardiovasc Res, November 1, 2007; 76(2): 361 - 372. [Abstract] [Full Text] [PDF]
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 A. V. Finn, G. Nakazawa, M. Joner, F. D. Kolodgie, E. K. Mont, H. K. Gold, and R. Virmani Vascular Responses to Drug Eluting Stents: Importance of Delayed Healing Arterioscler Thromb Vasc Biol, July 1, 2007; 27(7): 1500 - 1510. [Abstract] [Full Text] [PDF]
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