HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Figures Only Full Text (PDF) All Versions of this Article: 2241011253v1 224/2/529    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schillinger, M. Articles by Minar, E. Search for Related Content PubMed PubMed Citation Articles by Schillinger, M. Articles by Minar, E.

Inflammatory Response to Stent Implantation: Differences in Femoropopliteal, Iliac, and Carotid Arteries¹

¹ From the Departments of Angiology (M.S., W.M., M.H., R.A., E.M.) and Laboratory Medicine (M.E., H.R., O.W.), University of Vienna Medical School, Währinger Gürtel 18-20/6J, 1090 Vienna, Austria. Received July 23, 2001; revision requested September 12; revision received October 12; accepted December 10. Address correspondence to M.S. (e-mail: martin.schillinger@akh-wien .ac.at).

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
PURPOSE: To investigate the postintervention course of serum acute-phase reactants after stent implantation in the femoropopliteal, iliac, and carotid arteries.

MATERIALS AND METHODS: This prospective cohort study included 274 consecutive patients who underwent stent implantation in the femoropopliteal (n = 95), iliac (n = 70), and carotid (n = 109) arteries. C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen levels were measured at baseline and at 48 hours after intervention. Polynomial logistic regression analysis was applied to assess the independent association of the course of acute-phase reactants and the site of stent implantation.

RESULTS: Stent implantation in the femoropopliteal artery was associated with a higher postintervention increase in CRP (P = .01), SAA (P = .04), and fibrinogen (P = .01) values compared with values with iliac artery stent implantation, with adjustment for age, sex, fluoroscopy duration, contrast agent dose, complication occurrence, stenosis grade, total vessel occlusion, and stent cumulative length. No significant difference in the postintervention course of CRP (P = .9) and SAA (P = .1) levels was determined for stents implanted in the carotid artery compared with those implanted in the iliac artery; however, a higher increase in fibrinogen levels (P = .04) was noted.

CONCLUSION: Stent implantation in the muscular femoropopliteal artery was associated with a more extensive vascular inflammatory response than was stent implantation in the elastic iliac and carotid arteries, independent of lesion morphology and interventional factors.

© RSNA, 2002

Index terms: Arteries, stenosis or obstruction, 172.721, 9_*.721² • Stents and prostheses, 172.2079, 172.458, 172.629, 92.1268, 92.24, 98.1268, 98.24

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
The pathophysiology of the vascular wall reaction after stent implantation is not yet entirely understood. It is known that intimal and medial injury and lipid core penetration by the stent struts cause a perivascular inflammatory response (1). Various types of stents have been evaluated with regard to their potential for inflammatory response (2,3). However, differences in the inflammatory response according to the arterial site or vessel area of stent implantation, to our knowledge, have not been reported so far.

The severity of arterial injury during stent implantation correlates with increased inflammation (4). This vascular inflammatory process plays an important role in vascular smooth muscle cell proliferation and late neointimal growth (5,6). Vascular smooth muscle cell proliferation and subsequent hypertrophic neointima formation at the treated artery lead to in-stent restenosis.

Patency rates after percutaneous transluminal angioplasty (PTA) and stent implantation widely depend on the location of the treated lesion. Endovascular treatment of large elastic arteries, such as the internal carotid artery and the iliac arteries, is associated with a relatively low rate of recurrence (7–10). In contrast, in muscular arteries, such as the femoropopliteal artery, restenosis after PTA occurs in up to 50% of the patients within the 1st year (7,11–17). Hemodynamic and wall characteristics at each vessel segment are believed to influence the susceptibility for restenosis. However, the extent of the inflammatory response might also contribute to the specific pattern of in-stent restenosis in femoropopliteal, iliac, and carotid arteries. Recently, baseline levels of C-reactive protein (CRP) were demonstrated to be an independent predictor of restenosis after balloon angioplasty of the femoropopliteal artery (18).

The perivascular inflammatory process after stent implantation can be adequately quantified by means of measurement of serum acute-phase reactants (19,20). We hypothesized that the postintervention course of serum acute-phase reactants varies according to the arterial site of stent implantation in large elastic or muscular arteries. The aim of this study was to investigate the postintervention course of serum acute-phase reactants after stent implantation in the femoropopliteal, iliac, and carotid arteries.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Study Design
The study was designed as a prospective cohort study. We included 274 consecutive patients (180 [66%] men; median age, 67 years; interquartile range, 60th to 75th percentile) who underwent PTA and stent implantation in the arteries of the lower limbs and in the internal carotid artery between March 1, 2000, and March 1, 2001. Age data in 94 (34%) women were similar to those in men. Primary stent implantation was performed in carotid interventions, and in the iliac and femoropopliteal vessel area, stent implantation was performed after primary suboptimal PTA. We included patients with arterial occlusive disease, whereas patients with aneurysmal disease were not eligible for the study. Furthermore, patients who underwent local thrombolysis were excluded. The study was performed in accordance with the Declaration of Helsinki and was approved by the local ethics committee. All patients gave their written informed consent.

Definitions
The Fontaine classification was used to categorize the clinical stage of peripheral arterial disease (PAD) (7). Patients with PAD in Fontaine II, III, and IV classifications and lesions with at least 50% reduction in diameter in the iliac (common and external iliac arteries) or the femoropopliteal artery were scheduled for endovascular interventions of the lower limbs. Assessment of data in patients with PAD was in accordance with the TransAtlantic Inter-Society Concensus for treatment of PAD (7). Carotid artery interventions were performed in asymptomatic patients with internal carotid artery stenosis of 90% or greater and in symptomatic patients with internal carotid artery stenosis of 70% or greater (8). Cerebral vascular occlusive disease was categorized as stage I if it was asymptomatic, stage II if it was associated with a recent transitory ischemic attack, stage III if it was associated with a recent prolonged reversible ischemic neurologic deficit, and stage IV if it was associated with a recent stroke.

At the time of hospital admission, patients’ age, sex, body mass index, medical history, cardiovascular risk factors, and comorbidities were recorded, according to a standardized questionnaire, by two independent observers (M.S., W.M.). Data sets of both observers were then compared to identify any inconsistency in data collection. Hypercholesterolemia was defined as a baseline serum cholesterol level greater than 200 mg/dL (5.17 mmol/L) or serum low-density lipoprotein value greater than 130 mg/dL (3.36 mmol/L). Diabetes mellitus was classified in patients with a history of diabetes, in patients with fasting blood glucose levels greater than 110 mg/dL (6.1 mmol/L) measured on three occasions, in patients with oral glucose tolerance test results suggestive of disease, and in patients with a glycosylated hemoglobin level greater than 0.06 (6.5%).

Laboratory Investigations
A complete series of routine laboratory investigations, including glycosylated hemoglobin level, low- and high-density lipoprotein cholesterol values, complete blood cell count, and serum creatinine value, was performed at baseline before PTA. Antecubital venous blood samples were obtained for determination of CRP, serum amyloid A (SAA), and fibrinogen values at baseline before the intervention and at 48 hours after the intervention. For measurement of serum CRP values, the high-sensitivity assay (N Latex CRP Mono; Dade Behring, Vienna, Austria) was used. SAA level was measured with a high-sensitivity assay (N Latex SAA; Dade Behring). Fibrinogen level also was measured with a test (Fibrinogen Clauss; Stago, Roche, Vienna, Austria). The detection levels of CRP, SAA, and fibrinogen assays, respectively, were 0.03 mg/dL (0.3 mg/L), 3.8 mg/L (3.8 U/L), and 20 mg/dL (2.0 g/L), respectively. The coefficients of variation of CRP, SAA, and fibrinogen values were 4.6%, 6.4%, and 5.2%, respectively.

Interventions
PTA and stent implantation were performed according to a standardized protocol. All interventions were performed by using the transfemoral access. Length and grade of lesion were calculated from the initial angiogram in at least two planes. Predilation was routinely performed in all vessel areas with the balloon diameter corresponding to the proximal nondiseased vessel diameter. Indication for interventional treatment and diameter, length, and number of stents implanted were routinely documented. The diameter of the stent was chosen according to the proximal nondiseased vessel area. For all carotid artery interventions, an over-the-wire carotid stent (Carotid Wallstent OTW; Boston Scientific, Natick, Mass) was used. All carotid artery interventions were performed by one experienced interventionist (R.A.) with experience in more than 300 procedures before initiation of the study. Implantation of stents in iliac arteries was performed by using one of three self-expandable stents (Easy Wallstent and Symphony Stent, Boston Scientific; Dynalink Stent, Guidant, Santa Clara, Calif).

In the femoropopliteal vessel area, self-expandable stents, including one made by another manufacturer (SmartStent; Cordis, Miami, Fla), were implanted. Peripheral interventions were performed by two authors (R.A. or E.M.) with more than 15 years of interventional experience. Duration of fluoroscopy and dose of contrast agent and amount of intraarterially administered heparin were recorded. The nonionic low-osmolality contrast agent ioversol (Optiray 320; Mallinckrodt, St Louis, Mo) in a dilution of 50% was used for all interventions. Peri- and postintervention complications at the site of arterial puncture and at the dilated vessel were documented up to 48 hours after the intervention. All complications that could be managed conservatively were classified as minor complications and included hematoma or pseudoaneurysm at the site of puncture and a significant dissecting membrane at the dilated vessel segment or peripheral emboli. Major bleeding (hemoglobin decrease > 2 mg/dL [0.02 g/L]) and all complications that necessitated emergency surgery within 48 hours were classified as major complications.

Standardized medication administered after stent implantation, irrespective of the site of intervention, included 100 mg of acetylsalicylic acid and 75 mg of clopidogrel bisulfate (Sanofi Pharma Bristol-Myers Squibb, Paris, France) daily. Pharmacologic treatment was initiated at least 1 day before the intervention.

Statistical Analysis
Continuous data were presented as the median and the interquartile range (range, 25th to the 75th percentile) or, if adequate, as the mean and the SD. Percentages were calculated for dichotomous variables. For univariate comparison of continuous data, the Kruskal-Wallis test or, if adequate, the Mann Whitney U test was used. Categorical data were compared by means of the ² test. Spearman rank correlation coefficient was calculated for correlation of continuous variables. The course of laboratory values before intervention to 48 hours after intervention was measured by means of the relative change (ie, relative change in CRP [CRP], relative change in SAA [SAA], and relative change in fibrinogen [fibrinogen]).

Multivariate polynomial logistic regression analysis was performed to assess the independent association of the course of acute-phase reactants and the location of stent implantation and to adjust for confounding factors and preselection bias. Variables that differed between the two groups at a level of significance with a P value less than .2 in univariate analysis were entered into the models as possible confounders. The results of the logistic regression model were presented as the odds ratio and the 95% CI. All P values were two sided; a P value less than .05 was considered statistically significant. Calculations were performed with statistical software (SPSS, version 10.0, for Microsoft Windows; SPSS, Chicago, Ill).

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Within the 12-month study period, 274 consecutive patients underwent stent implantation in the femoropopliteal artery (n = 95), in the iliac arteries (n = 70), and in the internal carotid arteries (n = 109). All patients were included in the final analysis. The median age was 67 years (interquartile range, 60th to 75th percentile), and 180 patients (66%) were men. Ninety-four (34%) patients were women, and age data were similar to those in men. Cardiovascular risk factors and comorbidities were found in the majority of patients (Table 1).

Carotid artery interventions were performed in 76 (70%) of 109 asymptomatic patients with internal carotid artery stenosis of 90% or greater. Thirty-three (30%) of these patients had a symptomatic internal carotid artery stenosis and recent neurologic events: 24 (22%) patients had a transitory ischemic attack, two (2%) patients had a prolonged reversible ischemic neurologic deficit, and seven (6%) patients had a major stroke and were examined 6 weeks afterward.

Baseline characteristics and interventional data in the 274 patients according to the arterial site of stent implantation are shown in Table 2. Patients who underwent revascularization of the carotid artery were substantially older compared with patients who underwent interventions in the iliac and femoropopliteal arteries. Patients with femoropopliteal artery stent implantation more frequently had complete vessel occlusion and an overall higher grade of stenosis compared with the grade of stenosis in other vessel areas. Furthermore, femoropopliteal artery lesions were longer compared with carotid and iliac artery lesions, and longer stents were implanted in this vessel area. Internal carotid artery stenoses were the shortest treated lesions, with a maximum length of 30 mm. Duration of carotid and iliac artery interventions was shorter compared with duration of femoropopliteal artery endovascular treatment (Table 2). The rate of complications was similar after stent implantation in the carotid, iliac, and femoropopliteal arteries; in particular, no differences in vessel dissection before stent implantation were observed in the three groups. No significant differences were observed between male and female patients within the three intervention groups.

View larger version (34K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Graph shows mean CRP before to 48 hours after stent implantation in iliac (n = 70), femoropopliteal (n = 95), and carotid (n = 109) arteries. Error bars represent 95% CI.

View larger version (33K): [in this window] [in a new window] [Download PPT slide]   Figure 2. Graph shows mean SAA before to 48 hours after stent implantation in iliac (n = 70), femoropopliteal (n = 95), and carotid (n = 109) arteries. Error bars represent 95% CI.

View larger version (36K): [in this window] [in a new window] [Download PPT slide]   Figure 3. Graph shows mean fibrinogen before to 48 hours after stent implantation in iliac (n = 70), femoropopliteal (n = 95), and carotid (n = 109) arteries. Error bars represent 95% CI.

Multivariate polynomial logistic regression analysis was performed to independently assess differences in the postintervention course of acute-phase parameters with regard to the arterial site of stent implantation. The models were adjusted for possible confounding factors, as indicated by univariate comparison (Table 2). Patients with iliac stent implantation served as the reference group. Because of colinearity between the acute-phase reactants, separate models were applied for the courses of CRP, SAA, and fibrinogen values. The final models were adjusted for age, sex, fluoroscopy duration, contrast agent dose, complications, stenosis grade, total vessel occlusion, and cumulative stent length.

Femoropopliteal artery stent implantation was independently associated with a higher increase in CRP (Table 4), SAA (Table 5), and fibrinogen (Table 6) values compared with the values in the reference group of patients with iliac artery stent implantation. Carotid artery stent implantation was associated with a similar course of postintervention CRP (Table 4) and SAA (Table 5) values compared with the course of these values with iliac stent implantation; however, a more pronounced increase in fibrinogen (Table 6) level was noted. The final models had an acceptable fit (P < .001, log likelihood ratio).

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

Intimal and medial injuries after balloon dilation and stent implantation induced a perivascular inflammatory response (1,4,6,21). Differences in the extent of the inflammatory process depended on the type of stent used (2,22). In particular, the material of the stent mesh, such as stainless steel or nitinol, and the presence of a covered fabric, such as polytetrafluoroethylene or synthetic polyester fiber (ie, Dacron), influenced the local vascular reaction at the site of implantation (2,22). Furthermore, the distribution of shear stress after arterial stent implantation correlated with in-stent neointimal hyperplasia (23), which was a result of the inflammatory reaction.

However, the postimplantation reaction after stent deployment may also depend on the arterial site. So far, to our knowledge, large elastic arteries and muscular vessels have not been investigated with regard to their inflammatory potential in response to stent implantation. A marked increase in CRP, SAA, and fibrinogen values was described 48 hours after peripheral and coronary PTA and stent implantation (19,20). These acute-phase parameters, therefore, seemed adequate to quantify inflammation after stent implantation in muscular or elastic arteries.

Elastic and geometric properties of the vascular wall and local hemodynamics significantly vary in the carotid, iliac, and femoropopliteal arteries (24). In particular, maintenance of brisk flow through the carotid and iliac arteries in diastole as opposed to the diastolic flow characteristic in the femoropopliteal arteries may contribute to the patency of stents. Furthermore, atherosclerotic lesions in these three vessel areas were shown to differ with regard to plaque morphology and remodeling to luminal narrowing (25). Similarly, results in studies with animal models used for interventions to prevent coronary and peripheral artery restenosis are not uniformly predictive, depending on the arterial site of stent implantation (26).

Local vessel wall properties of muscular and elastic arteries probably cause the observed differences in the postimplantation inflammatory reaction. The distribution and density of vascular smooth muscle cells significantly vary between elastic and muscular arteries. Vascular smooth muscle cells may be the key factors in the chain of vascular inflammatory processes. However, the specific mechanisms of the more extensive inflammatory response to stent implantation in the femoropopliteal artery compared with those of the response to stent implantation in the carotid and iliac arteries remain unclear so far.

Balloon angioplasty and stent implantation apply a transient strain to the vessel wall that activates smooth muscle cells and modulates a proliferative and inflammatory phase of vessel repair (27). Migration of smooth muscle cells through the meshes of the stent and lumen-narrowing proliferation are the hallmarks of in-stent restenosis. Initial lumen diameter, flow characteristics, and endogenous antiinflammatory and antiproliferative mechanisms influence the occurrence of restenosis (23,28). However, the specific differences in the inflammatory response at various arterial sites are also likely to contribute to different patterns of restenosis after stent implantation in femoropopliteal, iliac, and carotid arteries.

Baseline CRP and SAA values have been reported to be independent predictors of restenosis after coronary angioplasty (29,30). Recently, the baseline CRP level before intervention was shown to be an independent predictor of restenosis after angioplasty in the femoropopliteal artery as well (18). The finding that stent implantation in the femoropopliteal artery induces a more extensive inflammatory response than do interventions in the carotid or iliac artery may have a potential effect on the understanding of mechanisms of restenosis. Further studies may reveal whether the postintervention increase in these acute-phase reactants is also associated with the occurrence of restenosis in the individual patient.

Limitations
These findings are derived from a between-patient comparison and the use of different types of stents. Therefore, we adjusted for several possible confounding factors, such as lesion morphology and length of the stent. Lesion morphology and stent characteristics were not associated with the postintervention inflammatory reaction. Furthermore, there was no relationship between a given stent in a given vessel and CRP, SAA, and fibrinogen. However, it cannot be entirely excluded that different stent materials caused an altered inflammatory response and influenced the course of acute-phase parameters. However, all stent meshes were of comparable fabricates and geometries, no covered stents were implanted, and experimental studies suggest that a similar degree of inflammatory response can be expected from each of the stents used in this patient series (2,3).

In conclusion, stent implantation in the muscular femoropopliteal artery was associated with a more extensive vascular inflammatory response than was stent implantation in the elastic iliac and carotid arteries, independent of lesion morphology and interventional factors. The enhanced inflammatory response after stent implantation in the femoropopliteal artery might contribute to the higher rates of restenosis in this vessel area.

	FOOTNOTES

 
² 9_*. Vascular system, location unspecified

Abbreviations: CRP = C-reactive protein, CRP = relative change in CRP, fibrinogen = relative change in fibrinogen, SAA = relative change in serum amyloid A, PAD = peripheral arterial disease, PTA = percutaneous transluminal angioplasty, SAA = serum amyloid A

Author contributions: Guarantors of integrity of entire study, E.M., M.S.; study concepts, M.S., E.M.; study design, M.E., W.M., M.H.; literature research, M.S., W.M.; clinical studies, R.A., E.M.; data acquisition, M.S., W.M.; data analysis/interpretation, E.M., R.A., H.R., O.W.; statistical analysis, M.S.; manuscript preparation, all authors; manuscript definition of intellectual content, E.M., M.S.; manuscript editing, revision/review, and final version approval, all authors.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 

1. Farb A, Sangiorgi G, Carter AJ, et al. Pathology of acute and chronic coronary stenting in humans. Circulation 1999; 99:44-52.[Abstract/Free Full Text]
2. Barth KH, Virmani R, Froelich J, et al. Paired comparison of vascular wall reactions to Palmaz stents, Strecker tantalum stents, and Wallstents in canine iliac and femoral arteries. Circulation 1996; 93:2161-2169.[Abstract/Free Full Text]
3. Cejna M, Virmani R, Jones R, et al. Biocompatibility and performance of the Wallstent and several covered stents in a sheep iliac artery model. J Vasc Interv Radiol 2001; 12:351-358.[Medline]
4. Virmani R, Farb A. Pathology of in-stent restenosis. Curr Opin Lipidol 1999; 10:499-506.[CrossRef][Medline]
5. Kornowski R, Hong MK, Tio FO, et al. In-stent restenosis: contributions of inflammatory responses and arterial injury to neointimal hyperplasia. J Am Coll Cardiol 1998; 31:224-230.[Abstract/Free Full Text]
6. Yutani C, Ishibashi-Ueda H, Suzuki T, et al. Histologic evidence of foreign body granulation tissue and de novo lesions in patients with coronary stent stenosis. Cardiology 1999; 92:171-177.[CrossRef][Medline]
7. Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD): TASC Working Group—TransAtlantic Inter-Society Concensus (TASC). J Vasc Surg 2000; 31(1 pt 2):S1-S296.[CrossRef][Medline]
8. Ahmadi R, Wilifort A, Lang W, et al. Carotid artery stenting: effect of learning curve and intermediate-term morphological outcome. J Endovasc Ther 2001; 8:539-546.[CrossRef][Medline]
9. Tetteroo E, van der Graaf Y , Bosch JL, et al. Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease: Dutch Iliac Stent Trial Study group. Lancet 1998; 351:1153-1159.[CrossRef][Medline]
10. Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology 1997; 204:87-96.[Abstract/Free Full Text]
11. Gallino A, Mahler F, Probst P, Nachbur B. Percutaneous transluminal angioplasty of the arteries of the lower limbs: a 5 year follow-up. Circulation 1984; 70:619-623.[Abstract/Free Full Text]
12. Krepel VM, van Andel GJ, van Erp WF, Breslau PJ. Percutaneous transluminal angioplasty of femoropopliteal artery: initial and long term results. Radiology 1985; 156:325-328.[Abstract/Free Full Text]
13. Maca T, Ahmadi R, Derfler K, et al. Elevated lipoprotein(a) and increased incidence of restenosis after femoropopliteal PTA: rationale for the higher risk of recurrence in females? Atherosclerosis 1996; 127:27-34.[CrossRef][Medline]
14. Cejna M, Illiasch H, Waldenberger P, Horvath W, Thurnher SA, Lammer J. PTA versus Palmaz stent in femoropopliteal obstructions: a prospective randomized trial—long-term results (abstr). Radiology 1998; 209(P):492.
15. Matsi PJ, Manninen HI, Vanninen RL, et al. Femoropopliteal angioplasty in patients with claudication: primary and secondary patency in 140 limbs with 1-3-year follow-up. Radiology 1994; 191:727-733.[Abstract/Free Full Text]
16. Adar R, Critchfield GC, Eddy DM. A confidence profile analysis of the results of femoropopliteal percutaneous transluminal angioplasty in the treatment of lower-extremity ischemia. J Vasc Surg 1989; 10:57-67.[CrossRef][Medline]
17. Jeans WD, Armstrong S, Cole SE, Horrocks M, Baird RN. Fate of patients undergoing transluminal angioplasty for lower-limb ischemia. Radiology 1990; 177:559-564.[Abstract/Free Full Text]
18. Schillinger M, Haumer M, Schlerka G, Mlekusch W, Exner M, Minar E. Restenosis after percutaneous transluminal angioplasty in the femoropopliteal segment: the role of inflammation. J Endovasc Ther 2001; 8:477-483.[CrossRef][Medline]
19. Gottsauner-Wolf M, Zasmeta G, Hornykewycz S, et al. Plasma levels of C-reactive protein after coronary stent implantation. Eur Heart J 2000; 21:1152-1158.[Abstract/Free Full Text]
20. Schillinger M, Exner M, Mlekusch W, et al. Balloon angioplasty and stent implantation induce a vascular inflammatory reaction. J Endovasc Ther 2002; 9:59-66.[CrossRef][Medline]
21. Azar RR, McKay RG, Kiernan FJ, et al. Coronary angioplasty induces a systemic inflammatory response. Am J Cardiol 1997; 80:1476-1478.[CrossRef][Medline]
22. Schurmann K, Vorwerk D, Bucker A, et al. Perigraft inflammation due to Dacron-covered stent-grafts in sheep iliac arteries: correlation of MR imaging and histopathologic findings. Radiology 1997; 204:757-763.[Abstract/Free Full Text]
23. Wentzel JJ, Krams R, Schuurbiers JC, et al. Relationship between neointimal thickness and shear stress after Wallstent implantation in human coronary arteries. Circulation 2001; 103:1740-1745.[Abstract/Free Full Text]
24. Li JK, Melbin J, Riffle RA, Noordergraad A. Pulse wave propagation. Circ Res 1981; 49:442-452.[Abstract/Free Full Text]
25. Pasterkamp G, Schoneveld AH, van Wolferen W, et al. The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely with the arterial system: a postmortem study. Arterioscler Thromb Vasc Biol 1997; 17:3057-3063.[Abstract/Free Full Text]
26. Johnson GJ, Griggs TR, Badimon L. The utility of animal models in the preclinical study of interventions to prevent human coronary artery restenosis: analysis and recommendations. On behalf of the Subcommittee on Animal, Cellular and Molecular Models of Thrombosis and Haemostasis of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis. Thromb Haemost 1999; 81:835-843.
27. Geary RL, Nikkari ST, Wagner WD, Williams JK, Adams MR, Dean RH. Wound healing: a paradigm for lumen narrowing after arterial reconstruction. J Vasc Surg 1998; 27:96-106.[CrossRef][Medline]
28. Exner M, Schillinger M, Minar E, et al. Heme oxygenase-1 gene promoter microsatellite polymorphism is associated with restenosis after percutaneous transluminal angioplasty. J Endovasc Ther 2001; 8:433-440.[CrossRef][Medline]
29. Buffon A, Liuzzo G, Biasucci LM, et al. Preprocedural serum levels of C-reactive protein predict early complications and late restenosis after coronary angioplasty. J Am Coll Cardiol 1999; 34:1512-1521.[Abstract/Free Full Text]
30. Blum A, Kaplan G, Vardinon N, et al. Serum amyloid type A may be a predictor of restenosis. Clin Cardiol 1998; 21:655-658.[Medline]

This article has been cited by other articles:

				A. L. Hogh, J. Joensen, J. S. Lindholt, M. R. Jacobsen, and L. Ostergaard C-Reactive Protein Predicts Future Arterial and Cardiovascular Events in Patients With Symptomatic Peripheral Arterial Disease Vascular and Endovascular Surgery, August 1, 2008; 42(4): 341 - 347. [Abstract] [PDF]

				G. Tepe, P. Muschick, M. Laule, F. Reddig, C. D. Claussen, L. M. Dinkelborg, H. Tielemans, M. Wehrmann, and S. H. Duda Prevention of Carotid Artery Restenosis After Sirolimus-Coated Stent Implantation in Pigs Stroke, February 1, 2006; 37(2): 492 - 494. [Abstract] [Full Text] [PDF]

				S. P. Lownie, D. M. Pelz, D. H. Lee, S. Men, I. Gulka, and P. Kalapos Efficacy of Treatment of Severe Carotid Bifurcation Stenosis By Using Self-Expanding Stents without Deliberate Use of Angioplasty Balloons AJNR Am. J. Neuroradiol., May 1, 2005; 26(5): 1241 - 1248. [Abstract] [Full Text] [PDF]

				B. J. Pearce and J. F. McKinsey Current Status of Intravascular Stents as Delivery Devices to Prevent Restenosis Vascular and Endovascular Surgery, July 1, 2003; 37(4): 231 - 237. [Abstract] [PDF]

				D. F. Denny Jr Prediction of Restenosis after Carotid Artery Stent Implantation Radiology, May 1, 2003; 227(2): 316 - 318. [Full Text] [PDF]

This Article Abstract Figures Only Full Text (PDF) All Versions of this Article: 2241011253v1 224/2/529    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schillinger, M. Articles by Minar, E. Search for Related Content PubMed PubMed Citation Articles by Schillinger, M. Articles by Minar, E.