Influence of Balloon Pressure During Stent Placement in Native Coronary Arteries on Early and Late Angiographic and Clinical Outcome

Transcription

1 Influence of Balloon Pressure During Stent Placement in Native Coronary Arteries on Early and Late Angiographic and Clinical Outcome A Randomized Evaluation of High-Pressure Inflation Josef Dirschinger, MD; Adnan Kastrati, MD; Franz-Josef Neumann, MD; Peter Boekstegers, MD; Shpend Elezi, MD; Julinda Mehilli, MD; Helmut Schühlen, MD; Jürgen Pache, MD; Eckhard Alt, MD; Rudolf Blasini, MD; Gerhard Steinbeck, MD; Albert Schömig, MD Background High-pressure dilatation is considered a better stent placement strategy, but this has not yet been proved by appropriately designed studies. The objective of this randomized trial was to assess the role of high-pressure dilatation in the early and late outcome of patients undergoing coronary stent placement. Methods and Results Consecutive patients with coronary stent placement were randomly assigned to high- (15 to 20 atm, 468 patients) or low- (8 to 13 atm, 466 patients) balloon-pressure dilatation. The primary end point of the study was the event-free survival at 1 year. Secondary end points were the incidence of stent thrombosis at 30 days and angiographic restenosis ( 50% diameter stenosis) at 6 months. The incidence of stent thrombosis was 1.7% in the high-pressure and 1.9% in the low-pressure group (relative risk 0.89; 95% CI 0.30 to 2.56). During the first 30 days, although there was no significant difference in the incidence of Q-wave myocardial infarction, the incidence of non Q-wave infarction was 6.4% in the high-pressure and 3.4% in the low-pressure group (relative risk 1.87; 95% CI 1.02 to 3.42). The restenosis rate was 30.4% in the high-pressure and 31.4% in the low-pressure group (relative risk 0.97; 95% CI 0.75 to 1.26). Event-free survival at 1 year was not significantly different between the groups, with 78.8% in high-pressure patients and 75.5% in patients assigned to low-pressure dilatation (hazard ratio 0.85; 95% CI 0.65 to 1.11). Conclusions The systematic use of high-balloon-pressure inflation (15 to 20 atm) during coronary stent placement is not associated with any significant influence on the 1-year outcome of patients undergoing this intervention. (Circulation. 1999;100: ) Key Words: stents balloon thrombosis restenosis trials The enthusiasm engendered by the initial randomized trials demonstrating the advantages of coronary stenting over conventional percutaneous transluminal balloon angioplasty (PTCA) was overshadowed by the increase in bleeding complications associated with the anticoagulation therapy imposed by the thrombogenic nature of the stent. 1,2 Improvement in the rheology of the stented coronary lumen 3 was a first logical attempt to reduce the risk of stent thrombosis and the need for aggressive anticoagulation. Colombo and his team 4,5 were the first to propose high-pressure dilatation as a strategy that ensures complete stent apposition, better flow characteristics, and decreased risk of thrombosis and obviates the anticoagulation. This strategy was rapidly embraced by the large community of interventional cardiologists and became an integral part of recent recommendations on coronary stenting. 6 The switch to the high-pressure strategy, however, has coincided with the introduction of ticlopidine plus aspirin as a poststenting therapy. The demonstration of the pivotal role of platelets in stent thrombosis 7,8 and of the superiority of the combined antiplatelet therapy over anticoagulation for its prevention 9,10 necessitates specifically designed studies to clarify the independent role of high-pressure dilatation in the reduction of the risk for stent thrombosis. High-pressure dilatation may also exert a positive influence on restenosis as a result of the better acute lumen achieved 11 and improvement in flow characteristics. 12 The objective of this randomized trial was to assess the role of high-pressure dilatation in the early and late outcome of patients undergoing coronary stent placement. Methods Patients Patients with symptomatic coronary artery disease treated with stenting were eligible for this study. Exclusion criteria were acute Received January 14, 1999; revision received May 24, 1999; accepted June 2, From the 1. Medizinische Klinik rechts der Isar der Technischen Universität (J.D., H.S., J.P., E.A.); the Deutsches Herzzentrum (A.K., F.J.N., S.E., J.M., R.B., A.S.); and the 1. Medizinische Klinik, Klinikum Großhadern der Ludwig-Maximilians-Universität (P.B., G.S.), Munich, Germany. Correspondence to Dr Josef Dirschinger, 1. Medizinische Klinik rechts der Isar der TU, Ismaningerstraße 22, München, Germany American Heart Association, Inc. Circulation is available at 918

2 Dirschinger et al High- vs Low-Pressure Coronary Stenting 919 3myocardial infarction (within 48 hours before intervention), target lesion in a venous bypass graft, prior randomization, and unwillingness or inability to provide written informed consent for participation in the trial. The randomization sequence was specified before the study began. All patients were randomly assigned to a balloonpressure strategy by means of sealed envelope before the intervention. Patients gave informed consent for a routine control angiography at 6 months. The study was conducted according to the principles of the Declaration of Helsinki and was approved by the Ethics Committees at each participating center. Stent Placement and Poststenting Treatment During the intervention, patients received intravenous heparin and aspirin. Patients considered at higher risk for stent thrombosis (large residual dissections, thrombus at the stent site) received abciximab. Heparin infusion was continued for 12 hours after the intervention. All patients received 250 mg ticlopidine started immediately after the intervention and continued twice daily for 4 weeks as well as 100 mg aspirin taken twice daily indefinitely. The stents implanted were those in use in our institutions at the time at which the study was performed. They were all composed of stainless steel material and were multicellular in design. We used the Inflow stent (Inflow Dynamics), Multi-Link stent (Guidant, Advanced Cardiovascular Systems), NIR stent (Scimed, Boston Scientific), Palmaz-Schatz stent (Johnson & Johnson Interventional Systems), and Pura-A stent (Devon Medical). Lesion predilatation with conventional angioplasty balloon catheters was performed before the stent placement. Except for the Multi-Link type, all stents were firmly hand-crimped on conventional balloon catheters before delivery. For Multi-Link stents, the delivery system provided by the manufacturer was used. The balloon size for stent deployment was chosen on the basis of the estimated vessel size in a nondiseased portion. High pressure was defined as a pressure in the range of 15 to 20 atm on the basis of the values used by Colombo et al 4,5 and achieved with noncompliant or minimally compliant balloons. Low pressure was defined as a pressure in the range of 8 to 13 atm to allow a safe inflation with conventional angioplasty balloons below the rated burst pressure. The procedural results were assessed by angiography only; no intravascular ultrasound studies were performed. The procedure was considered successful when stent placement was associated with a residual stenosis of 30% and Thrombolysis in Myocardial Infarction (TIMI) flow grade 2. Angiographic Evaluation Lesion complexity and calcifications were defined according to Ellis et al. 13 Left ventricular function was assessed qualitatively on the basis of biplane angiograms with a 7-segment division; the diagnosis of reduced left ventricular function required the presence of hypokinesia in 2 segments. Offline quantitative angiographic analysis was performed by operators not involved in the procedure and unaware of the pressure strategy to which the patient was assigned. Digital angiograms were analyzed with the automated edge detection system CMS (Medis Medical Imaging Systems). Matched views were selected for angiograms recorded before and immediately after the intervention and at follow-up. The parameters obtained were minimal lumen diameter (MLD), reference diameter, diameter stenosis, and diameter of the maximally inflated balloon during stent placement. Acute elastic recoil was measured as the difference between balloon diameter and MLD at the end of the procedure. Acute lumen gain was the difference between MLD at the end of the intervention and MLD before balloon dilatation. Late lumen loss was calculated as the difference in MLD between immediately after the procedure and follow-up. Definitions and End Points of the Study The primary end point of the study was event-free survival at 1 year after the procedure. Death, myocardial infarction, and target vessel revascularization (PTCA or aortocoronary bypass surgery) were considered adverse events. The diagnosis of acute myocardial infarction was established in the presence of a clinical episode of TABLE 1. Baseline Clinical Characteristics Age, y Women Arterial hypertension Diabetes Smoking Hypercholesterolemia Unstable angina Previous PTCA Previous CABG Reduced left ventricular function Number of diseased vessels Single-vessel disease Two-vessel disease Three-vessel disease prolonged chest pain and a rise in serum creatine kinase (CK) levels to at least twice the upper normal limit or the appearance of 1 new pathological Q waves on the ECG. 14 CK was determined before and immediately after the procedure, every 8 hours for the first 24 hours after stenting, and then daily until discharge. Target vessel revascularization was performed in the presence of angiographic restenosis and symptoms or signs of ischemia. Cardiac events were monitored throughout the follow-up period. The assessment was made on the basis of the information provided by hospital readmission records, referring physician, or phone interview with the patient. For all those patients who showed cardiac symptoms during the interview, at least a clinical and ECG checkup was performed at the outpatient clinic or by the referring physician. Secondary end points of the study were based on angiographic outcomes after stenting. First, the incidence of stent thrombosis was assessed during the early 30-day period. The diagnosis was made on the basis of a TIMI flow grade of 0 or 1 at angiography. Second, the incidence of restenosis (defined as a diameter stenosis of 50%) was assessed from the 6-month follow-up angiography. Statistical Analysis The number of patients included in the study was based on the sample size estimation for our primary end point, the occurrence of any major adverse event during the first year after the procedure. We assumed a 1-year event rate of 20% for patients with low-pressure stenting and 13% for those with high-pressure dilatation. The study was designed to have an 80% power for detecting a significant difference between these 2 strategies with an level of 0.05, and a sample size of 466 patients for each group was estimated. All analyses were performed on an intention-to-treat basis. Results are expressed as mean SD or as proportions (%). The differences between groups were assessed by 2 test for categorical data and t test for continuous data. The relative risk for an adverse event associated with high-pressure inflation was also calculated. Survival analysis was made by the Kaplan-Meier method. Differences in survival parameters were assessed for significance by means of the log-rank test, and the hazard ratio associated with high-pressure inflation was calculated by Cox regression analysis. Statistical significance was accepted for all values of P Results Of the 934 patients enrolled in the study, 468 were assigned to high-pressure and 466 to low-pressure dilatation. Table 1 shows the baseline clinical characteristics of the patients,

3 920 Circulation August 31, 1999 TABLE 2. Baseline Angiographic Characteristics Vessel Left main LAD LCx RCA ACC/AHA lesion type A B B C Calcified lesions Chronic occlusions Ostial lesions Lesion length, mm Vessel size, mm Preprocedural diameter stenosis, % * LAD indicates left anterior descending coronary artery; LCx, left circumflex coronary artery; RCA, right coronary artery; and ACC/AHA, American College of Cardiology/American Heart Association. *P 0.05 vs low-pressure group. which were comparable between the groups. Table 2 lists the baseline angiographic characteristics of the patients. Diameter stenosis was higher in patients of the high-pressure group, whereas all other data were not significantly different between the groups. Table 3 shows the procedural data. On average, there was a difference of 6 atm in the actual balloon pressure used, and the distribution of this parameter in either group is displayed in Figure 1. In 45 patients of the low-pressure group (14 with calcified lesions), the operator TABLE 3. Procedural Data Maximal balloon pressure, atm * Balloon-to-vessel ratio Number of implanted stents Stent type Inflow NIR Palmaz-Schatz Pura-A Multi-Link Residual dissection after stenting Administration of abciximab Final diameter stenosis, % * Acute elastic recoil, mm Acute lumen gain, mm * Procedural success *P 0.05 vs low-pressure group. Figure 1. Histogram of actual balloon pressures used in each randomization arm. considered it more appropriate to use a pressure above the range specified in the study protocol because of suboptimal angiographic results. In 24 of these 45 patients (53%), the balloon pressure used was only 1 atm above the upper limit of 13 atm, ie, intermediate between low and high pressure. In 48 patients of the high-pressure group, the operator used a pressure below the range specified in the study protocol because of increased risk or presence of a progressive dissection or when it was impossible or hazardous to reach the stented lesion with an additional noncompliant balloon. In 20 of these 48 patients (42%), the balloon pressure used was only 1 atm below the lower limit of 15 atm, ie, intermediate between low and high pressure. Thus, in 6.0% of highpressure patients, we used a pressure within the low-pressure range and in 4.5% of low-pressure patients, a pressure within the high-pressure range. Early 30-Day Outcome There were no cases of coronary artery perforation in either group. Table 4 indicates the number of patients with untoward events within the first 30 days after the procedure and the respective relative risk associated with high-pressure inflation. During this period, there was a higher incidence of non Q-wave myocardial infarction (CK or CK-MB elevation 3 times normal) in the group of high balloon pressure, 6.4%, versus 3.4% in the low-pressure group; relative risk 1.87; 95% CI 1.02 to Figure 2 shows the incidence of myocardial infarction defined according to the criteria applied in the EPISTENT trial. 8 TABLE 4. Adverse Events Recorded During the Early 30 Days Relative Risk Stent occlusion 8 (1.7) 9 (1.9) 0.89 [ ] Death 2 (0.4) 4 (0.9) 0.50 [ ] Nonfatal Q-wave 4 (0.9) 2 (0.4) 2.00 [ ] myocardial infarction CABG 1 (0.2) 1 (0.2) 1.00 [ ] Repeat PTCA 9 (1.9) 11 (2.4) 0.81 [ ] Any clinical event 13 (2.8) 14 (3.0) 0.92 [ ] Data are number of patients (%).

4 Dirschinger et al High- vs Low-Pressure Coronary Stenting 921 TABLE 6. Results of the 1-Year Survival Analysis Figure 2. Bar graph presenting, for both study groups, 30-day incidence of myocardial infarction (MI) defined according to criteria used in EPISTENT trial. 8 Angiographic Follow-Up and 1-Year Clinical Outcome Patients without adverse events within the first 30 days after the procedure were considered eligible for a 6-month angiographic control. It was carried out in 372 (83.0%) of the eligible patients in the high-pressure group and 370 (82.2%) of the eligible patients in the low-pressure group. The results of the quantitative assessment of the follow-up angiogram are presented in Table 5. The incidence of restenosis was 30.4% in the high-pressure group and 31.4% in the low-pressure group, and the relative risk associated with high-pressure inflation was 0.97 (95% CI 0.75 to 1.26). As shown in Table 6, our primary end point, event-free survival, was not significantly different between the 2 groups, with 78.8% in patients assigned to high-pressure dilatation and 75.5% in patients assigned to low-pressure dilatation, with a hazard ratio of 0.85 (0.65 to 1.11). Repeat PTCA was required in 77 patients (16.4%) of the high-pressure arm, compared with 78 patients (16.7%) in the low-pressure arm; relative risk of 0.98 (0.72 to 1.35). Primary end-point analysis performed in different subgroups defined by the stent model used, the presence of complex or calcified lesions, or lesions located in small vessels did not show any significant influence of high-pressure dilatation (Table 7). Table 8 shows the main findings in subgroups defined by the random assignment and actual pressure used. For both study groups, the results achieved in patients in whom a pressure outside the assigned range was applied were not significantly different from those achieved in patients in whom a pressure within the limits specified by the protocol was used. TABLE 5. Results of the 6-Month Angiographic Follow-Up (n 372) (n 370) Relative Risk Diameter stenosis, % Late lumen loss, mm Loss index Incidence of restenosis [ ] Stenoses [ ] Total occlusions [ ] High Pressure Low Pressure Hazard Ratio* Overall survival [ ] Survival free of Q-wave [ ] myocardial infarction Survival free of Q-wave myocardial infarction and target lesion revascularization [ ] Data are percentages. *Hazard ratio indicates the risk for an adverse outcome associated with high-pressure inflation. Discussion This randomized study compared 2 strategies of balloon dilatation pressure during stent placement in native coronary vessels of 934 patients with coronary artery disease. It showed that systematic use of high pressure is not associated with any appreciable reduction in the incidence of stent thrombosis and restenosis. Most importantly, the rate of adverse clinical events during the 1 year after the intervention was comparable for both treatment strategies. High Balloon Pressure and Early Adverse Events The overall incidence of stent thrombosis within the first 30 days after the procedure was 1.8% in the present study. This is in the range of stent thrombosis rate reported for patients treated with combined antiplatelet agents after stenting. 4,5,15,16 We could not show any significant difference in the incidence of this complication between high- and low-pressure inflation, but we should also take into account that this study was not sufficiently powered for the analysis of the secondary end point of stent thrombosis. Earlier observational studies reported a low incidence of stent thrombosis with high-pressure inflation and dual antiplatelet therapy with ticlopidine plus aspirin. 5,16 More recently, 2 randomized trials demonstrated the independent preventive effect of ticlopidine plus aspirin against stent thrombosis. 9,10 This therapy was particularly beneficial in patients with high risk for stent thrombosis. 17 TABLE 7. Risk for an Adverse 1-Year Outcome (Death, Q-Wave Myocardial Infarction or Target Vessel Revascularization) Associated With High-Pressure Inflation in Different Subgroups Hazard Ratio Patients with Inflow stent 0.89 [ ] Patients with Multi-Link stent 1.16 [ ] Patients with NIR stent 1.00 [ ] Patients with Plamaz-Schatz stent 0.84 [ ] Patients with Pura-A stent 0.70 [ ] Patients with ACC/AHA type B2/C lesions 0.79 [ ] Patients with calcified lesions 1.25 [ ] Patients with stents in vessels 0.78 [ ] 2.8 mm ACC/AHA indicates American College of Cardiology/American Heart Association.

5 922 Circulation August 31, 1999 TABLE 8. Main Findings in Subgroups Defined by the Random Assignment and Actual Pressure Used atm (n 420) 15 atm (n 48) 8 13 atm (n 421) 13 atm (n 45) Actual balloon pressure, atm Stent occlusion Incidence of restenosis Survival free of myocardial infarction and target lesion revascularization The rates of early clinical events such as death, Q-wave myocardial infarction, and reintervention were also comparable between the 2 groups with different pressure inflation strategies. Another important finding of this study is the higher incidence of CK elevation after stenting with highpressure inflation, which may be of concern considering the most recent data about its clinical significance. 18 Our results, however, should not be interpreted as contradicting a positive role conceived for optimal stent expansion. Bermejo et al 19 recently demonstrated with intravascular ultrasound investigation that despite high-pressure deployment, lumen dimensions after stenting are only 57% of the maximum achievable because of inadequate balloon expansion and elastic recoil. These issues were not the focus of the present study, and it remains to be demonstrated which is the best strategy to achieve an optimal stent expansion. High Balloon Pressure and Restenosis Final lumen achieved after stenting is one of the most powerful predictors of restenosis at follow-up. 20 Highpressure inflation is expected to afford a better lumen at the end of the intervention. In fact, a slight yet significant difference in residual stenosis was verified in the present study in favor of the high-pressure strategy. Conversely, the use of high balloon pressure may engender concerns about a potential exacerbation of the hyperplastic response from the injured vessel wall. The present randomized trial demonstrated that restenosis after coronary stent placement is not a function of the balloon pressure strategy used. All angiographic and clinical indexes of restenosis were comparable between the high- and low-pressure arms. Conversely, our findings did not justify the concerns that this approach may serve as a stimulus for excessive neointimal hyperplasia after stenting. Limitations of the Study Studies that assess the role of various pressure inflation strategies during coronary stent placement suffer from the lack of a clear-cut definition of high pressure. The pressure used in the high-pressure arm of the present study complies well with the values applied by the team that proposed this strategy for the first time 4,5 and also corresponds to the recent recommendations of the American College of Cardiology Expert Consensus Document. 6 Similarly, there is no clear definition of low pressure. In their initial experience, Schatz et al used pressure ranges of 6 to 10 atm 21 or 9 to 12 atm. 22 Our average inflation pressure of 11.1 atm in the low-pressure group is also comparable to that of 10 8 atm used in the BENESTENT trial 1 before the advent of high-pressure strategy. Even with minimally compliant balloons, balloon size and consequently balloon-to-vessel ratio are not completely independent from the inflation pressure. If both pressure and balloon-to-vessel ratio vary concomitantly, it may be difficult to estimate the independent role of inflation pressure. The results presented here should not be extrapolated to procedures in which the combination of high-pressure inflation with compliant balloons may significantly increase the balloon-to-vessel ratio. Our primary goal was to keep a comparable balloon-to-vessel ratio between the 2 groups and to test the independent role of inflation pressure. Appropriately designed studies are required to evaluate which is the best balloon-to-vessel ratio to be used during coronary stent deployment to achieve an optimal result. Another limitation of the study is that not all patients have been treated with an inflation pressure within the assigned range. However, the deviation from the predefined range was mostly minimal, and only 6.0% of the high-pressure patients and 4.5% of low-pressure patients crossed over to the opposite inflation pressure range. These data also indicate that a unique inflation pressure strategy may not be applied for all kinds of lesions. Conclusions The systematic use of high-pressure inflation during coronary stent placement is not associated with any significant influence on the 1-year outcome of patients undergoing this intervention. Depending on lesion characteristics, the operator may take advantage of a wider range of balloon inflation pressures that may be used to achieve optimal results. References 1. Serruys PW, de Jaegere P, Kiemeneij F, Macaya C, Rutsch W, Heyndrickx G, Emanuelsson H, Marco J, Legrand V, Materne P, Belardi J, Sigwart U, Colombo A, Goy JJ, van den Heuvel P, Delcan J, Morel MA. A comparison of balloon-expandable-stent implantation with

6 Dirschinger et al High- vs Low-Pressure Coronary Stenting 923 balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994;331: Fischman DL, Leon MB, Baim DS, Schatz RA, Savage MP, Penn I, Detre K, Veltri L, Ricci D, Nobuyoshi M, Cleman M, Heuser R, Almond D, Teirstein PS, Fish RD, Colombo A, Brinker J, Moses J, Shaknovich A, Hirshfeld J, Bailey S, Ellis S, Rake R, Goldberg S. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331: Serruys PW, Di Mario C. Who was thrombogenic: the stent or the doctor? Circulation. 1995;91: Colombo A, Hall P, Nakamura S, Almagor Y, Maiello L, Martini G, Gaglione A, Goldberg SL, Tobis JM. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation. 1995;91: Nakamura S, Hall P, Gaglione A, Tiecco F, Di Maggio M, Maiello L, Martini G, Colombo A. High pressure assisted coronary stent implantation accomplished without intravascular ultrasound guidance and subsequent anticoagulation. J Am Coll Cardiol. 1997;29: Holmes DR Jr, Hirshfeld J Jr, Faxon D, Vlietstra RE, Jacobs A, King SB III. ACC Expert Consensus document on coronary artery stents. Document of the American College of Cardiology. J Am Coll Cardiol. 1998;32: Neumann FJ, Gawaz M, Ott I, May A, Mössmer G, Schömig A. Prospective evaluation of hemostatic predictors of subacute stent thrombosis after coronary Palmaz-Schatz stenting. J Am Coll Cardiol. 1996;27: The EPISTENT Investigators. Randomized placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-iib/iiia blockade. Lancet. 1998;352: Schömig A, Neumann FJ, Kastrati A, Schühlen H, Blasini R, Hadamitzky M, Walter H, Zitzmann-Roth E, Richardt G, Alt E, Schmitt C, Ulm K. A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronary artery stents. N Engl J Med. 1996;334: Leon MB, Baim DS, Popma JJ, Gordon PC, Cutlip DE, Ho KKL, Giambartolomei A, Diver DJ, Lasorda DM, Williams DO, Pocock SJ, Kuntz RE. A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. N Engl J Med. 1998;339: Kuntz RE, Gibson CM, Nobuyoshi M, Baim DS. Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. J Am Coll Cardiol. 1993;21: Liu MW, Roubin GS, King SB III. Restenosis after coronary angioplasty: potential biologic determinants and role of intimal hyperplasia. Circulation. 1989;79: Ellis SG, Vandormael MG, Cowley MJ, DiSciascio G, Deligonul U, Topol EJ, Bulle TM. Coronary morphologic and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease: implications for patient selection. Circulation. 1990;82: Joint International Society and Federation of Cardiology/World Health Organization Task Force on Standardization of Clinical Nomenclature. Nomenclature and criteria for diagnosis of ischemic heart disease. Circulation. 1979;59: Karrillon GJ, Morice MC, Benveniste E, Bunouf P, Aubry P, Cattan S, Chevalier B, Commeau P, Cribier A, Eiferman C, Grollier G, Guerin Y, Henry M, Lefevre T, Livarek B, Louvard Y, Marco J, Makowski S, Monassier JP, Pernes JM, Rioux P, Spaulding C, Zemour G. Intracoronary stent implantation without ultrasound guidance and with replacement of conventional anticoagulation by antiplatelet therapy: 30 day clinical outcome of the French Multicenter Registry. Circulation. 1996;94: Albiero R, Hall P, Itoh A, Blengino S, Nakamura S, Martini G, Ferraro M, Colombo A. Results of a consecutive series of patients receiving only antiplatelet therapy after optimized stent implantation: comparison of aspirin alone versus combined ticlopidine and aspirin therapy. Circulation. 1997;95: Schühlen H, Hadamitzky M, Walter H, Ulm K, Schömig A. Major benefit from antiplatelet therapy for patients at high risk for adverse cardiac events after coronary Palmaz-Schatz stent placement: analysis of a prospective risk stratification protocol in the ISAR trial. Circulation. 1997; 95: Califf RM, Abdelmeguid AE, Kuntz RE, Popma JJ, Davidson CJ, Cohen EA, Kleiman NS, Mahaffey KW, Topol EJ, Pepine CJ, Lipicky RJ, Granger CB, Harrington RA, Tardiff BE, Crenshaw BS, Bauman RP, Zuckerman BD, Chaitman BR, Bittl JA, Ohman EM. Myonecrosis after revascularization procedures. J Am Coll Cardiol. 1998;31: Bermejo J, Botas J, Garcia E, Elizaga J, Osende J, Soriano J, Abeytua M, Delcan JL. Mechanisms of residual lumen stenosis after high-pressure stent implantation: a quantitative coronary angiography and intravascular ultrasound study. Circulation. 1998;98: Kastrati A, Schömig A, Elezi S, Schühlen H, Dirschinger J, Hadamitzky H, Wehinger A, Hausleiter J, Walter H, Neumann FJ. Predictive factors of restenosis after coronary stent placement. J Am Coll Cardiol. 1997; 30: Schatz RA, Baim DS, Leon M, Ellis SG, Goldberg S, Hirshfeld JW, Cleman MW, Cabin HS, Walker C, Stagg J, Buchbinder M, Teirstein PS, Topol EJ, Whitworth H, Sousa JE, Tio F, Almagor Y, Ponder R, Penn IM, Leonard B, Levine SL, Fish RD, Palmaz JC. Clinical experience with the Palmaz-Schatz coronary stent: initial results of a multicenter study. Circulation. 1991;83: Haude M, Erbel R, Straub U, Dietz U, Schatz R, Meyer J. Koronare Gefäßstützenimplantation bei Patienten mit symptomatischen Dissektionen nach Ballondilatation. Z Kardiol. 1990;79: