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Long-term outcome after coronary stenting
Trials volume 1, Article number: 48 (2000)
The present review assesses the data on long-term outcome after coronary stenting. Histological, angiographical and intravascular imaging data have shown that the insertion of stents constitutes only a transient stimulus to lumen renarrowing, that this process is almost complete at 6 months and that a certain degree of neointima regression is also possible after this time. Clinical data have confirmed the sustained benefit of stenting in the long term. Careful selection of optimal stent designs and application of the recent advances in adjunctive pharmacological therapy are currently effective strategies to improve both short-and long-term results with coronary stenting. However, further efforts are needed and are ongoing to combat restenosis, a process that counters the excellent short-term results of stenting in the long term.
Since the introduction of percutaneous transluminal coronary angioplasty (PTCA), the first use of coronary stenting in clinical practice in 1986  was the major breakthrough in the treatment of patients with coronary artery disease. Coronary stenting was introduced to combat two limitations of conventional PTCA: acute vessel closure and late lumen renarrowing. Now, after 15 years of continuous refinement, stenting has become the dominant percutaneous coronary intervention. Over these years, stent designs, stent delivery systems, stent deployment techniques and adjunctive antithrombotic therapy have all changed dramatically .
The earliest concern with the use of stenting was its thrombogenicity and potential for disastrous early severe thrombotic complications . Potent anticoagulation therapy with prolonged heparin administration followed by coumarin derivatives only amplified the risk of bleeding complications, without resolving the problem of stent thrombosis . Considerable efforts were then focused on understanding the principal mechanisms of stent thrombosis , on technical refinements aimed at improving the immediate lumen gain through high-pressure inflation under the guidance of intravascular ultrasound , and on the search for more effective antithrombotic therapies .
The ISAR (Intracoronary Stenting and Antithrombotic Regimen) trial in 1996  and the other trials that followed in 1998 [9,10] definitively established the role of the combined antiplatelet therapy (ticlopidine plus aspirin) in minimizing the risk of stent thrombosis. The favourable results achieved more recently with newer antiplatelet agents such as glycoprotein IIb/IIIa inhibitors  further strengthened the value of the pharmacological approach in the prevention of thrombotic events after stenting. The trials mentioned above were critical in defining stent placement protocols and in guiding future efforts in this field; this became even more apparent after the demonstrated failure of high-pressure deployment to favourably impact on the risk of thrombosis and restenosis after stenting .
Several randomized trials have examined the value of coronary stenting in various subsets of lesions and patients. For selected lesions situated in native coronary vessels with a diameter of 3 mm or more, the BENESTENT (Belgium-Netherland Stent)  and STRESS (Stent Restenosis Study)  trials demonstrated a significant reduction in angiographic restenosis and need for target vessel revascularization (TVR) achieved with stenting compared with PTCA. Stenting also proved superior to PTCA for lesions in coronary bypass grafts, as shown by the significant reduction in incidence of adverse clinical events at 8 months and the trend toward a lower rate of angiographic restenosis . However, these advantages of stenting could not be reproduced for lesions in smaller native vessels .
When compared with primary PTCA, primary stenting in acute myocardial infarction (AMI) was associated with decreased restenosis and need for TVR, but without any benefit in hard end-points such as death or reinfarction . In contrast, optimizing the adjunctive antithrombotic therapy with the addition of glycoprotein IIb/IIIa blockade (abciximab) enabled greater myocardial salvage and better clinical outcome with stenting than with thrombolysis in patients with AMI . However, the present review does not discuss the results of primary stenting in AMI due to the paucity of long-term data.
There is no doubt about the excellent acute and good mid-term results achieved with stenting. This is the reason why this treatment option is used so frequently, even for indications that have not been proven by properly designed randomized trials. However, there are doubts regarding the long-term advantages of this intervention. The introduction of a new treatment strategy often raises the question of long-term results. This question is even more important in the case of stenting. Stenting consists of the permanent implantation of a foreign body, with the potential of adverse effects in the long term through the lasting interaction with the vessel wall and the chronic strain imposed on that structure. On the other extreme of concerns regarding this treatment, stents might collapse with time, thereby abrogating the initial benefit. The 15 years of experience with this treatment and the plethora of data from histopathological, angiographical, intravascular imaging and clinical studies have enabled a more realistic perspective about the long-term efficacy of coronary stenting.
The pathobiological responses of the vessel wall to stent insertion have been characterized by numerous animal studies and fewer human investigations that used stented vessels obtained at autopsy, stented vein grafts excised at surgery and vessel wall tissue specimens retrieved with atherectomy. The response of the vessel wall to stenting is qualitatively characterized by the typical features of a response to injury. Stent-induced injury triggers a sequence of events that may be categorized as thrombosis, inflammation and proliferation . Stents provoke a higher degree of injury than does balloon dilatation alone, and this is followed by mural deposition of platelet-rich thrombi, which occurs within the first few days  and is demonstrable until 30 days after the intervention . Another important response to stent-induced injury is the inflammatory reaction, as demonstrated by the accumulation at the injury site of acute inflammatory cells (neutrophils) during the first 30 days and chronic inflammatory cells (lymphocytes and macrophages) thereafter . The degree of the inflammatory reaction correlates with the degree of injury, and both thrombosis and inflammation are also dependent on the stent design used .
The higher degree of injury, thrombosis and inflammation observed after stenting is associated with more extensive neointima formation than after plain PTCA . Restenotic tissue from patients after stenting is richer in smooth muscle cells and is poorer in collagen than restenotic tissue from patients after PTCA . Also, neointima presents more apoptosis after stenting than after PTCA . Both inhibition of smooth muscle cell proliferation and/or enhancement of apoptosis are logical targets of strategies for prevention of restenosis. Finally, remodelling, which is the principal mechanism of restenosis after PTCA, plays almost no role at all in in-stent restenosis .
Although the differences in the magnitude of the components of restenosis between stenting and PTCA have been well described, an accurate characterization of the time course of the restenotic processes that occur after these interventions is still lacking. The data available from separate pathological studies suggest that the healing process after stenting does not take much longer than that after PTCA. Full re-endothelialization and stability of the neointima overlying the stent seem to be achieved by 12 weeks after stenting, on the basis of autopsy studies in humans . Therefore, the histopathological data do not provide reasons to believe that the documented advantages of stenting over PTCA will be eliminated in the long run.
Angiographic and intravascular imaging data
Although stenting reduces the incidence of angiographic restenosis by 25-30% in comparison with PTCA [13,14], restenosis remains the major drawback for this intervention also. Restenosis mostly affects particular subsets of patients , and baseline conventional clinical, lesion-related and procedure-related variables may only partly explain the risk for this complication . A significant part of this risk appears to be related to known or as yet unknown genetic factors .
Intravascular ultrasound investigations  have confirmed neointima formation and remodelling as the major contributors to restenosis after stenting and PTCA, respectively. The temporal pattern of luminal changes appears to be similar within the first 6 months after stenting and PTCA . Most of the lumen renarrowing takes place within the first 3 months after stenting, with virtually no change occurring between 6 and 12 months; the incidence of restenosis was 22% after 3 months, 32% after 6 months, and remained essentially constant at 33% by 1 year . More importantly, the minimal lumen at the stented site initially was surprisingly enlarged during the interval between 1 and 3 years after the procedure . In fact, serial angioscopy in patients after stenting has shown that thinning of neointima occurs after 6 months . The mechanism that may lead to altered expression of genes that interfere with apoptosis in the neointima tissue remains to be investigated. If confirmed, these findings may also have important implications regarding how asymptomatic patients with in-stent restenosis should be managed.
Routine angiographic follow up is believed by some to increase the risk of 'oculostenotic reflex', which increases the number of reinterventions. The number of reinterventions was twice as high among stent patients who were subrandomized to angiographic restudy than among those assigned only clinical follow up in the BENESTENT II trial . On the other hand, PTCA patients with systematic angiographic follow up at 6 months had a higher rate of reinterventions, but a lower mortality at 10 years after the procedure than did their counterparts without angiographic restudy at 6 months .
Table 1 shows the clinical results at 1 year that were reported by the major randomized trials that compared stenting with conventional PTCA or coronary artery bypass grafting (CABG). Where data are available, the incidence of angiographic restenosis at 6 months is also shown. The BENESTENT [13,37], BENESTENT II  and STRESS [14,38] trials included selected subsets of patients and lesions. The ARTS (Arterial Revascularization Therapy Study)  enrolled patients with multivessel interventions. The device used was the Palmaz-Schatz stent (Cordis, a Johnson & Johnson Company, Warren, NJ, USA) in the BENESTENT, STRESS and EPISTENT (Evaluation of Platelet IIb/IIIa Inhibitor for Stenting)  trials, the heparin-coated Palmaz-Schatz stent in the BENESTENT II trial, and Crown (Cordis) or CrossFlex (Cordis) stent in the ARTS trial. As adjunctive pharmacological therapy to stenting, full anticoagulation was used in the BENSTENT and STRESS trials, and aspirin plus ticlopidine in the BENESTENT II, EPISTENT and ARTS trials. In addition, glycoprotein IIb/IIIa inhibition with abciximab was given periprocedurally in the EPISTENT trial.
As shown in Table 1, stenting is associated with a relative reduction of 20-30% in the cumulative 1-year incidence of adverse clinical events when compared with PTCA. This is exclusively the result of the reduced need for reinterventions. On the other hand, the ARTS trial showed that multivessel stenting may achieve similar clinical results at 1 year to those of CABG in terms of hard endpoints, such as mortality and myocardial infarction, at the cost of more frequent need for reinterventions, mostly percutaneous coronary interventions. However, when the ARTS results are interpreted in the context of the previous trials that compared PTCA with CABG, multivessel stenting seems to reduce the difference in the incidence of adverse clinical events between the surgical and the percutaneous approaches.
In addition to the experimental evidence, there are now sufficient clinical data to support the independent role of stent type in the long-term results achieved with stenting. In a randomized comparison of five stent types , 1-year event-free survival varied from 69.4 to 78.9% (P <0.02) depending on the stent design used. These findings show the potential of stent technologies to improve the long-term outcome of patients treated with this technique.
For several years, the use of stents remained limited and mostly confined to bail-out situations or coronary bypass grafts. Following reports of advantages of stenting over PTCA and the radical improvement in antithrombotic therapy, there has been a great increase in the use of stents during the past 5 years. This explains why studies with follow-up periods longer than 1 year usually include a limited number of patients. Several factors should be considered that can have a profound influence on the long-term clinical findings. The results with coronary stenting are dependent on the characteristics of patients included , on the antithrombotic regimen used as an adjunct to stenting [8,10,11], and on the particular stent design implanted [40,41]. Long-term outcome after stenting also reflects the progression of coronary atherosclerosis, prevention of which should represent the primary focus of the management of these patients.
A summary of the long-term results reported by studies with a follow-up period of at least 24 months is presented in Table 2. The risk profile of the patients included in these studies is considerably different, with only selected lesions in native vessels for some studies [13,14,33] and bail-out situations in others [4,42]. The Palmaz-Schatz stent was used in most of the studies [4,33,43,44,45,46]. Eeckhout et al  used the Wallstent (Boston Scientific Corp, Natick, MA, USA) and van Domburg et al  use different stents, including the Wallstent. Except for the study of van Domburg et al , all of the other studies applied full anticoagulation as the poststenting regimen.
Two studies reported on the long-term results of randomized comparisons between stent and PTCA. At 5 years, BENESTENT investigators  reported a 34.5% rate of adverse events after stenting, and a 40.2% rate after PTCA, which represents a nonsignificant relative reduction of 14%. This was exclusively due to a significant reduction of 37% in the need for repeat PTCA (17.3% in the stent and 27.6% in the PTCA arm). Similar results were reported by the other randomized trial, conducted by Betriu et al . The incidence of adverse events at 4 years decreased significantly from 29.9% after PTCA to 16.9% after stenting, mostly because of the reduction in the rate of repeat PTCA from 22.3% to 10.7%.
In the retrospective study of van Domburg et al , a comparative analysis between the subgroup treated with anticoagulation therapy and that treated with antiplatelet agents was performed at 2 years after stenting. Interestingly, the advantages of antiplatelet therapy in terms of reduced risk of myocardial infarction and need for repeat interventions were maintained over the entire follow-up period. The concept that even short-term antithrombotic therapy is able to achieve a long-term benefit is best illustrated by the EPISTENT  results: adding abciximab to the periprocedural therapy was associated with a significant 57% reduction in 1-year mortality (1.0% in stent plus abciximab versus 2.3% in stent plus placebo). It is readily conceivable that this is the result of the drastic reduction in the rate of postprocedural myocardial infarction observed with abciximab. These findings indicate another source of improvement of long-term results after stenting, namely further optimization of the adjunctive pharmacological therapy.
In-stent restenosis poses a major threat to long-term outcome after stenting; it may be focal or diffuse . Particularly when diffuse, in-stent restenosis is a real management challenge for interventional cardiologists because of its high recurrence rate. Various forms of percutaneous coronary intervention, including plain PTCA, repeat stenting, directional and rotational atherectomy, and excimer laser angioplasty, have been used to treat in-stent restenosis. Considering that lumen encroachment in the stented site is the consequence of an exuberant neointimal tissue growth, debulking techniques appear to be attractive strategies for treating this complication. Contrary to expectations, however, rotational atherectomy, followed by low-pressure balloon dilatation proved to be inferior to plain PTCA in the ARTIST (Angioplasty versus Rotation for the Treatment of In-Stent Stenosis/Occlusion) randomized trial .
The experience to date indicates that several strategies designed to prevent restenosis have yielded disappointing results, but brachytherapy may have promise. In a small series of 55 patients with a particularly high risk for restenosis who were randomly assigned to either intra-coronary γ-radiation or placebo therapy during the intervention , there was a significant reduction in the need for reintervention at 3 years, from 48.3 to 15.4%. Encouraging results in reducing the recurrence of in-stent restenosis were also reported with the use of intracoronary β-radiation . Intensive work is being done in this field and results from large clinical trials are still pending.
Coronary stenting is increasingly being used because of the excellent short-term results, the ability to prevent abrupt vessel closure that may occur after plain PTCA, and the reduced risk of restenosis that has been demonstrated for a number of indications. Histologic, angiographic and intravascular imaging data have evidenced the different mechanisms of restenosis between stenting and PTCA. They have also shown that the insertion of stents constitutes only a transient stimulus to lumen renarrowing, that this process is almost complete at 6 months, and that a certain degree of neointima regression is also possible after this time. Clinical data have confirmed the sustained benefit of stenting in the long term. Careful selection of optimal stent designs and application of the recent advances in adjunctive pharmacological therapy are currently effective strategies to improve both short-term and long-term results with coronary stenting. However, further efforts are needed and are on-going to combat restenosis, a process that counters the excellent short-term results of stenting in the long term.
Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L: Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med. 1987, 316: 701-706.
Schömig A, Kastrati A: Long lesions, long stents and the long process of stent optimization [editorial]. J Am Coll Cardiol. 1999, 34: 660-662. 10.1016/S0735-1097(99)00302-2.
Serruys PW, Strauss BH, Beatt KJ, Bertrand ME, Puel J, Rickards AF, Meier B, Goy JJ, Vogt P, Kappenberger L, Sigwart U: Angiographic follow-up after placement of a self-expanding coronary-artery stent. N Engl J Med. 1991, 324: 13-17.
Schömig A, Kastrati A, Mudra H, Blasini R, Schühlen H, Klauss V, Richardt G, Neumann FJ: Four-year experience with Palmaz-Schatz stenting in coronary angioplasty complicated by dissection with threatened or present vessel closure. Circulation. 1994, 90: 2716-2724.
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: 15-21. 10.1016/0735-1097(95)00433-5.
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: 1676-1688.
Gawaz M, Neumann FJ, Ott I, May A, Schömig A: Platelet activation and coronary stent implantation: effect of antithrombotic therapy. Circulation. 1996, 94: 279-285.
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: 1084-1089. 10.1056/NEJM199604253341702.
Urban P, Macaya C, Rupprecht HJ, Kiemeneij F, Emanuelsson H, Fontanelli A, Pieper M, Wesseling T, Sagnard L: Randomized evaluation of anticoagulation versus antiplatelet therapy after coronary stent implantation in high-risk patients: the multicenter aspirin and ticlopidine trial after intracoronary stenting (MATTIS). Circulation. 1998, 98: 2126-2132.
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: 1665-1671. 10.1056/NEJM199812033392303.
Topol EJ, Mark DB, Lincoff AM, Cohen E, Burton J, Kleiman N, Talley D, Sapp S, Booth J, Cabot CF, Anderson KM, Califf RM: Outcomes at 1 year and economic implications of platelet glycoprotein IIb/IIIa blockade in patients undergoing coronary stenting: results from a multicentre randomised trial. EPISTENT Investigators. Evaluation of Platelet IIb/IIIa Inhibitor for Stenting. Lancet. 1999, 354: 2019-2024. 10.1016/S0140-6736(99)10018-7.
Dirschinger J, Kastrati A, Neumann FJ, Boekstegers P, Elezi S, Mehilli J, Schühlen H, Pache J, Alt E, Blasini R, Steinbeck G, Schömig A: 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. Circulation . 1999, 100: 918-923.
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 balloon angioplasty in patients with coronary artery disease. N Engl J Med. 1994, 331: 489-495. 10.1056/NEJM199408253310801.
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, Sha-knovich 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: 496-501. 10.1056/NEJM199408253310802.
Savage MP, Douglas JS, Fischman DL, Pepine CJ, King SB, Werner JA, Bailey SR, Overlie PA, Fenton SH, Brinker JA, Leon MB, Goldberg S: Stent placement compared with balloon angioplasty for obstructed coronary bypass grafts. N Engl J Med. 1997, 337: 740-747. 10.1056/NEJM199709113371103.
Kastrati A, Schömig A, Dirschinger J, Mehilli J, Dotzer F, von Welser N, Neumann FJ: A randomized trial comparing stenting with balloon angioplasty in small vessels in patients with symptomatic coronary artery disease. Circulation.
Grines CL, Cox DA, Stone GW, Garcia E, Mattos LA, Giambartolomei A, Brodie BR, Madonna O, Eijgelshoven M, Lansky AJ, WW ON, Morice MC: Coronary angioplasty with or without stent implantation for acute myocardial infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group. N Engl J Med. 1999, 341: 1949-1956. 10.1056/NEJM199912233412601.
Schömig A, Kastrati A, Dirschinger H, Mehilli J, Schricke U, Pache J, Martinoff S, Neumann FJ, Schwaiger M: A randomized trial comparing primary stenting plus glycoprotein IIb/IIIa blockade with tissue plasminogen activator for myocardial salvage in acute myocardial infarction. N Engl J Med.
Edelman ER, Rogers C: Pathobiologic responses to stenting. Am J Cardiol. 1998, 81: 4E-6E. 10.1016/S0002-9149(98)00189-1.
Farb A, Sangiorgi G, Carter AJ, Walley VM, Edwards WD, Schwartz RS, Virmani R: Pathology of acute and chronic coronary stenting in humans. Circulation. 1999, 99: 44-52.
Komatsu R, Ueda M, Naruko T, Kojima A, Becker AE: Neointimal tissue response at sites of coronary stenting in humans: macroscopic, histological, and immunohistochemical analyses. Circulation. 1998, 98: 224-233.
Rogers C, Edelman ER: Endovascular stent design dictates experimental restenosis and thrombosis. Circulation. 1995, 91: 2995-3001.
Karas SP, Gravanis MB, Santoian EC, Robinson KA, Anderberg KA, King SA: Coronary intimal proliferation after balloon injury and stenting in swine: an animal model of restenosis. J Am Coll Cardiol . 1992, 20: 467-474.
Moreno PR, Palacios IF, Leon MN, Rhodes J, Fuster V, Fallon JT: Histopathologic comparison of human coronary in-stent and post-balloon angioplasty restenotic tissue. Am J Cardiol. 1999, 84: 462-466. 10.1016/S0002-9149(99)00334-3.
Kollum M, Kaiser S, Kinscherf R, Metz J, Kübler W, Hehrlein C: Apoptosis after stent implantation compared with balloon angioplasty in rabbits. Role of macrophages. Arterioscler Thromb Vasc Biol. 1997, 17: 2383-2388.
Grewe PH, Deneke T, Machraoui A, Barmeyer J, Muller KM: Acute and chronic tissue response to coronary stent implantation: pathologic findings in human specimen. J Am Coll Cardiol. 2000, 35: 157-163. 10.1016/S0735-1097(99)00486-6.
Schömig A, Kastrati A, Elezi S, Schühlen H, Dirschinger J, Dannegger F, Wilhelm M, Ulm K: Bimodal distribution of angiographic measures of restenosis six months after coronary stent placement. Circulation. 1997, 96: 3880-3887.
Kastrati A, Schömig A, Elezi S, Schühlen H, Wilhelm M, Dirschinger J: Interlesion dependence of the risk for restenosis in patients with coronary stent placement in multiple lesions. Circulation. 1998, 97: 2396-2401.
Kastrati A, Dirschinger J, Schomig A: Genetic risk factors and restenosis after percutaneous coronary interventions. Herz. 2000, 25: 34-46.
Mintz GS, Popma JJ, Hong MK, Pichard AD, Kent KM, Satler LF, Leon MB: Intravascular ultrasound to discern device-specific efects and mechanisms of restenosis. Am J Cardiol. 1996, 78(Suppl 3A): 18-22. 10.1016/S0002-9149(96)00493-6.
Kimura T, Nosaka H, Yokoi H, Iwabuchi M, Nobuyoshi M: Serial angiographic follow-up after Palmaz-Schatz stent implantation: comparison with conventional balloon angioplasty. J Am Coll Cardiol. 1993, 21: 1557-1563.
Kastrati A, Schömig A, Dietz R, Neumann FJ, Richardt G: Time course of restenosis during the first year after emergency coronary stenting. Circulation. 1993, 87: 1498-1505.
Kimura T, Yokoi H, Nakagawa Y, Tamura T, Kaburagi S, Sawada Y, Sato Y, Yokoi H, Hamasaki N, Nosaka H, Nobuyoshi M: Three-year follow-up after implantation of metallic coronary-artery stents. N Engl J Med. 1996, 334: 561-566. 10.1056/NEJM199602293340903.
Asakura M, Ueda Y, Nanto S, Hirayama A, Adachi T, Kitakaze M, Hori M, Kodama K: Remodeling of in-stent neointima, which became thinner and transparent over 3 years: serial angiographic and angioscopic follow-up. Circulation. 1998, 97: 2003-2006.
Serruys PW, van Hout B, Bonnier H, Legrand V, Garcia E, Macaya C, Sousa E, van der Giessen W, Colombo A, Seabra-Gomes R, Kiemeneij F, Ruygrok P, Ormiston J, Emanuelsson H, Fajadet J, Haude M, Klugmann S, Morel MA: Randomised comparison of implantation of heparin-coated stents with balloon angioplasty in selected patients with coronary artery disease (Benestent II). Lancet. 1998, 352: 673-681. 10.1016/S0140-6736(97)11128-X.
Rupprecht HJ, Espinola-Klein C, Erbel R, Nafe B, Brennecke R, Dietz U, Meyer J: Impact of routine angiographic follow-up after angioplasty. Am Heart J. 1998, 136: 613-619.
Macaya C, Serruys PW, Ruygrok P, Suryapranata H, Mast G, Klug-mann S, Urban P, den Heijer P, Koch K, Simon R, Morice MC, Crean P, Bonnier H, Wijns W, Danchin N, Bourdonnec C, Morel MA: Continued benefit of coronary stenting versus balloon angioplasty: one-year clinical follow-up of Benestent trial. Benestent Study Group. J Am Coll Cardiol. 1996, 27: 255-261. 10.1016/0735-1097(95)00473-4.
George CJ, Baim DS, Brinker JA, Fischman DL, Goldberg S, Holubkov R, Kennard ED, Veltri L, Detre KM: One-year follow-up of the Stent Restenosis (STRESS I) Study. Am J Cardiol. 1998, 81: 860-865. 10.1016/S0002-9149(98)00004-6.
Ferguson JJ: Meeting highlights. Highlights of the 21st Congress of the European Society of Cardiology. ARTS (Presented by P.Serruys). Circulation. 1999, 100: e126-e131.
Kastrati A, Dirschinger J, Boeckstegers P, Elezi S, Schühlen H, Pache J, Steinbeck G, Schmitt C, Ulm K, Neumann FJ, Schömig A: Influence of stent design on one-year outcome after coronary stent placement: a randomized comparison of 5 stent types in 1147 unselected patients. Cathet Cardiovasc Intervent. 2000, 50: 290-297. 10.1002/1522-726X(200007)50:3<290::AID-CCD5>3.0.CO;2-W.
Kastrati A, Schömig A, Dirschinger J, Mehilli J, von Welser N, Pache J, Schühlen H, Schilling T, Schmitt C, Neumann FJ: Increased risk of restenosis after placement of gold-coated stents. Results of a randomized trial comparing gold-coated with uncoated steel stents in patients with coronary artery disease. Circulation. 2000, 101: 2478-2483.
Eeckhout E, Goy JJ, Vogt P, Stauffer JC, Sigwart U, Kappenberger L: Complications and follow-up after intracoronary stenting: critical analysis of a 6-year single-center experience. Am Heart J. 1994, 127: 262-272.
Klugherz BD, DeAngelo DL, Kim BK, Herrmann HC, Hirshfeld JW, Kolansky DM: Three-year clinical follow-up after Palmaz-Schatz stenting. J Am Coll Cardiol. 1996, 27: 1185-1191. 10.1016/0735-1097(95)00574-9.
Laham RJ, Carrozza JP, Berger C, Cohen DJ, Kuntz RE, Baim DS: Long-term (4- to 6-year) outcome of Palmaz-Schatz stenting: paucity of late clinical stent-related problems. J Am Coll Cardiol. 1996, 28: 820-826. 10.1016/S0735-1097(96)00244-6.
Betriu A, Masotti M, Serra A, Alonso J, Fernandez-Aviles F, Gimeno F, Colman T, Zueco J, Delcan JL, Garcia E, Calabuig J: Randomized comparison of coronary stent implantation and balloon angioplasty in the treatment of de novo coronary artery lesions (START): a four-year follow-up. J Am Coll Cardiol. 1999, 34: 1498-1506. 10.1016/S0735-1097(99)00366-6.
The BENESTENT-I Study Group : Continued benefit of coronary stenting versus balloon angioplasty: five-year clinical follow-up of BENESTENT-I trial [abstract]. Circulation. 1999, 100(Suppl I): 1-233.
van Domburg RT, Foley DP, de Jaegere PP, de Feyter P, van den Brand M, van der Giessen W, Hamburger J, Serruys PW: Long term outcome after coronary stent implantation: a 10 year single centre experience of 1000 patients. Heart. 1999, 82(Suppl 2): 1127-1134.
Mehran R, Dangas G, Abizaid AS, Mintz GS, Lansky AJ, Satler LF, Pichard AD, Kent KM, Stone GW, Leon MB: Angiographic patterns of in-stent restenosis: classification and implications for long-term outcome. Circulation. 1999, 100: 1872-1878.
Ferguson JJ: Meeting highlights. Highlights of the 21st Congress of the European Society of Cardiology. ARTIST (Presented by J. vom Dahl). Circulation. 1999, 100: e126-e131.
Teirstein PS, Massullo V, Jani S, Popma JJ, Russo RJ, Schatz RA, Guarneri EM, Steuterman S, Sirkin K, Cloutier DA, Leon MB, Tripuraneni P: Three-year clinical and angiographic follow-up after intra-coronary radiation: results of a randomized clinical trial. Circulation. 2000, 101: 360-365.
Waksman R, Bhargava B, White L, Chan RC, Mehran R, Lansky AJ, Mintz GS, Satler LF, Pichard AD, Leon MB, Kent KK: Intracoronary beta-radiation therapy inhibits recurrence of in-stent restenosis. Circulation. 2000, 101: 1895-1898.
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Kastrati, A., Hall, D. & Schömig, A. Long-term outcome after coronary stenting. Trials 1, 48 (2000) doi:10.1186/cvm-1-1-048
- coronary artery disease
- long-term outcome