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Rapid Responses: Rapid Responses published:
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A little more about Drug Eluting Stents
- Russell W J Millner (19 December 2006)
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Heparin and glycoprotein IIb/IIIa antagonist-induced thrombocytopaenia increase bleeding and death in cardiac patients – platelets may not help
- Amit Patel (21 December 2006)
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Drug eluting stents: A wake up call?
- Kiran CR Patel (21 December 2006)
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Coronary stent thrombosis and oral antiplatelet “low responders” – should we be looking harder and treating harder?
- Andrew J Wiper, David H Roberts (26 December 2006)
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Risks of bleeding
- A G hameed (26 December 2006)
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Premature discontinuation of clopidogrel - the need for patient empowerment
- Sotiris Antoniou, Martin T Rothman, Professor of Interventional Cardiology, Barts and the London NHS Trust (1 January 2007)
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Antiplatelets alone won't do the job.
- Hans Van Brabandt (4 January 2007)
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We already have a problem
- Phil S Jones (8 January 2007)
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Stent Thrombosis: Fine Tuning Opinion
- Anthony H Gershlick, Gail Richardson, Consultant Cardiologist, University Hospitals of Leicester, LE3 9QP (2 February 2007)
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Russell W J Millner, Consultant cardiothoracic Surgeon Blackpool Victoria Hospital, Whinney Heys Road, Blackpool, FY3 8NR
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Editor Drs Gershlick and Richardson write an editorial in response to the outcome of the recent FDA panel convened to discuss issues raised about adverse outcomes after Drug Eluting Stenting (DES) insertion for coronary artery disease. It seems to me that the best the FDA could say is that DES are safe for licensed indications. Unfortunately they then pointed out that in the USA (and therefore in the UK??) about 60% of implants are outside the terms of the license. The authors make a point that DES are as safe as Bare Metal Stents (BMS) and that 75,000 procedures were performed in the UK against 25,000 CABG. I suspect that whilst there were very close to 25,000 patients treated with CABG, rather less than 75,000 patients were treated with stents! It is interesting to note than when a number of studies were produced recently, such as the S.O.S trial (which showed survival benefit for CABG over BMS out to 5 years) or the New York Registry data of 37,221 patients showing the benefit of CABG over stenting (N Engl J Med 2005;352:2174-83.) these studies were generally dismissed by the phrase "we've got Drug Eluting Stents now". Funny how the issue is now "are DES as safe as BMS?" and the obvious implication that they are not as safe therefore as coronary surgery is completely ignored. The New York registry data shows clear survival benefit for risk matched patients for CABG over stenting in every patient group. I simply quote the results section from the abstract: "Risk-adjusted survival rates were significantly higher among patients who underwent CABG than among those who received a stent in all of the anatomical subgroups studied. For example, the adjusted hazard ratio for the long-term risk of death after CABG relative to stent implantation was 0.64 (95 percent confidence interval, 0.56 to 0.74) for patients with three-vessel disease with involvement of the proximal left anterior descending coronary artery and 0.76 (95 percent confidence interval, 0.60 to 0.96) for patients with two-vessel disease with involvement of the nonproximal left anterior descending coronary artery. Also, the three-year rates of revascularization were considerably higher in the stenting group than in the CABG group (7.8 percent vs. 0.3 percent for subsequent CABG and 27.3 percent vs. 4.6 percent for subsequent PCI)." I do fully agree with the editorials authors that informed consent is paramount. When elective patients are consented, type of stent can not be the only discussion! The relative survival benefits of stenting against CABG must also be a part of the discussion, particularly if here in the UK we are replicating the American experience that 60% of stents are put in outside the terms of the licence, and into patients who would get a survival benefit with a strategy of surgery rather than stenting. Peter K. Smith, M.D., chief of thoracic surgery at Duke University when commenting on the discussions of the FDA panel is reported as quoting a figure based on the data from registries in thousands for the number of patients who have died in the US who would have survived if they had had CABG as their treatment.(http://www.medpagetoday.com/Cardiology/PCI/tb2/4668?pfc=101&spc=253) Let us hope that further analysis in the UK does not show the same sort of figures. Hopefully the rush of recent years to increase coronary re-vascularisation by any route to reduce the waiting times for CABG will not have had any unpleasant side effects. However, I do wonder whether it will ever be safe to stop clopidogrel in some of these patients, and I wonder what impact that will have on their lives in the future. Finally, I think it is entirely appropriate, indeed important that the BMJ has chosen this topic for an editorial. I am also pleased to see that the authors have disclosed competing interests: "AHG is on the advisory board and is an educational adviser and panel speaker for all drug eluting stent companies. GR is on the advisory board of Abbott Vascular." Competing interests: Cardiac Surgeon |
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Amit Patel, Academic Clinical Fellow & Specialist Registrar in Haematology The Hammersmith Hospitals NHS Trust, Charing Cross Hospital, London, W6 8RF, UK
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Gershlick[1] highlights the high morbidity and mortality of late drug eluting stent thrombosis, particularly associated with premature cessation of clopidogrel therapy to reduce the risk of bleeding from procedures. Glycoprotein (GP) IIb/IIIa antagonist use in cardiology patients, in combination with aspirin, clopidogrel and heparin, has increased markedly in the acute setting, particularly in those receiving percutaneous intervention (PCI). Adjusted registry data suggest that they increase the risk of bleeding at least twofold in these patients, particularly when combined with heparin.[2] Both heparin and GP IIb/IIIa antagonists can cause thrombocytopaenia and increase the risk of mucosal, gastrointestinal and intracranial bleeding. The reported incidence of thrombocytopaenia associated with GP IIb/IIIa antagonists varies depending on the agent and platelet definition used. However, its presence is associated with an increase in severe bleeding, a higher risk of recurrent myocardial infarction, a greater transfusion requirement, and an increased 30-day[3] and one-year risk of death.[4] Platelet transfusion with heparin-induced thrombocytopaenia (HIT) is contraindicated and markedly increases the risk of thrombosis. Conversion to a heparinoid with immune-modulatory therapy may improve the platelet count. Premature platelet transfusion with GP IIb/IIIa antagonist -induced thrombocytopaenia may also contribute to stent thrombosis. Combined aspirin and clopidogrel therapy alone increases the risk of adverse events from bleeding, including upper gastrointestinal.[5] However, continuation of clopidogrel maybe recommended in the latter if it occurs soon after PCI, with a high dose 72 hour proton pump inhibitor infusion, on a case by case basis in the context of non-variceal gastrointestinal bleeding, with appropriate maintenance of blood pressure using blood product and fluid support, in close consultation with a haematologist. [1] Gershlick AH, Richardson G. Drug eluting stents. BMJ 2006;333:1233-4. [2] Horwitz PA, Berlin JA, Sauer WH, Laskey WK, Krone RJ, Kimmel SE. Bleeding risk of platelet glycoprotein IIb/IIIa receptor antagonists in broad-based practice (results from the Society for Cardiac Angiography and Interventions Registry). Am J Cardiol 2003;91:803-6. [3] Merlini PA, Rossi M, Menozzi A, Buratti S, Brennan DM, Moliterno DJ, Topol EJ, Ardissino D. Thrombocytopenia caused by abciximab or tirofiban and its association with clinical outcome in patients undergoing coronary stenting. Circulation 2004;109:2203-6. [4] Scirica BM, Cannon CP, Cooper R, Aster RH, Brassard J, McCabe CH, Charlesworth A, Skene AM, Braunwald E. Drug-induced thrombocytopenia and thrombosis: Evidence from patients receiving an oral glycoprotein IIb/IIIa inhibitor in the Orbofiban in Patients with Unstable coronary Syndromes- (OPUS-TIMI 16) trial. J Thromb Thrombolysis 2006;22:95-102. [5] Jesper Hallas, Michael Dall, Alin Andries, Birthe Søgaard Andersen, Claus Aalykke, Jane Møller Hansen, Morten Andersen, Annmarie Touborg Lassen. Use of single and combined antithrombotic therapy and risk of serious upper gastrointestinal bleeding: population based case-control study. BMJ 2006;333:726-28. Competing interests: None declared |
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Kiran CR Patel, Consultant Cardiologist and Honorary Senior Lecturer Sandwell and West Birmingham NHS Trust
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Gershlick and Richardson (1) present a cogent argument for more appropriately guided trials in the field of interventional cardiology. Optimism bias has resulted in an explosion in the use of drug eluting stents outside of licensed indications, of which patients are often unaware. Whilst many of these uses are deemed reasonable within the fraternity, I suspect many cardiothoracic surgeons would argue to the contrary. There are clearly roles for both percutaneous coronary intervention and surgical coronary artery bypass grafting in management strategies for coronary artery disease, but until the fraternity either independently, or with the philanthropic qualities of industry behind it, undertakes to perform the requisite real world trials with long term follow up and generation of data on safety and outcomes (both morbidity and mortality), optimism bias within both cardiology and cardiac surgery will challenge the arrival of sensible strategies to coronary revascularisation by perpetuating polarised views. 1. Gershlick AH, Richardson G. Drug eluting stents. BMJ 2006;333:1233 -4. Competing interests: None declared |
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Andrew J Wiper, Cardiology Registrar Lancashire Cardiac Centre, Blackpool, David H Roberts
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Dear Sir, Drs Gershlick and Richardson [1] discussed the issue of coronary stent thrombosis. There appears to be an increased risk of stent thrombosis in patients treated with drug eluting stents when compared to bare metal stents, particularly when clopidogrel is stopped prematurely. The authors suggested that this increased risk may be attributable to prolonged exposure of the stent struts. We also suggest that stent thrombosis is partly attributable to clopidogrel and aspirin “low responders”, and that this patient subgroup should be identified pre percutaneous coronary intervention (PCI) and alternative oral antiplatelet strategies considered. It has been shown in multiple trials that between 5-40% of patients treated with clopidogrel display suboptimal inhibition of platelet aggregation (IPA), when evaluated ex vivo by optical aggregometry and flow cytometry. These patients are often deemed clopidogrel “low responders”. A similar phenomenon – aspirin “low responders” – is reported in 5-20% of cases. The latter group are more likely to be women and have diabetes mellitus and also have a reduced response to clopidogrel [2]. It would seem logical that patients categorised as clopidogrel or aspirin “low responders”, will have suboptimal levels of IPA in the ensuing months or years post PCI and thus be prone to an increased risk of stent thrombosis. Bed side platelet inhibition assays have been available for some time (eg VerifyNow P2Y12 assay, Accumetrics USA) and are able to identify aspirin and clopidogrel “low responders” prior to PCI. We suggest that these patients could be treated with increased oral antiplatelet loading and maintenance doses, although data concerning the efficacy of these strategies is limited. There are several other oral antiplatelet therapies ( eg prasugrel, AZD6140) which do not yet have a UK licence but have shown great promise specifically with a low incidence of pharmacodynamic “low responders” [3]. Data concerning these new antiplatelet strategies are long overdue. References 1) A H Gershlick, G Richardson. Drug eluting stents. BMJ 2006;333:1233-1234. 2) Lev EI, Patel RT, Maresh KJ, Guthikonda S et al. Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance. J Am Coll Cardiol. 2006 Jan 3;47(1):27-33. 3) Jernberg T, Payne CD, Winters KJ, Darstein C et al. Prasugrel achieves greater inhibition of platelet aggregation and a lower rate of non-responders compared with clopidogrel in aspirin-treated patients with stable coronary artery disease. Eur Heart J. 2006 May;27(10):1166-73. Competing interests: None declared |
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A G hameed, Locum Registrar in Cardiology Nottingham, UK
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Several benefits and concerns about DES's have been highlighted by Gershlick et Al. However in addition to late stent thrombosis, do the authors of the editorial have any data availble to to report the rates of Significant Bleeding (particularly Gastrointestinal ) associated with long term dual Antiplatelet therapy in their respected cardiac patients? Recent communtiy data highlight the higher risk of bleeding with dual aspirin/clopidogrel therapy OR 7.4 (3.5-15)[1] This may have implications for patients expected in making informed decisons about selecting the most appropriate treatment for their coronary disease. [1]Use of single and combined antithrombotic therapy and risk of serious upper gastrointestinal bleeding: population based case-control study BMJ, Oct 2006; 333: 726 ; doi:10.1136/bmj.38947.697558.AE Competing interests: none. |
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Sotiris Antoniou, Principal Pharmacist, Cardiac Services & Chair of Cardiac Committee, UKCPA Barts and the London NHS Trust, EC1A 7BE, Martin T Rothman, Professor of Interventional Cardiology, Barts and the London NHS Trust
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Dear Editor Drs Gershlik and Richardson write an editorial and discuss the FDA recommendation about drug eluting stents (DES). The authors point out that the greatest risk factor for stent thrombosis at any time is premature discontinuation of clopidogrel. The length of course of the combination therapy is dependent on numerous factors, including the pre- existing condition of the patient, procedure(s) undertaken and type of stent deployed. This information also needs to be communicated across the interface (primary and secondary sectors) to ensure continuation of therapy. There have been a number of initiatives aimed at improving communication at interface, but evidence suggests that there is still vast room for improvement[1]. Due to the importance of adequate duration of clopidogrel post DES, there is a need for patients to take ownership of their therapy, to prevent inappropriate abruption of therapy. The authors mention the use of warning cards that indicate the recommended length of clopidogrel therapy. The United Kingdom Clinical Pharmacy Association (UKCPA) has developed the Barts and the London clopidogrel card designed to be given to all patients receiving combination therapy following angioplasty. The aim of the card is to support ownership by the patient of their clopidogrel therapy, through facilitating education, communication. Thus use of the card is aimed at preventing admission to emergency centres with in-stent thrombosis following inappropriate discontinuation of anti- platelet therapy. The card informs the patient of the importance of dual therapy, and the reasons why clopidogrel has been initiated, daily dose, the combination with aspirin, together with the planned duration of treatment, and possible adverse effects. It also encourages the patient to show the card to any medical personnel and thereby offers important information regarding the clopidogrel and aspirin treatment to both patient and medical personnel, such that doctors and other para-medical personnel do not discontinue therapy without due consideration. The card offers encouragement for further discussion and liaison regarding their treatment with their GP, or with the hospital initiating therapy. We developed the card and have made arrangements for it to be available nationally to prevent local ‘re-invention of the wheel’ – in a way similar to the generic warfarin booklet. The card is freely available to all, and we would urge all centres performing angioplasties to consider issuing these, or similar cards, to patients. This card has been endorsed by the British Cardiovascular Society, and British Cardiac Intervention Society. Cards are available free of charge from UKCPA (tel: 0116 2776999 or via email: admin@ukcpa.com) References 1) Bellingham C. How to improve medicines management at the primary/secondary care interface. Pharm J, 2004; 272:210-211 Competing interests: None declared |
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Hans Van Brabandt, cardiologist B2800 Mechelen, Belgium
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Premature antiplatelet therapy discontinuation is a risk factor for stent thrombosis. In Iakovou’s series (1) DES-thrombosis occurred in 5 of 17 patients (29%) who prematurely discontinued dual antiplatelet therapy. One of them only discontinued clopidogrel and the others stopped both antiplatelets (aspirin and clopidogrel or ticlopidine). This is erroneously reported in the editorial of Gershlick (2) which states that premature discontinuation of clopidogrel is the greatest risk factor for stent thrombosis. We do not know whether continuation of aspirin alone would have been adequate to prevent DES-thrombosis. Moreover, in only a minority of patients in Iakovou’s register (5 out of 29, i.e. 17%) discontinuation of antiplatelets seemed to play a role in the occurrence of stent thrombosis. The tragedy of DES is not the risk of late stent thrombosis but the fact that these devices have only a limited effect on our patients well- being. It has been shown in several randomized trials (3) that they do not lead to a lower mortality and they do not affect the incidence of acute myocardial infarction. On the other hand, recently presented meta-analyses (4) and data from registries (5) suggest that DESs might increase the occurence of acute infarctions and even late mortality. The question at hand is not for how long and how many antiplatelets should be continued following DES implant but whether we should continue to use this kind of coronary stents in our patients. 1. Iakovou I, Mehran R, Dangas G. Thrombosis after implantation of drug-eluting stents. Hellenic J Cardiol 2006;47(1):31-8. 2. Gershlick AH, Richardson G. Drug eluting stents. BMJ 2006;333(7581):1233-4. 3. Roiron C, Sanchez P, Bouzamondo A, Lechat P, Montalescot G. Drug eluting stents: an updated meta-analysis of randomised controlled trials. Heart 2006;92(5):641-9. 4. Nordmann AJ, Briel M, Bucher HC. Mortality in randomized controlled trials comparing drug-eluting vs. bare metal stents in coronary artery disease: a meta-analysis. Eur Heart J 2006;27(23):2784-814. 5. Pfisterer M, Brunner-La Rocca HP, Buser PT, Rickenbacher P, Hunziker P, Mueller C, et al. Late clinical events after clopidogrel discontinuation may limit the benefit of drug-eluting stents: an observational study of drug-eluting versus bare-metal stents. J Am Coll Cardiol 2006;48(12):2584- 91. Competing interests: None declared |
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Phil S Jones, Consultant in Intensive Care Medicine & Cardiothoracic Anaesthesia St Bartholomew's Hospital, London EC1A 7BE
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The recent FDA announcement in the United States with regard to the use of Drug Eluting Stents (DES) should prompt sober reflection, but Gershlik & Richardson’s editorial [1], although welcome, hardly scratches the surface of the problems we now already face following the widespread use of DES. DES remain associated with catastrophic cardiac events months or even years after the procedure and if stenting per se is not superior anyway to Coronary Artery Bypass Surgery (CABG) [2] patients are entitled to wonder just what we have all been doing. It is not improper to ask if patients have died who needn’t have, due to DES being widely used without the proper long term follow-up trials being conducted first to demonstrate their efficacy and safety. Defining narrow indications for DES doesn’t seem to have protected patients in the USA, where the FDA say that most DES were just inserted anyway outside the licensed indications [1]. One wonders what the patients were told. I still do. Giving ever-more novel treatments to millions of patients around the world without having long term data is not ideal. In addition, though, we now have a vast, ever-growing cohort of patients in whom nobody even knows how long their dual antiplatelet therapy should continue. Many such patients will eventually be referred for CABG, at which stage they have been made more difficult to manage because their medication increases the risk of serious bleeding [3], besides the fact that surgeons are tasked with creating delicate anastomoses in coronaries clad in “full metal jackets”. It is hardly surprising that surgical complications are more common following prior percutaneous intervention (PCI) [4] and patients might enquire why, exactly, were they not offered surgery after their initial coronary angiogram? The situation is, if anything, even more problematic in non-cardiac surgery where patients with DES are faced with the invidious choice of stopping their antiplatelet therapy and risking an acute coronary thrombosis, or continuing with it and risking more perioperative bleeding. It is easy to recommend the latter option but there are many operations where even a small increase in bleeding either obscures the surgical field or causes serious problems post-operatively (infection, wound dehiscence, skin necrosis, reoperation). For patients who develop complications as a result of their DES or its associated drug regimen, the burden is high, as is the cost of treating them. We find ourselves in a position where, in the long term, PCI for coronary artery disease has become a quite expensive way of obtaining debatable outcomes, particularly in diabetic patients where the restenosis rates are much higher. PCI has also started to interfere with most surgical specialties’ routine work to boot. It remains perfectly possible that we are on the right road, but before we go any further perhaps we should get a map? References [1] Gershlick AH, Richardson G. Drug eluting stents. BMJ 2006;333:1233-1234. [2] Hannan EL. Racz MJ. Walford G. Jones RH. Ryan TJ. Bennett E. et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation N Engl J Med 2005;352:2174-83. [3] Kapetanakis EI. Medlam DA. Boyce SW. Haile E. Hill PC. Dullum MK et al. Clopidogrel administration prior to coronary artery bypass grafting surgery: the cardiologist's panacea or the surgeon's headache? Eur Heart J. 2005; 26(6):576-83. [4] Thielmann M, Leyh R, Massoudy P, Neuhauser M, Aleksic I, Kamler M et al. Prognostic significance of multiple previous percutaneous coronary interventions in patients undergoing elective coronary artery bypass surgery. Circulation 2006; 114(1 Suppl): I441-7. Competing interests: Consultant Cardiac Anaesthetist; Member of Hospital Transfusion Committee |
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Anthony H Gershlick, Consultant Cardiologist University Hospitals of Leicester, LE3 9QP, Gail Richardson, Consultant Cardiologist, University Hospitals of Leicester, LE3 9QP
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Dear Sir The fundamental aim of our editorial at the time of writing was to highlight the relatively rare but potentially serious issue of stent thrombosis (ST) and its association with premature discontinuation of clopidogrel in patients treated with drug eluting stents (DES) [1]. Most importantly it was written to convey to non-cardiological medical and surgical colleagues the possible implications of stopping the drug without discussion or knowledge of the interventional procedure, as might be considered in patients who had had an allergic reaction, who had bled or who were at risk of doing so in the context of a planned non-cardiac surgical procedure. The use of specific cards to improve levels of communication, as we suggested in the article, is further endorsed by the comments of Antoniou and Rothman [2]. Communication regarding the management of such patients was the fundamental to the tenet of the article. ST whilst occurring in only around 2% of patients treated with DES may have major clinical implications; up to 50% of these patients will suffer death or acute myocardial infarction [3]. Whilst clopidogrel may protect against early (up to 1 month post procedure) and late ST (up to 1 year post procedure) it appears to have little effect beyond that time although there are little large randomised clinical trial data to support this. Thus both BCIS and the FDA currently recommend that all patients treated with DES are prescribed clopidogrel for 12 months. Clopidogrel therapy in some patients is associated with increased bleeding. In a recent publication, the risk of GI bleeding with combination aspirin and clopidogrel therapy has been shown to be increased 7-fold compared to controls [4], although it appears most such patients can be managed conservatively. The risk of post-operative bleeding is much more difficult to quantify. In other patients however, clopidogrel can be less than effective, as measured by platelet function tests. These “non-responders” appear to have increased rates of thrombotic events even when compliance is good [5]. However, this is a poor association between compliance, clinical events and platelet function testing, dependant on definition, and our understanding of the relationship between these variables remains poor. Perhaps rather than undertake platelet function testing all in patients treated with clopidogrel – as suggested by Wiper et al [6] - we should wait for the newer thienopyridines, such as prasugrel, to become available, although again more data will need to be collected before we can be sure that they are better than those drugs currently being used. Early data suggest that they may be particularly useful in the small numbers of patients with “proven” thienopyridine resistance. This editorial was never intended to be a debate about DES vs. bare metal stents (BMS) or DES vs. surgery. There are no available randomised clinical trial data comparing DES vs. CABG – especially in high risk patients. In the ARTS 2 trial, major adverse cardiac event rates at 1 year for patients with multi vessel disease were the same with CABG and DES, although these are not randomised data [7]. The CARDIA and SYNTAX trials, among others, are ongoing. In one response to our editorial, data from the New England Journal of Medicine were quoted comparing outcomes from surgery and PCI [8]. These involved patients treated between 1997 and 2000 – i.e the BMS era. They are observational data and it is difficult therefore to know how patients were selected for each revascularisation option or to use then to draw comparisons between DES and CABG. The numbers of patients undergoing surgery is falling and likely to continue to do so. Currently in the UK, however, our ratio of stenting to CABG is 3:1, compared to ratios of up to 8:1 in Europe. Even the FDA is waiting for the results of ongoing clinical trials before it opines on the benefits of CABG vs. DES in patients with high risk multi-vessel disease. A reversal of the current trend should not be predicated on the basis of the risk of ST alone. Whilst there are little randomised clinical trial data currently available on DES vs. CABG, there are many data comparing DES with BMS both in terms of efficacy and safety. The RAVEL, SIRIUS and TAXUS, ENDEAVOR and SPIRIT series of trials have shown DES to achieve a significant 60%-80% reduction in both recurrence of angina and in angiographic restenosis and late loss compared to BMS [9 - 13]. Assessment of safety has been much more difficult because of relatively low adverse event rates. With the standardisation of definitions of ST and assessment of core patient data from the Cypher and Taxus trials, death and MI rates have been shown to be non-significantly different between BMS and DES although rates of very late ST (> 1 year post procedure) are higher with DES. However the ST thrombosis rate with BMS is not and never has been zero. It is associated with increasing complexity of procedure and with the availability of DES and the certainty of longer term sustained benefit, the patients treated with PCI are becoming ever more complex. The main issue highlighted by those who responded to our article was the lack of good randomised clinical trial data addressing the issue of ST and comparing DES with CABG. The former is being addressed by large clinical trials, PROTECT and INSIGHT, aiming to recruit 8,000 – 10,000 patients and 2 large registries, E-SELECT and the stent thrombosis trial. Patients will be followed-up for 2 – 5 years. There are a number of ongoing clinical trials comparing outcomes with DES and CABG in patients with multi vessel and left main stem disease, CARDIA and SYNTAX being 2 of these. Until these data become available, experts suggest that DES are implanted after due thought and consideration and that clopidogrel is prescribed for 12 months. It is essential that cardiologists, their medical colleagues and patients are aware of both the need for clopidogrel therapy and the consequences of its premature discontinuation. If all these factors are taken into consideration, it appears that DES usage is safe. To suggest that we return to BMS or CABG just because there are not enough data to answer all our questions now, is not a good enough reason to take such a retrograde step. Competing interests: Competing interests: AHG is on the advisory board and is an educational advisor adviser and panel speaker for all drug eluting stent companies. GR is on the advisory board of Abbott Vascular. |
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