Published online before print March 16, 2009, doi: 10.1161/CIRCULATIONAHA.108.813667
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(Circulation. 2009;119:1634-1642.)
© 2009 American Heart Association, Inc.
Interventional Cardiology |
Safety of Short-Term Discontinuation of Antiplatelet Therapy in Patients With Drug-Eluting Stents
From the Divisions of Cardiology and Clinical Epidemiology, Jewish General Hospital/McGill University (M.J.E., P.R.R., D.L., K.B.F.), Department of Epidemiology, Biostatistics, and Occupational Health (M.J.E., K.B.F.), McGill University, and Division of Clinical Epidemiology, McGill University Health Center (K.B.F.), Montreal, Quebec, Canada.
Correspondence to Mark J. Eisenberg, MD, MPH, Professor of Medicine, Divisions of Cardiology and Clinical Epidemiology, Jewish General Hospital/McGill University, 3755 Cote Ste Catherine Rd, Suite A-118, Montreal, Quebec, Canada H3T 1E2. E-mail mark.eisenberg{at}mcgill.ca
Received August 8, 2008; accepted January 13, 2009.
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Abstract |
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Background— Antiplatelet therapy is often discontinued in patients with drug-eluting stents who are undergoing surgical procedures. However, discontinuation of antiplatelet therapy is an important risk factor for late stent thrombosis. Our objective was to examine the safety of short-term discontinuation of antiplatelet therapy.
Methods and Results— We systematically searched Medline for reported cases of late stent thrombosis and very late stent thrombosis published between January 2001 and July 2008. We restricted our search to Academic Research Consortium–defined definite cases. We identified 161 cases of late stent thrombosis or very late stent thrombosis from 84 articles (79 from case reports, 61 from registries, and 21 from randomized clinical trials). Patients had a mean age of 58.4±13.4 years, and 88% were male. A total of 19 cases occurred in patients who were receiving dual antiplatelet therapy at the time of the event. If patients stopped both antiplatelet agents simultaneously, the median time to event was 7 days. If patients had previously stopped a thienopyridine with no ill effect and subsequently stopped acetylsalicylic acid, the median time to event was also 7 days from the time of acetylsalicylic acid cessation. If the thienopyridine was stopped but acetylsalicylic acid was maintained, the median time to event was 122 days. Among the 48 patients who stopped both agents, 36 cases (75%) occurred within 10 days. Among the 94 patients who discontinued a thienopyridine but continued acetylsalicylic acid, only 6 cases (6%) occurred within 10 days.
Conclusion— If acetylsalicylic acid therapy is maintained, short-term discontinuation of a thienopyridine may be relatively safe in patients with drug-eluting stents.
Key Words: angioplasty • antiplatelet therapy • drug-eluting stents • prevention • thrombosis
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Introduction |
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Discontinuation of antiplatelet therapy, including acetylsalicylic acid (ASA) and thienopyridines, is the dominant risk factor for the occurrence of late stent thrombosis (LST) and very late stent thrombosis (VLST) in patients with drug-eluting stents (DES).1–6 For this reason, treatment guidelines now recommend maintaining dual antiplatelet therapy for at least 12 months.7,8 However, patients with DES sometimes require surgical procedures for which antiplatelet agents are typically held. The risk associated with short-term discontinuation of antiplatelet therapy is a hotly debated issue.9–12 We sought to examine the safety of short-term antiplatelet discontinuation among patients with DES by performing a systematic review of reported cases of LST and VLST in DES patients.
Clinical Perspective p 1642
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Methods |
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Search Strategy
We systematically searched Medline to identify reported cases of LST and VLST in patients with DES. According to the Academic Research Consortium, LST is defined as stent thrombosis occurring between 30 days and 1 year after stent implantation, and VLST is defined as stent thrombosis occurring >1 year after implantation.13 Throughout the remainder of this article, we use the term LST to refer to both LST and VLST. We searched text words and MeSH terms related to coronary disease, DES, and thrombosis and combined these search results (Figure I of the online Data Supplement). Our search was limited to publications involving humans published in English or French between January 2001 and July 2008. References of identified studies and those of previous reviews were searched manually to identify additional cases. All data were independently extracted by 2 reviewers, with disagreements resolved by consensus or, if necessary, by a third reviewer.
Inclusion Criteria
We included all published cases of LST in DES patients for which detailed clinical information was available. To avoid potential misclassification, we limited our study to Academic Research Consortium–defined definite cases of LST.13 Consequently, all cases were angiographically confirmed, had pathological evidence obtained via thrombectomy, or had evidence of occlusion or thrombus in the DES-treated artery at autopsy. We restricted our study to patients with sirolimus-eluting or paclitaxel-eluting stents, and all patients were required to receive dual antiplatelet therapy after percutaneous coronary intervention (PCI). We excluded patients with cardiac events within 30 days of PCI and those for which the timing of LST was unknown.
Statistical Analysis
We categorized cases on the basis of their antiplatelet (ASA and/or thienopyridine) therapy at the time of LST. We divided the patients into 4 exposure categories: (1) patients who simultaneously discontinued both ASA and thienopyridine therapy, (2) patients who discontinued ASA therapy after previously discontinuing thienopyridine therapy, (3) patients who discontinued thienopyridine therapy but continued ASA, and (4) patients who did not discontinue dual antiplatelet therapy.
Continuous data are presented as medians with 95% CIs and were compared by use of Mann-Whitney U tests. Discrete data were compared by use of 
2 or Fisher’s exact test as appropriate. To examine the potential effects of publication bias, we conducted sensitivity analyses in which we stratified cases by publication type (case report/case series versus registry/randomized clinical trial [RCT]). Our a priori hypothesis for these sensitivity analyses was that, if the observed differences in treatment were larger when restricted to case reports, publication bias might explain any observed differences. All tests were 2 tailed, and values of P
0.05 were considered significant. Analyses were conducted with SAS version 9.1 (SAS Institute, Cary, NC).
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Our search identified 1665 articles, 80 of which met our inclusion criteria (supplemental Figure II). We identified 4 additional studies through our manual search, resulting in a total of 84 included articles. These articles contained a total of 161 cases (supplemental Table).
Patients had a mean age of 58.4±13.4 years, and 88% were male (Table). The numbers of cases associated with sirolimus-eluting and paclitaxel-eluting stents were similar. LST occurred predominantly in DES placed in the left anterior descending artery. The 161 cases included 118 nonfatal acute coronary syndromes and 18 deaths. Of the 18 patients who died, 17 died after presenting with an acute coronary syndrome, and 1 died suddenly. The vital status for 25 cases was not reported.
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The median time from index PCI to LST was 395 days (range, 31 to 1338 days [3.7 years]; Table). The median time from PCI to LST appeared to be longer among cases with sirolimus-eluting stents (508 days; 95% CI, 335 to 639) compared with those with paclitaxel-eluting stents (335 days; 95% CI, 258 to 426) (P=0.03). Among patients who did not discontinue dual antiplatelet therapy yet still had an event, the median time from PCI to LST was 183 days (95% CI, 91 to 258). The minimum time from PCI to LST in this group was 31 days; the maximum time was 868 days (2.4 years).
If patients stopped both a thienopyridine and ASA simultaneously, the median time to event was 7 days (Figures 1 and 2
). If patients had previously stopped their thienopyridine with no ill effect and subsequently stopped ASA, the median time to event was also 7 days from the time of ASA cessation. If the thienopyridine was stopped but ASA was maintained, the median time to event was 122 days (P<0.0001 compared with each of the other 2 groups). No LST cases were reported in patients who stopped ASA and were still receiving a thienopyridine. In 10 cases, ticlopidine was used instead of clopidogrel.
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The importance of maintaining ASA is highlighted by an examination of the number of cases that occurred within 10 days of antiplatelet discontinuation (Figure 2). Of the 94 cases of LST among those who discontinued a thienopyridine but continued ASA, only 6 (6%) occurred within 10 days of discontinuation and only 2 (2%) occurred within 5 days. In contrast, LST occurred within 10 days among 26 of 33 patients (79%) who discontinued both agents simultaneously and among 10 of 15 patients (67%) who discontinued ASA after already discontinuing a thienopyridine (P<0.0001 for each). Among those who discontinued both agents simultaneously, 13 cases (39%) occurred within 5 days of discontinuation (P<0.0001 compared with those who discontinued a thienopyridine but continued ASA). Similarly, LST occurred within 5 days of discontinuation in 4 cases (27%) among those who discontinued ASA after already discontinuing a thienopyridine (P=0.0006 compared with those who discontinued a thienopyridine but continued ASA).
Sensitivity analyses revealed similar results regardless of publication type. Among cases reported in case reports or case series (n=79), the median time to LST among those who discontinued a thienopyridine but maintained ASA therapy was 183 days (95% CI, 84 to 371). The median time to LST among those who discontinued ASA after having already discontinued a thienopyridine was 8.5 days (95% CI, 7 to 14), and the median time to LST among those who discontinued both agents simultaneously was 7 days (95% CI, 5 to 10). Among cases obtained from registries or RCTs (n=82), the median time to LST was 122 days (95% CI, 76 to 251) among those who discontinued a thienopyridine but maintained ASA therapy, 7 days (95% CI, 3 to 56) among those who discontinued ASA therapy after already having discontinued a thienopyridine, and 6 days (95% CI, 5 to 7) among those who discontinued both agents simultaneously.
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Discussion |
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Our study was designed to examine the safety of short-term discontinuation of antiplatelet therapy in patients with DES. These patients often require surgical procedures for which antiplatelet therapy is temporarily discontinued. However, cessation of antiplatelet therapy is the dominant risk factor for LST.14 Because LST is such a rare event, it has been difficult to determine its exact incidence rate.15–18 The rarity of this event has also made it difficult to identify whether short-term discontinuation of antiplatelet therapy is safe. To examine this issue, we systematically identified all reported cases of LST in DES patients for whom detailed information was available regarding the timing of cessation of antiplatelet therapy. We found that patients who discontinued their thienopyridine but maintained their ASA therapy had a substantially longer time to LST compared with those who discontinued both agents (either simultaneously or separately). Importantly, for those patients who maintained their ASA therapy, only 6% of cases occurred within 10 days of cessation of their thienopyridine, and only 2% of cases occurred within 5 days of cessation. In contrast, the vast majority of all cases in the other groups occurred within 2 weeks of antiplatelet discontinuation.
Previous studies have identified important risk factors for DES-associated LST. These risk factors include cessation of antiplatelet therapy, inadequate stent expansion and deployment, the presence of bifurcation lesions, reduced ejection fraction, and persistent platelet reactivity despite treatment with antiplatelet therapy.9–12,14 However, when the odds ratios associated with each of these risk factors are considered, it becomes apparent that cessation of antiplatelet therapy is by far the most important.14 For this reason, great concern has arisen in the medical community,19 with physicians becoming very reluctant to stop antiplatelet therapy in patients with DES who are scheduled to undergo surgical procedures. This reluctance has been fueled by reports of fatal cases of LST occurring within days of cessation of antiplatelet therapy.20–22 In contrast, physicians who perform surgical or invasive procedures are often reluctant to perform these procedures in patients who continue to receive antiplatelet therapy because of their increased risk of bleeding. However, our results suggest that for those patients at high risk of bleeding, it may be relatively safe to stop thienopyridine therapy in patients with DES over a short period of time if ASA is maintained.
Variability in platelet response and rebound platelet activation may be responsible for the variation in timing and occurrence of LST that we observed after the cessation of antiplatelet therapy. Multiple studies have demonstrated variability in platelet response among different individuals.23 This variability may be due to the different methods used to assess platelet responsiveness,24 to different levels of compliance with antiplatelet agents, or to genetic variability that modulates platelet responsiveness. In any case, platelet resistance has been linked to the likelihood of developing adverse cardiovascular events.25 In addition, depending on the method used to identify platelet reactivity, between 5% and 65% of the population may be aspirin resistant.23 Thus, the likelihood of developing LST during short-term cessation of antiplatelet agents may, at least partially, be due to whether an individual is resistant to antiplatelet agents.
Rebound platelet activation may also be responsible for the results that we observed. Several in vitro studies have documented an increase in platelet activation shortly after the cessation of thienopyridine therapy.26–28 These studies have been complemented by clinical studies documenting the clustering of cardiovascular events shortly after the cessation of antiplatelet therapy. These events occurred after the cessation of both thienopyridine therapy29 and ASA therapy.30 Our finding that LST occurs soon after the cessation of dual antiplatelet therapy but is delayed if ASA therapy is maintained is consistent with the idea of rebound platelet activation.
Importantly, any decision about short-term cessation of antiplatelet therapy needs to take into consideration the potential risks and benefits for an individual patient. Although our results suggest that short-term cessation of antiplatelet agents in many patients appears to be relatively safe, there are clearly subgroups of patients in whom the risk of LST is higher than average (eg, presence of multiple, long DES used in bifurcation lesions) or in whom the occurrence of LST could be catastrophic (eg, DES in a left main coronary artery in the presence of a left-dominant circulation). At the same time, the risks of bleeding during surgery in the setting of noncessation of antiplatelet agents also need to be considered. For high-risk procedures in which significant bleeding would prove to be catastrophic, the risk-to-benefit ratio might favor the short-term cessation of antiplatelet agents. Our results suggest that, if at all possible, patients should continue ASA therapy before, during, and after surgery if a thienopyridine is temporarily withheld. Again, however, the decision about short-term cessation of antiplatelet therapy needs to be tailored to the individual patient.
With the above caveats in mind, we present a potential management strategy based on our results: For a patient undergoing noncardiac surgery that could present a bleeding risk, the procedure should ideally be delayed until 1 year after stenting. For a patient who is undergoing a procedure that cannot be delayed, a thienopyridine could potentially be held for 5 days, the patient could undergo the procedure, and the thienopyridine could be restarted on day 6. Low-dose ASA would need to be maintained throughout the perioperative period. If at all possible, it would be optimal to continue both agents throughout the perioperative period. If the patient is deemed to be at such a high risk of bleeding that both aspirin and thienopyridine therapy need to be stopped, they should be stopped no sooner than 5 days before the surgery, and they should be restarted as soon as possible after the surgery, certainly within 5 days of the procedure. The above strategy should be used only in cases when the bleeding risk outweighs the risk of LST. A better assessment of the risks and benefits of antiplatelet therapy would require improved knowledge about bleeding risks. Unfortunately, the reports that we reviewed did not provide information regarding bleeding. Thus, we were unable to address this issue and other side effects related to the discontinuation of antiplatelet therapy.
Patients who are scheduled to undergo cardiac surgery and who are currently receiving dual antiplatelet therapy warrant special consideration. These patients usually have thienopyridines held and have their ASA continued. This practice is based largely on data from the Clopidogrel in Unstable Angina to Prevent Recurrent Ischemic Events (CURE) trial, which showed that patients who undergo cardiac surgery while receiving thienopyridines within the previous 5 days are at higher risk of perioperative bleeding and need for transfusions.31 Our results are not in conflict with this strategy. However, it must be recognized that most of these patients were receiving thienopyridine therapy because of a preceding acute coronary syndrome. Only a minority of these patients had a preceding PCI with a DES. In these cases, it would be particularly important to maintain ASA therapy while thienopyridine therapy is being withheld.
As the risk of LST has become evident, guidelines statements have evolved in their recommendations regarding the suggested duration of antiplatelet therapy after DES placement.7,32,33 In 2001, the American College of Cardiology/American Heart Association (ACC/AHA) guidelines for PCI recommended that thienopyridine therapy be used for 2 to 4 weeks after bare metal stent placement.32 The 2005 ACC/AHA/Society for Cardiac Angiography and Interventions (SCAI) guidelines recommended a minimum of 3 months of thienopyridine therapy after sirolimus-eluting stent implantation and 6 months after paclitaxel-eluting stent implantation.33 These guidelines recommended that, if possible, thienopyridine therapy should be maintained beyond this minimum period and ideally for 12 months after DES implantation. Similarly, the 2005 European Society of Cardiology guidelines for PCI recommended that thienopyridine therapy be maintained for 6 to 12 months after DES implantation.34 Most recently, the 2007 ACC/AHA/SCAI focused update of their 2005 guidelines recommends a minimum of 12 months of dual antiplatelet therapy and indefinite ASA therapy.7 Long-term results from various trials and cohort studies suggest that the risk of LST does not decline over time. Even for patients who have stopped thienopyridines but maintained ASA for long periods without ill effects, cases of LST have been reported. Thus, it may be prudent to maintain these patients indefinitely on dual antiplatelet therapy, and for patients who have previously stopped thienopyridine, it may be prudent to restart their therapy. It is possible that, over time, there is a decline in the likelihood of LST associated with the short-term cessation of antiplatelet therapy. However, although our study was underpowered to examine this issue, we did not observe any evidence of such an effect.
Our choice of study design merits discussion. Optimally, the issue of short-term discontinuation of antiplatelet therapy would be examined in an RCT. An RCT would overcome many potential limitations associated with a case-only design, including that of confounding by indication and lack of controls. However, such a trial would require tens of thousands of patients, and these patients would have to be followed up for many years. An RCT may also be ethically problematic given the currently available evidence.
Another potential design is a nested case-control study. However, a nested case-control study would require an extremely large cohort of patients who had received a DES. Within this large cohort, patients who had developed LST would need to be identified, and then appropriate control subjects would have to be selected. After the identification of cases and controls, antiplatelet exposure status would need to be assessed. Unfortunately, most of these types of databases are administrative in nature and contain limited clinical data. Consequently, these databases might be used to identify whether a patient had LST or not, but they likely could not be used to identify which antiplatelet agents the patients were on and when these agents were stopped. Administrative databases often lack adequate clinical detail to distinguish between definite and probable cases of LST as identified by Academic Research Consortium definitions.
We used a modified case-only design. Case-only designs are typically used in genetic studies, particularly for examinations of the effects of potential gene-environment or gene-gene interactions, for which these designs are statistically efficient.35 Other types of case-only designs include case-crossover designs and self-controlled case-series designs, which are often used to study acute effects after an acute exposure (eg, adverse events after vaccination).36 One advantage of case-only designs is that they are very efficient for the study of rare events such as LST. Because we needed a large number of LST cases with detailed information regarding antiplatelet therapy use, we used a modified case-only design in which cases were identified through a systematic literature search. Despite the limitations associated with a lack of control subjects, we believe that this design is currently the most feasible approach to address this important clinical question. The use of control subjects would potentially strengthen the conclusions from our study. However, the unbiased identification of representative control subjects is not feasible with a literature-based case-only design. As a result of this lack of control subjects, this design produced data that were more heterogeneous than those typically produced by RCTs or cohort studies, potentially limiting the strength of our conclusions.
The effects of censoring must also be considered when a case-only design is used. It is possible that some patients may be censored before experiencing an episode of LST. However, it is most likely that such censoring is random and unrelated to the discontinuation of antiplatelet therapy. Furthermore, the vast majority of patients do not experience LST and are therefore censored, with this censoring occurring independently of their antiplatelet therapy. Despite some of the features inherent to a case-only design, it is currently the only feasible design to examine clinically important questions like short-term discontinuation of antiplatelet therapy.
Limitations
Our study has several potential limitations. First, we examined only reported cases of LST. Clearly, there have been many cases that have not been reported in the literature. Nonetheless, there is little reason to believe that reported cases of this rare event differ substantially from unreported cases. In addition, there are also large numbers of patients who have had thienopyridines and ASA withheld before procedures who have not developed LST. Thus, the likelihood of developing LST in a large group of patients who stop antiplatelet agents for a short period of time is relatively small. When this information is added to the information that we have developed in our study, it becomes evident that the chance of developing LST in the short term, if the patient is maintained on ASA therapy, is relatively low.
A second potential limitation is that we restricted our study to cases of LST published in English or French. Our results may therefore be affected by language and/or publication bias. However, from our systematic search, we estimate that <5% of cases have been reported in other languages, and we believe it is unlikely that these cases differ substantially from those published in English or French. In addition, only a minority of LST cases have been reported in the literature, and these cases are more likely to have been reported if their occurrence was preceded by antiplatelet discontinuation. Consequently, the major impact of any potential publication bias is likely to overestimate the magnitude of the effect of discontinuation of antiplatelet therapy. To examine the potential effects of publication bias, we conducted sensitivity analyses in which we stratified our results by publication type. These stratified analyses provided results similar to those reported in our primary analyses, suggesting that, if publication bias is present, it should not affect our conclusions.
Finally, our data are observational in nature and may therefore be affected by confounding by indication. Physicians are more likely to stop antiplatelet therapy before procedures if they think that the patient is at high risk for bleeding. It is conceivable that these patients could also be at high risk of LST if antiplatelet agents are withheld. Thus, the patients who have antiplatelet therapy stopped and then develop LST may be a higher-risk subgroup of the total population of patients. However, the risk for bleeding and the risk for LST do not necessarily proceed in tandem. Rather, the risk for bleeding is closely related to the type of procedure the patient is undergoing, and this fact should be independent of the risk for LST. Thus, we believe that confounding by indication is not likely to be a major limitation of our study. Furthermore, because of the large differences we observed in the timing of LST, any such bias could affect the magnitude of the differences but is unlikely to affect the overall conclusions from our study.
Conclusions
Our study was designed to examine the safety of short-term discontinuation of antiplatelet therapy in patients with DES. We found that very few cases of LST occurred within 10 days of stopping a thienopyridine if ASA was maintained. These data suggest that it may potentially be feasible for patients with DES to stop their thienopyridine therapy for a short period of time if required for invasive or surgical procedures. Although there is still a risk for LST with this strategy, short-term cessation of thienopyridine therapy may be relatively safe if ASA is maintained.
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Acknowledgments |
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We would like to thank Sandra Derghazarian, Brooke Wilson, and Priyanka Dixit for their help with the literature search and Dr Ganesan Karthikeyan for his comments on an early draft of this manuscript. We also thank the reviewers for their helpful comments and suggestions.
Sources of Funding
Dr Eisenberg is a National Researcher of the Quebec Foundation for Health Research. K.B. Filion is supported in part by a bursary from the Quebec Foundation for Health Research.
Disclosures
None.
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The online Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.108.813667/DC1.
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