How Long to Continue Eliquis Post Stent
Antithrombotic therapy reduces cardiovascular events in patients following acute coronary syndrome (ACS). Since antithrombotic therapy increases the risk of bleeding, clinicians must utilize therapies in a manner that maximizes efficacy while minimizing risk. Whether the optimal strategy to balance ischemic and bleeding risk involves an anticoagulant, antiplatelet, or some combination remains unknown.1
The advent of percutaneous coronary intervention (PCI) dramatically changed the treatment of coronary artery disease (CAD) and ACS. Balloon angioplasty—the first form of PCI—was effective but was limited by high rates of acute vessel closure. Coronary stents were developed to mitigate this problem but were themselves initially plagued by high rates of stent thrombosis. Regimens that included low-molecular-weight dextran, aspirin, dipyramidole, and heparin followed by vitamin K antagonists (VKAs) were developed. While these regimens lowered thrombotic complications, they dramatically increased the risk of bleeding and duration of hospitalization.2
The development of P2Y12 inhibitors and improvements in stent design shifted strategies away from anticoagulants and toward antiplatelet therapies. Initial studies using intravascular ultrasound showed that with adequate stent expansion, antiplatelet therapies without anticoagulation were effective.3 Subsequent studies and the STARS (Stent Anticoagulation Restenosis Study) found that dual antiplatelet therapy (DAPT) with aspirin and ticlopidine—a P2Y12 inhibitor—improved efficacy and safety compared with regimens of aspirin and VKA.4,5
Due to safety concerns for ticlopidine, clopidogrel became the preferred agent.6 More potent P2Y12 inhibitors, prasugrel and ticagrelor, have since been developed and have demonstrated improved outcomes compared with clopidogrel, albeit with higher rates of bleeding.7,8 While debate exists on the preferred P2Y12 inhibitor, DAPT with aspirin and a P2Y12 inhibitor has become the standard of care to reduce ischemic outcomes and the risk of stent thrombosis in patients post-PCI.
Compounds that directly inhibit thrombin (dabigatran) or factor Xa (apixaban, edoxaban, and rivaroxaban) are now guideline recommended to reduce the risk of thrombotic events in patients with atrial fibrillation (AF) due to lower rates of mortality, stroke, systemic embolism, and intracranial hemorrhage (ICH) compared with VKA.9
Patients with stable CAD, sometimes referred to as chronic coronary syndromes, benefit from intensive medical therapy.10 The development of novel oral anticoagulants (NOAC) has led to renewed interest in the use of anticoagulation in patients with chronic coronary syndromes, particularly in those patients after ACS and PCI. This review article will explore the most recent trials that have evaluated the use of NOACs with antiplatelet therapy following PCI in patients with and without a traditional indication for anticoagulation.
Treatment Strategies for Patients Following PCI Who Require Oral Anticoagulation
The prevalence of CAD in patients with AF is estimated to range from 17% to 47% with ≈5% to 10% having undergone prior treatment with PCI.11 As a result, decisions regarding how to manage antiplatelet therapy and anticoagulation after PCI are common.
When PCI was first developed, triple therapy, defined as oral anticoagulation (OAC) plus DAPT, was the predominant anticoagulation strategy for patients undergoing PCI with AF. It was associated with high rates of major bleeding, which spurred investigation into alternative strategies such as OAC with a single antiplatelet agent (double therapy).1 Some have hypothesized that potent P2Y12 inhibition alone may sufficiently reduce platelet reactivity without the need for COX-1 inhibition with aspirin, whereas others have suggested that aspirin has benefits that cannot be replicated by a P2Y12 inhibitor alone.12 Data for the superiority of P2Y12 inhibition over aspirin come from the CAPRIE study (Clopidogrel Versus Aspirin in Patients at Risk of Ischemic Events), which compared clopidogrel and aspirin monotherapy for secondary prevention. CAPRIE found clopidogrel more effectively prevented ischemic events while reducing the rate of gastrointestinal bleeding. Recent studies evaluating alternative treatment regimens in patients with an indication for anticoagulation have uniformly discontinued aspirin.12
The WOEST trial (What Is the Optimal Antiplatelet and Anticoagulant Therapy in Patients With Oral Anticoagulation and Stenting) was the initial study evaluating triple versus double therapy and randomized patients who were taking a VKA for AF, mechanical heart valve, or venous thromboembolism (VTE) and underwent PCI to either clopidogrel or clopidogrel plus aspirin. Patients randomized to double therapy had significantly lower rates of bleeding when compared with those randomized to triple therapy.13 Ischemic events were lower in the double therapy arm, although this was not statistically significant nor was the study powered for this end point. Nevertheless, these data suggested that P2Y12 inhibition alone may obviate the need for aspirin.
The PIONEER study (the Open-Label, Randomized, Controlled, Multicenter Study Exploring Two Treatment Strategies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With Atrial Fibrillation Who Undergo Percutaneous Coronary Intervention) was the first randomized trial comparing double therapy with a NOAC to triple therapy with a VKA. Patients with AF who underwent PCI were randomized into 3 groups: rivaroxaban 15 mg plus P2Y12 inhibitor, rivaroxaban 2.5 mg BID plus DAPT, or VKA plus DAPT. The rate of clinically significant bleeding—a composite of Thrombolysis in Myocardial Infarction (TIMI) major/minor bleeding or bleeding requiring medical attention—was lower in both rivaroxaban cohorts compared with VKA (16.8% versus 18.0% versus 26.7%; P<0.001). There were no significant differences in a composite end point of death, myocardial infarction, or stroke between the rivaroxaban 15 mg plus P2Y12 inhibitor and the VKA plus DAPT cohort (hazard ratio [HR], 1.08 [95% CI, 0.69–1.68]); however, the study was not powered for ischemic outcomes. Of note, rivaroxaban 2.5 mg BID is not a traditional anticoagulant dose and may not be sufficient to prevent thromboembolism from AF.14
Double therapy with dabigatran was compared with triple therapy with VKA in the RE-DUAL-PCI study (Randomized Evaluation of Dual Antithrombotic Therapy With Dabigatran Versus Triple Therapy With Warfarin in Patients With Nonvalvular Atrial Fibrillation Undergoing Percutaneous Coronary Intervention).15 The primary end point of the International Society on Thrombosis and Haemostasis major or clinically relevant nonmajor bleeding occurred less often in the dabigatran 110 mg (HR, 0.52 [95% CI, 0.42–0.63]) and 150 mg (HR, 0.72 [95% CI, 0.58–0.88]) cohorts compared with triple therapy with VKA.16 Notably, the rates of ICH were lower in the double therapy cohorts. A noninferiority analysis found no difference in rates of combined thrombotic events or death between the 2 cohorts.
The AUGUSTUS trial (Antithrombotic Therapy After Acute Coronary Syndrome or PCI in Atrial Fibrillation) trial compared regimens with both VKA and apixaban. This study randomized patients with AF who presented with ACS and underwent PCI in a 2×2 factorial design to either apixaban or VKA and then to either a P2Y12 inhibitor with aspirin or with placebo. The International Society on Thrombosis and Haemostasis major bleeding and clinically relevant nonmajor bleeding was found to be lower with apixaban compared with VKA (HR, 0.69 [95% CI, 0.58–0.81]). The composite rate of bleeding was higher in those receiving aspirin compared with those receiving placebo (HR, 1.89 [95% CI, 1.59–2.24]).17 Although not statistically significant, there was a trend toward increased rates of stent thrombosis in the arm receiving placebo versus aspirin (0.63% versus 1.08%; HR, 0.58 [95% CI, 0.28–1.22]).18
The ENTRUST-AF PCI trial (Edoxaban Treatment Versus Vitamin K Antagonists in Patients With Atrial Fibrillation Undergoing Percutaneous Coronary Intervention) was the first major trial comparing double therapy with a NOAC to triple therapy with a VKA that did not show statistically significant lower rates of bleeding. The trial compared edoxaban and clopidogrel to VKA and DAPT in patients with AF who underwent PCI.19 The rate of major or clinically relevant bleeding was similar between the 2 groups (P=0.12 for superiority and P=0.01 for noninferiority) with no difference in the secondary outcome of ischemic events. Additional details on these studies are shown (Figure 1; Table I in the Data Supplement).
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Figure 1. Summary of primary bleeding end points for major trials evaluating double vs triple therapy. Primary bleeding end point for each trial: WOEST (What Is the Optimal Antiplatelet and Anticoagulant Therapy in Patients With Oral Anticoagulation and Stenting): composite of Thrombolysis in Myocardial Infarction (TIMI), GUSTO (Global Utilization of Streptokinase and tPA for Occluded Arteries) definition of bleeding, and BARC (Bleeding Academic Research Consortium). PIONEER (The Open-Label, Randomized, Controlled, Multicenter Study Exploring Two Treatment Strategies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With Atrial Fibrillation Who Undergo Percutaneous Coronary Intervention): TIMI. RE-DUAL PCI (Randomized Evaluation of Dual Antithrombotic Therapy With Dabigatran Versus Triple Therapy With Warfarin in Patients With Nonvalvular Atrial Fibrillation Undergoing Percutaneous Coronary Intervention), AUGUSTUS (Antithrombotic Therapy After Acute Coronary Syndrome or PCI in Atrial Fibrillation), and ENTRUST-AF (Edoxaban Treatment Versus Vitamin K Antagonists in Patients With Atrial Fibrillation): International Society on Thrombosis and Haemostasis. HR indicates hazard ratio; NOAC, novel oral anticoagulants; and VKA, vitamin K antagonist. *Noninferiority.
A meta-analysis of WOEST, RE-DUAL PCI, PIONEER, and AUGUSTUS (n=10 026 patients) compared bleeding and efficacy of different combinations of triple and double therapy. Compared with VKA plus DAPT, NOAC plus P2Y12 inhibitor had significantly lower rates of TIMI major bleeding and ICH. NOAC plus DAPT trended toward lower rates of TIMI major bleeding and ICH compared with VKA plus DAPT but did not reach statistical significance. There were no statistically significant differences in ischemic events or risk of stent thrombosis between the various cohorts.20
There are important challenges when interpreting and mixing these various trials. First, the primary end point for all of these trials was a bleeding/safety end point, and none of them were powered for ischemic end points. Second, the studies did not use the same bleeding end points, used various dosages of NOAC, and were studied in different populations. Lastly, the WOEST trial was the only study that included indications for OAC other than AF. Patients with VTE inherently have differences in their clotting mechanics compared with those without VTE and studies in populations of only AF may not be completely generalizable to every patient who has an indication for OAC.
Experts from North America and the European Society of Cardiology (ESC) published separate updates on the use of OAC following PCI for patients with an indication for anticoagulation. The North American Consensus white paper recommends the default strategy to be triple therapy during the peri-PCI period (defined as time of PCI to discharge). Upon discharge, the majority of patients should be treated with double therapy with a NOAC and P2Y12 inhibitor. After 12 months, the North American Consensus statement recommends discontinuing antiplatelet therapy and continuing OAC monotherapy. Therapy can be tailored based on whether a patient is at high risk of ischemia or bleeding and can include the option of triple therapy for 1 month.21
The 2018 ESC guidelines provide similar recommendations to those of the North America Consensus statement, with some key differences.22 Patients at high risk of ischemic events can have triple therapy extended up to 6 months. The ESC recommends that clopidogrel be the only P2Y12 inhibitor used in combination with anticoagulation, whereas the North American Consensus document allows for the consideration of ticagrelor in patients at high risk of ischemia. Potential ways to risk stratify ischemic and bleeding risk as recommended by the ESC are shown23 (Table).
| Unfavorable for triple therapy |
| Short life expectancy |
| Malignancy |
| Poor expected adherence |
| Poor mental status |
| End-stage renal disease |
| Advanced age |
| Prior major bleeding/hemorrhagic stroke |
| Chronic alcohol abuse |
| Anemia |
| Clinically significant bleeding on dual antithrombotic therapy |
| High risk for ischemia |
| Prior stent thrombosis on adequate antiplatelet therapy |
| Stenting of the last remaining patent coronary artery |
| Diffuse multivessel disease, especially diabetic patients |
| Chronic kidney disease |
| At least 3 stents implanted |
| At least 3 lesions treated |
| Bifurcation with 2 stents implanted |
| Total stented length >60 mm |
| Treatment of chronic total occlusion |
| History of ST-segment–elevation MI |
| PCI to the left main artery or proximal LAD |
Both the North American Consensus document and the ESC guidelines recommend OAC monotherapy as the default strategy 12 months after PCI. This recommendation was further supported by the AFIRE trial (Atrial Fibrillation and Ischemic Events With Rivaroxaban in Patients With Stable Coronary Artery Disease), which was the first prospective, randomized trial to evaluate the optimal combination of antithrombotic agents in stable CAD in patients with AF. Patients >1 year from PCI or coronary artery bypass grafting were randomized to receive rivaroxaban 15 mg daily (dose reduced to 10 mg for patients with glomerular filtration rate of 15–49 mL/min) plus aspirin or rivaroxaban monotherapy. The trial was stopped early due to increased mortality in the rivaroxaban-plus-aspirin arm as compared with the monotherapy arm (HR, 0.59 [95% CI, 0.39–0.89]). There were no differences in the primary efficacy end point of all-cause mortality, myocardial infarction, stroke, unstable angina requiring revascularization, or systemic embolism (HR, 0.72 [95% CI, 0.55–0.95] for noninferiority).24
In summary, numerous trials suggest that double therapy, with a NOAC and a P2Y12 inhibitor, should be the default strategy for most patients who require anticoagulation post-PCI. Triple therapy can be considered but should be limited to only those at high risk of ischemia and only for a limited period of time (Figure 2).21 However, it is important to note that none of the studies were powered for ischemic outcomes and may not have sufficient power to identify small differences in rare events, such as stent thrombosis. Further study is warranted to delineate which patients, if any, could benefit from a short treatment course of triple therapy following PCI. Similarly, identifying which patients benefit from continued double therapy beyond 12 months is another important area of research.
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Figure 2. North American Consensus white paper suggested algorithm for management of antithrombotic therapy in patients with atrial fibrillation who undergo percutaneous coronary intervention. All patients should be treated with triple therapy in the peri-percutaneous coronary intervention (PCI) period. Patients can be stratified at discharge into standard risk, high risk for ischemia, or high risk for bleeding based on patient characteristics. In double therapy, a P2Y12 inhibitor is preferred over aspirin. Novel oral anticoagulants (NOACs) are preferred over vitamin K antagonist unless contraindicated. Clopidogrel is the P2Y12 inhibitor of choice unless higher risk of ischemia and then ticagrelor can be considered. Prasugrel should be avoided. After 12 mo, antiplatelet therapy should be discontinued in most patients. Double therapy is reasonable in patients with high ischemic and low bleeding risk. OAC indicates oral anticoagulation. Adapted from Angiolillo et al21 with permission. Copyright © 2018, American Heart Association, Inc.
Treatment Strategies for Patients Following PCI Who Do Not Require Anticoagulation
Given their improved safety profile and reliable pharmacodynamics, NOACs have also been evaluated for use in secondary prevention in patients without a traditional indication for anticoagulation. This strategy, termed dual pathway inhibition (DPI), hypothesizes that targeting a second antithrombotic pathway, independent from antiplatelet mechanisms, may have synergistic effects to prevent future ischemic events.25
The ATLAS ACS2-TIMI 51 study (Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects With Acute Coronary Syndrome–Thrombolysis in Myocardial Infarction 51) evaluated the use of rivaroxaban in patients with ACS without an indication for anticoagulation. Stable patients who were within 7 days of ACS were randomized to either rivaroxaban 2.5 mg BID, rivaroxaban 5 mg BID, or placebo. The dosing of rivaroxaban was considerably lower than the standard 20-mg daily dose used for systemic anticoagulation for AF or VTE. The majority of patients had undergone revascularization with either coronary artery bypass grafting or PCI (60%), and most were on a P2Y12 inhibitor (93%) or aspirin (99%). Compared with placebo, low-dose rivaroxaban reduced the incidence of cardiovascular death (HR, 0.84 [95% CI, 0.74–0.96]), death from any cause (HR, 0.83 [95% CI, 0.72–0.97]), myocardial infarction (HR, 0.80 [95% CI, 0.67–0.95]), and stent thrombosis (HR, 0.69 [95% CI, 0.51–0.93]). The reductions in MI were primarily type 1 (spontaneous MIs).26 These benefits were offset by increased rates of TIMI major bleeding (2.1% versus 0.6%; P<0.05) and ICH (0.6% versus 0.2%; P<0.05) but without a significant increase in fatal bleeding (0.3% versus 0.2%; P=0.66).27
Not all studies of NOACs after ACS have suggested benefit. The GEMINI-ACS study (A Study to Compare the Safety of Rivaroxaban Versus Acetylsalicylic Acid in Addition to Either Clopidogrel or Ticagrelor Therapy in Patients With Acute Coronary Syndrome) randomized patients with ACS to either P2Y12 alone plus low-dose rivaroxaban (2.5 mg BID) or P2Y12 plus aspirin. The investigators found similar rates of bleeding without a significant difference in ischemic outcomes.28 This study was underpowered for ischemic events, and there were no qualitative differences in outcomes. In the APPRAISE-2 trial (Apixaban for Prevention of Acute Ischemic Events 2), patients with recent ACS, of whom 44% were treated with PCI, were randomized to receive apixaban 5 mg BID or placebo in addition to DAPT. The trial was stopped early due to increased bleeding events in the NOAC arm without a clear reduction in ischemic events. The results were similar in the subgroup of patients treated with revascularization.29
In addition to their use in the post-ACS setting, NOACs have recently been evaluated for long-term secondary prevention. In the COMPASS trial (Cardiovascular Outcomes for People Using Anticoagulation Strategies), 27 395 patients with CAD or peripheral arterial disease who were not on DAPT were randomized to rivaroxaban 5 mg daily, rivaroxaban 2.5 mg BID plus low-dose aspirin, or low-dose aspirin alone. The DPI cohort (rivaroxaban, 2.5 mg BID and aspirin) reduced the primary end point of cardiovascular death, myocardial infarction, or stroke (HR, 0.76 [95% CI, 0.66–0.86]) compared with aspirin monotherapy. The DPI cohort had a higher rate of major bleeding (HR, 1.70 [95% CI, 1.40–2.05]) but no differences in ICH (HR, 1.16 [95% CI, 0.67–2.00]). Rivaroxaban monotherapy had similar ischemic outcomes to aspirin monotherapy but with increased rates of ICH. The COMPASS trial suggests that DPI with rivaroxaban 2.5 mg BID and aspirin was the best strategy of the 3 for reducing ischemic events.30
Discordant results between these trials may be explained by the difference in degree of anticoagulation and timing of initiation. The studies of NOACs for use in secondary prevention post-ACS suggest that rivaroxaban at low doses (2.5 mg BID) in addition to aspirin reduces ischemic events, but the effectiveness is counterbalanced by higher rates of bleeding. Full-dose anticoagulation has no benefit and leads to excess bleeding. Currently, rivaroxaban is approved by both the European Medicines Agency to reduce cardiovascular events following ACS and the US Food and Drug Agency to reduce major cardiovascular events in patients with chronic CAD or peripheral arterial disease.
Many patients who undergo PCI will discontinue their P2Y12 inhibitor after the initial treatment period of 3 to 12 months. However, several studies have shown a reduction in cardiovascular events for prolonged DAPT beyond 12 months. The DAPT trial (Dual Antiplatelet Therapy), with clopidogrel and prasugrel, and the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared With Placebo on a Background of Aspirin–Thrombolysis in Myocardial Infarction 54), with ticagrelor, found decreased ischemic outcomes with prolonged DAPT, albeit with an increased risk of major bleeding.31,32 The DAPT score is one such tool that attempts to identify which patients would most benefit from prolonged DAPT by incorporating both risk factors for future cardiac and bleeding events.33
While prolonged antithrombotic therapy with DAPT or low-dose rivaroxaban is beneficial in reducing cardiovascular events in patients with stable CAD, these 2 strategies have not been directly compared. Continued investigation is warranted to more clearly define which subgroups of patients would benefit most from prolonged DAPT versus prolonged DPI. While the latest generation of stents have low rates of stent thrombosis that allow for shorter duration of antiplatelet therapy, prolonged therapy, either with low-dose rivaroxaban, reduced dose of ticagrelor (60 mg BID), or clopidogrel, lowers rates of ischemic events in patients with stable CAD.
Recommendations for Clinicians
The ESC has recently published a guideline for the treatment of patients with chronic coronary syndromes—a term that encompasses a wide array of clinical scenarios, including patients with stable CAD and angina, new-onset heart failure with suspected CAD, asymptomatic and symptomatic patients post-ACS with stabilized symptoms, microvascular disease, and asymptomatic patients in whom CAD is suspected.10 In patients without an indication for anticoagulation, rivaroxaban 2.5 mg BID should be considered in addition to aspirin for long-term secondary prevention in patients without significant risk of bleeding who are at high risk of ischemic events (class IIa, level of evidence A) and can be considered in patients at moderate risk of ischemic events (class IIb, level of evidence A). In patients who have an indication for anticoagulation and receive an uncomplicated PCI, early cessation (<1 week) of aspirin and continuation of dual therapy with an OAC and P2Y12 inhibitor can be used in most situations (class IIa, level of evidence B). A potential algorithm that summarizes the options for anticoagulation and antiplatelet therapy after PCI is shown (Figure 3).
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Figure 3. Pathway for secondary prevention following acute coronary syndrome (ACS) in patients without an indication for anticoagulation. ASA indicates aspirin; BID, twice a day; DAPT, dual antiplatelet therapy; and PCI, percutaneous coronary intervention.
Conclusions
Patients undergoing PCI frequently have a concomitant need for anticoagulation due to preexisting conditions such as AF or VTE. For these patients, multiple trials have shown that double therapy with a NOAC has lower risk of bleeding compared with triple therapy and should be the default strategy. However, none of the trials evaluating double and triple therapy were powered for ischemic outcomes, and triple therapy should be considered in certain circumstances.
Additionally, lower dose rivaroxaban reduces cardiovascular events in patients without a traditional indication for anticoagulation. While early studies proved the superiority of antiplatelet therapy over anticoagulation after PCI, studies with rivaroxaban suggest there may be benefits of DPI. Further research is still necessary to identify what combination and duration of antiplatelet and anticoagulant therapy best balances the risk of bleeding with the risk of thrombosis in the intermediate and long-term period post-PCI.
Nonstandard Abbreviations and Acronyms
| ACS | acute coronary syndrome |
| AF | atrial fibrillation |
| AFIRE | Atrial Fibrillation and Ischemic Events With Rivaroxaban in Patients With Stable Coronary Artery Disease |
| APPRAISE-2 | Apixaban for Prevention of Acute Ischemic Events 2 |
| ATLAS ACS2-Anti-Xa Therapy to Lower Car- TIMI 51 | diovascular Events in Addition to Standard Therapy in Subjects With Acute Coronary Syndrome–Thrombolysis in Myocardial Infarction 51 |
| AUGUSTUS | Antithrombotic Therapy After Acute Coronary Syndrome or PCI in Atrial Fibrillation |
| CAD | coronary artery disease |
| CAPRIE | Clopidogrel Versus Aspirin in Patients at Risk of Ischemic Events |
| COMPASS | Cardiovascular Outcomes for People Using Anticoagulation Strategies |
| DAPT | dual antiplatelet therapy |
| DAPT trial | Dual Antiplatelet Therapy |
| DPI | dual pathway inhibition |
| ENTRUST- | Edoxaban Treatment Versus AF PCI Vitamin K Antagonists in Patients With Atrial Fibrillation Undergoing Percutaneous Coronary Intervention |
| ESC | European Society of Cardiology |
| GEMINI-ACS | A Study to Compare the Safety of Rivaroxaban Versus Acetylsalicylic Acid in Addition to Either Clopidogrel or Ticagrelor Therapy in Patients With Acute Coronary Syndrome |
| HR | hazard ratio |
| ICH | intracranial hemorrhage |
| OAC | oral anticoagulation |
| PCI | percutaneous coronary intervention |
| PEGASUS- | Prevention of Cardiovascular TIMI 54 Events in Patients With Prior Heart Attack Using Ticagrelor Compared With Placebo on a Background of Aspirin–Thrombolysis in Myocardial Infarction 54 |
| PIONEER | The Open-Label, Randomized, Controlled, Multicenter Study Exploring Two Treatment Strategies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With Atrial Fibrillation Who Undergo Percutaneous Coronary Intervention |
| RE-DUAL-PCI | Randomized Evaluation of Dual Antithrombotic Therapy With Dabigatran Versus Triple Therapy With Warfarin in Patients With Nonvalvular Atrial Fibrillation Undergoing Percutaneous Coronary Intervention |
| STARS | Stent Anticoagulation Restenosis Study |
| TIMI | Thrombolysis in Myocardial Infarction |
| VKA | vitamin K antagonist |
| VTE | venous thromboembolism |
| WOEST | What Is the Optimal Antiplatelet and Anticoagulant Therapy in Patients With Oral Anticoagulation and Stenting |
Disclosures
Dr Cannon has received research grants from Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Janssen, Merck, and Pfizer and consulting fees from Aegerion, Alnylam, Amarin, Amgen, Applied Therapeutics, Ascendia, Boehringer Ingelheim, Bristol-Myers Squibb, Corvidia, HLS Therapeutics, Innovent, Janssen, Kowa, Merck, Pfizer, and Sanofi. Dr Cavender reports consulting fees from AstraZeneca, Boehringer Ingelheim, Edwards Lifesciences, Merck, and Sanofi-Aventis. He has received research funding (nonsalary) from Amgen, AstraZeneca, Bristol-Myers Squibb, Chiesi, GlaxoSmithKline, Novartis, and Takeda and research funding (salary) from Novo-Nordisk. The other author reports no conflicts.
Footnotes
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Source: https://www.ahajournals.org/doi/10.1161/CIRCINTERVENTIONS.119.008465
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