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Periprocedural management of antithrombotic therapy in patients receiving long-term oral anticoagulation and undergoing percutaneous coronary intervention

Periprocedural management of antithrombotic therapy in patients receiving long-term oral anticoagulation and undergoing percutaneous coronary intervention
Literature review current through: Jan 2024.
This topic last updated: Mar 15, 2023.

INTRODUCTION — All patients who undergo percutaneous coronary intervention (PCI) are at risk of periprocedural bleeding, a complication that results from the combination of vascular puncture and periprocedural antithrombotic therapy, the latter of which generally includes aspirin, a P2Y12 receptor blocker, and a parenteral anticoagulant. This bleeding risk is further increased in any patient receiving chronic anticoagulant therapy. Approximately 5 percent of patients undergoing PCI are treated with long-term oral anticoagulation (OAC) for conditions such as atrial fibrillation, venous thromboembolism, or prior placement of a mechanical heart valve [1,2]. (See "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures", section on 'Cardiac catheterization'.)

The optimal periprocedural antithrombotic strategy in these patients depends on the relative risks of thrombosis in patients who have their anticoagulant temporarily stopped and bleeding risk if it is continued. These risks are also impacted by whether the patient is undergoing an elective or urgent procedure (eg, acute coronary syndrome).

This topic discusses issues surrounding the periprocedural management of antithrombotic therapy in patients on OAC undergoing PCI. The issues surrounding the care of patients who are candidates for longer-term dual antiplatelet therapy and anticoagulant therapy are discussed separately. (See "Coronary artery disease patients requiring combined anticoagulant and antiplatelet therapy".)

DEFINING THE ISSUES — The management of periprocedural antithrombotic therapy in patients undergoing percutaneous coronary intervention (PCI) is challenging because of the competing risks of thrombosis and bleeding. Interrupting anticoagulation for this procedure transiently increases the risk of periprocedural thromboembolism while continuing anticoagulant therapy may increase the risk of periprocedural bleeding. In addition, if the patient has a bleeding complication, the anticoagulant is often discontinued for a variable length of time, resulting in a longer period of increased thromboembolic risk. (See "Periprocedural bleeding in patients undergoing percutaneous coronary intervention".)

It is estimated that 5 to 10 percent of patients referred for PCI have a strong indication for long-term anticoagulation, with atrial fibrillation (AF) being the most common [3-7].

The following are pivotal questions in these patients:

Does the need for long-term oral anticoagulation change the choice and timing of oral antiplatelet regimen? (See 'Dual antiplatelet therapy' below.)

Can oral anticoagulant therapy be interrupted? This has major implications in patients receiving anticoagulants for prosthetic heart valves. In most of these specific patients with prosthetic valves requiring urgent PCI, it cannot be interrupted. (See 'Preprocedural anticoagulant management' below and "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures", section on 'Cardiac catheterization'.)

If interrupted, is preprocedural heparin bridging needed? (See 'Preprocedural anticoagulant management' below.)

Is intraprocedural heparin needed and if so, at what dose? (See 'Intraprocedural anticoagulant management' below.)

When should the first dose of oral anticoagulant be given after an uncomplicated procedure? (See 'Postprocedural anticoagulant management' below.)

Bleeding risk — There is no validated method for estimating the risks of bleeding in this setting. The HAS-BLED score is able to assess the bleeding risk in patients with AF who receive oral anticoagulation (OAC). However, in patients with PCI who receive dual antiplatelet therapy, the HAS-BLED score does not predict major bleeding events and in patients with PCI and AF, a modified HAS-BLED score is also unable to predict bleeding events [8-10]. (See "High bleeding risk patients undergoing percutaneous coronary intervention", section on 'Assessing individual patient risk'.)

Risk factors for bleeding include older age, female sex, low body weight use of the femoral artery for access (compared with the radial artery), age greater than 75 years, and baseline comorbidities such as anemia and chronic kidney disease.

Thrombotic (ischemic) risk — Patients at relatively low thrombotic risk include patients with older deep vein thrombosis or atrial fibrillation with lower CHA2DS2-VASc score. Those at relatively high or very high thrombotic risk include individuals with a mechanical mitral valve or high CHA2DS2-VASc score (table 1).

DUAL ANTIPLATELET THERAPY — Most anticoagulated patients undergoing percutaneous coronary intervention (PCI) will require one week to one month of triple antithrombotic therapy with aspirin, a P2Y12 receptor blocker, and an oral anticoagulant (OAC). The combination of aspirin and a P2Y12 receptor blocker is referred to as dual antiplatelet therapy (DAPT); aspirin plus clopidogrel is our preferred combination for patients receiving OAC in the first weeks after PCI. (See "Coronary artery disease patients requiring combined anticoagulant and antiplatelet therapy".)

Aspirin should be started as soon as the diagnosis of coronary artery disease is made. For patients not previously taking aspirin, we load with 162 to 325 mg and treat with 81 to 100 mg daily. The need for chronic OAC does not change the dose or timing of aspirin. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".)

For most patients who will require some period of combined anticoagulant and antithrombotic therapy, we prefer clopidogrel to one of the more potent P2Y12 receptor blockers (prasugrel or ticagrelor), including patients who are being treated for an acute coronary syndrome. This recommendation is based on the following observations:

The randomized trials of DAPT in stable patients used clopidogrel rather than more potent P2Y12 receptor blockers.

There is an increase in the baseline bleeding risk in individuals taking OAC therapy and DAPT. Thus, even in acute coronary syndrome patients who would ordinarily receive a more potent P2Y12 receptor blocker, we prefer clopidogrel. (See "Coronary artery disease patients requiring combined anticoagulant and antiplatelet therapy", section on 'Bleeding' and "Acute non-ST-elevation acute coronary syndromes: Early antiplatelet therapy", section on 'Invasive management' and "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Patients receiving primary PCI'.)

Exceptions include those who are allergic to clopidogrel and those with prior stent thrombosis while taking clopidogrel. In patients who are considered for triple therapy, typically in most clinical practices, aspirin is used only for the shortest period of time (some people would say only one week), and then the patient is continued on clopidogrel and the oral anticoagulant.  

The timing and dose of clopidogrel is as follows:

For patients undergoing urgent PCI, we load with 600 mg at the time of diagnosis and continue 75 mg daily. In patients who present with an acute coronary syndrome while taking clopidogrel, we typically reload with either 300 or 600 mg. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'P2Y12 use' and "Acute non-ST-elevation acute coronary syndromes: Early antiplatelet therapy", section on 'P2Y12 use'.)

For stable patients whose coronary anatomy is not known and who are scheduled for diagnostic coronary angiography with possible PCI, we suggest withholding clopidogrel (600 mg loading dose) until after diagnostic coronary angiography, as many patients will either not have disease that needs revascularization or will have disease that requires coronary artery bypass surgery. Patients with prior diagnostic coronary angiography who are scheduled for PCI should receive clopidogrel (600 mg loading dose) at least two hours before PCI. (See "Antithrombotic therapy for elective percutaneous coronary intervention: General use", section on 'P2Y12 receptor blockers'.)

There are limited data on the role of newer P2Y12 inhibitors as part of triple therapy. In a prospective observational study of 377 patients who underwent drug-eluting stent placement and who had an indication for OAC, 5.6 percent received prasugrel and the rest clopidogrel [11]. All patients were treated with triple therapy for at least six months. The primary end point of Thrombolysis In Myocardial Infarction major and minor bleeding occurred more often in the prasugrel group (28.6 versus 6.7 percent; adjusted hazard ratio [HR] 3.2, 95% CI 1.1-9.1). There was no significant difference in the composite secondary end point (death, myocardial infarction [MI], ischemic stroke, or definite stent thrombosis). In this study, in most patients, the indication for prasugrel was high platelet reactivity on clopidogrel. (See "Clopidogrel resistance and clopidogrel treatment failure", section on 'Definitions'.)

In the RE-DUAL PCI trial, 2725 OAC patients who underwent DES placement were randomized to dabigatran 110 or 150 mg with P2Y12 inhibitor (ticagrelor or clopidogrel), or warfarin with P2Y12 inhibitor (ticagrelor or clopidogrel) and aspirin. In the group of patients treated with ticagrelor, the study treatment-independent incidence of the first ISTH major or clinically relevant nonmajor bleeding event was 26.3 percent, and in those treated with clopidogrel 20.1 percent (multivariable adjusted HR 1.35; 95% CI 1.05-1.72) [12,13].

PREPROCEDURAL ANTICOAGULANT MANAGEMENT — In most patients, we do not attempt to reverse (either with a reversal agent or by letting the anticoagulant effect wear off) the anticoagulant effect of the long-term anticoagulant prior to percutaneous coronary intervention (PCI). Arterial access using the radial artery significantly lowers the risk of access site bleeding and is part of the rationale for not reversing oral anticoagulation (OAC). (See 'Access site' below.)

Urgent patients — In patients taking long-term OAC who require urgent or emergent PCI, there is generally not sufficient time to stop the OAC (and its anticoagulant effect). By default, management decisions move to the periprocedural period. (See 'Intraprocedural anticoagulant management' below.)

Elective patients — For all patients, we assess the relative risk of periprocedural bleeding if anticoagulant is continued and thrombosis if it is withheld. Bleeding risk is discussed above. (See 'Bleeding risk' above.)

After considering the thrombosis and bleeding risks, we hold anticoagulant therapy only for those with a low thrombotic risk and high bleeding risk. For most patients taking direct-acting oral anticoagulants (DOAC; also referred to as non-vitamin K oral anticoagulants [NOAC]; eg, dabigatran, apixaban, rivaroxaban, or edoxaban) (see "Direct oral anticoagulants (DOACs) and parenteral direct-acting anticoagulants: Dosing and adverse effects"), we do not attempt to reverse the anticoagulant effect with newer reversal agents. For most patients taking warfarin, we do not routinely reverse its effect with vitamin K or fresh frozen plasma because with the former, reinitiation of warfarin is more difficult with uneven variation in INR until a stable level of warfarin has been reached.

In addition to the comments below, the management of warfarin prior to PCI is discussed in detail elsewhere. (See "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures".)

The following are guidelines for when to administer the last preprocedural anticoagulant dose:

For elective patients taking DOACs, we continue therapy until 24 hours before the procedure. In patients with renal insufficiency, we give the last dose 36 to 48 hours before the procedure, particularly with dabigatran. A detailed discussion of when to stop DOACs is found elsewhere. (See "Perioperative management of patients receiving anticoagulants", section on 'Timing of anticoagulant interruption'.)

When DOACs are temporarily paused, there is no need for bridging with low molecular weight heparin/unfractionated heparin. No study has shown a reduction in periprocedural thrombotic or embolic cardiovascular events with heparin bridging and at least two studies have shown an increase in periprocedural bleeding [14].

For patients taking warfarin, we measure the international normalized ratio (INR) in advance (at least two days) of the procedure. We make adjustments to the warfarin dose to allow the INR to be at the lower end of the target range (2.0 to 2.5) the morning of the procedure. If it is anticipated that a large sheath will be placed in the femoral artery, we may hold warfarin for longer and allow the INR to fall below 2.

In most cases we do not bridge with heparin even if the INR falls below 2. Exceptions include those with very high thrombotic risk such as mechanical heart valves, particularly in the mitral position or older aortic mechanical valves, those atrial fibrillation patients with a CHA2DS2-VASc score >5, patients with recent ischemic stroke within three months, or recent venous thromboembolism within three months.

Our recommendations regarding the preprocedural management of OAC in patients referred for elective PCI are based on observations only; randomized trials or high-quality observational studies are not available. Our approach to performing PCI without warfarin interruption (but at the lower end of the therapeutic INR level) is based on evidence obtained in other populations [15]:

The BRUISE CONTROL trial randomly assigned patients on warfarin undergoing implantation of a cardiac implantable electronic device to continuation of warfarin or heparin bridging [16]. This trial found a lower risk of bleeding in patients who continued warfarin. (See "Cardiac implantable electronic devices: Periprocedural complications", section on 'Bleeding'.)

A benefit of warfarin continuation rather than discontinuation with bridging was reported in the COMPARE trial, which randomly assigned patients with atrial fibrillation undergoing catheter ablation to continued warfarin or discontinuation of warfarin with bridging. In this trial, patients assigned to the warfarin group had a lower risk of stroke and less bleeding. (See "Catheter ablation to prevent recurrent atrial fibrillation: Anticoagulation", section on 'Patients taking long-term vitamin K antagonist'.)

A 2010 meta-analysis of eight moderate- to low-quality studies of patients undergoing elective coronary angiography with or without PCI found that a strategy of uninterrupted vitamin K antagonist lowered the risk of access site bleeding by approximately 50 percent, compared with interrupted vitamin K antagonist [17].

INTRAPROCEDURAL ANTICOAGULANT MANAGEMENT — Similar to preprocedural issues, intraprocedural decisions regarding antithrombotic therapy have not been well studied in patients taking long-term oral anticoagulant (OAC).

Our approach — The following are the sequential steps we take to optimize antithrombotic care during the procedure:

As the risk of bleeding at the catheterization site is significantly lower with the use of the radial artery, we prefer it to the femoral artery if possible in most patients. (See 'Access site' below and "Periprocedural complications of percutaneous coronary intervention", section on 'Radial artery access' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Radial artery'.)

We give intraprocedural unfractionated heparin to most patients, irrespective of whether the long-term anticoagulant is warfarin or a direct-acting oral anticoagulant (DOAC; also referred to as non-vitamin K oral anticoagulants [NOAC]). We acknowledge that there is some (weak) evidence to suggest that heparin may be omitted in patients taking therapeutic dose of warfarin [18]. (See "Anticoagulant therapy in non-ST elevation acute coronary syndromes", section on 'Anticoagulant Use' and "Antithrombotic therapy for elective percutaneous coronary intervention: General use", section on 'Heparin' and "Acute ST-elevation myocardial infarction: Management of anticoagulation", section on 'Primary percutaneous coronary intervention'.)

If the international normalized ratio (INR) is <2, we given full dose heparin.

For patients taking warfarin, we reduce the normal heparin dose if the INR is >2 and <2.5, we use reduced doses of heparin, and we typically keep the activated clotting time on the low side (200 to 225).

We prefer to delay elective PCI if the INR is >2.5. For patients with an INR >2.5 who must have PCI that day, we reduce the dose of heparin even further.

The use of glycoprotein (GP) IIb/IIIa inhibitors should be minimized. (See 'Use of GP IIb/IIIa inhibitors' below.)

Access site — In most patients undergoing PCI, access using the radial rather than the femoral artery decreases the risk of periprocedural bleeding. As patients receiving OAC therapy are at particularly high bleeding risk, we prefer radial access in most cases if possible. This issue is discussed in detail elsewhere. (See "Periprocedural bleeding in patients undergoing percutaneous coronary intervention", section on 'Access site' and "Periprocedural complications of percutaneous coronary intervention", section on 'Radial artery access' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Radial artery'.)

If a transradial approach is not an option, we strongly recommend using a micropuncture technique and ultrasound guidance. The use of a femoral vascular closure device (VCD) in patients on oral anticoagulation has shown that VCDs reduced the occurrence of pseudoaneurysms and time to hemostasis [19]. We choose the smallest diameter femoral sheath possible.

Stent type — For most anticoagulated patients undergoing PCI, we recommend newer-generation drug-eluting stents (DES) rather than bare metal stents (BMS) based on their superiority with regard to the rate of restenosis and their lower rate of stent thrombosis in many circumstances. (See "Intracoronary stents: Stent types".)

Use of GP IIb/IIIa inhibitors — In some patients undergoing PCI, antiplatelet therapy with intravenous GP IIb/IIIa inhibitors may be beneficial. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Summary and recommendations' and "Antithrombotic therapy for elective percutaneous coronary intervention: General use", section on 'GP IIb/IIIa inhibitors' and "Acute non-ST-elevation acute coronary syndromes: Early antiplatelet therapy", section on 'Invasive management'.)

However, due to the higher bleeding risk in patients who receive this class of antiplatelet therapy, we are very restrictive of their use in patients with concomitant OAC. We limit the use of these agents in our patients to those with a suboptimal angiographic result or those with a very high-risk lesions (large thrombotic burden in patients who have not received adequate clopidogrel load in time prior to the procedure).  

POSTPROCEDURAL ANTICOAGULANT MANAGEMENT — All patients should be reassessed for their need for chronic anticoagulation prior to reinitiation. This should include consideration of other approaches that could be used to avoid the need for long-term anticoagulation such as left atrial appendage occlusion. For patients in whom oral anticoagulant (OAC) will be restarted, and assuming no significant postprocedural bleeding has occurred, the next major decision is when to restart OAC.

The optimal time to restart anticoagulant therapy after percutaneous coronary intervention (PCI) is not known. For most patients, the goal is to restart anticoagulation as soon as possible after PCI. In the absence of evidence to support one approach or another, we suggest the following:

For patients who did not take their OAC the morning of the PCI, we restart OAC therapy the evening after the procedure in patients without evidence of bleeding, particularly if they have undergone radial artery access.

For patients treated with a femoral artery approach, it is reasonable to restart a newer OAC the morning following the procedure.

For patients at very high risk of thrombosis (eg, mechanical heart valves, high CHA2DS2-VASc score) who are taking warfarin, we continue therapeutic heparin after the procedure until the international normalized ratio (INR) is therapeutic. The INR should be monitored closely, particularly in the first four weeks after discharge (high-risk period for hemorrhage). This is particularly important for the uncommon patient in whom vitamin K was administered as it affects the INR for some time.

In the presence of significant, ongoing postprocedural bleeding, we delay initiation of OAC therapy. Similar to all patients, the timing of initiation must take  into account the benefits and risks of doing so.

If significant bleeding occurs after the procedure and the patient’s INR on warfarin before the procedure was >2, the use of fresh frozen plasma may be an option. (See "Warfarin and other VKAs: Dosing and adverse effects".)

PERIPROCEDURAL BLEEDING — If active bleeding is present or develops, or the international normalized ratio on warfarin is very high, we consider using vitamin K or fresh frozen plasma. This issue is discussed in detail elsewhere. (See "Periprocedural bleeding in patients undergoing percutaneous coronary intervention".)

RECOMMENDATIONS OF OTHERS — Major societal guidelines do not address the issue of how to manage patients taking oral anticoagulant therapy who are referred for percutaneous coronary intervention in any detail.

Our recommendations are generally consistent with those made in the 2020 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation, the 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines, and the 2021 European Heart Rhythm Association Practical Guide on the use of non-vitamin K antagonist anticoagulants in patients with nonvalvular atrial fibrillation [20-22].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Anticoagulation" and "Society guideline links: Percutaneous coronary intervention".)

SUMMARY AND RECOMMENDATIONS

Defining the issues – In patients who undergo percutaneous coronary intervention (PCI) with stenting, chronic oral anticoagulant (OAC) therapy, when added to dual antiplatelet therapy, increases the risk of periprocedural bleeding. Our recommendations for managing this increase in risk follow. (See 'Defining the issues' above.)

Approach in stable patients – For stable patients, we recommend clopidogrel rather any other P2Y12 receptor blocker (Grade 1A). For patients with acute coronary syndrome, we recommend clopidogrel rather any other P2Y12 receptor blocker (Grade 1C). (See 'Dual antiplatelet therapy' above.)

Patients who are taking warfarin – For patients taking warfarin, we measure the international normalized ratio (INR) in advance (at least two days) of the procedure. We make adjustments to the warfarin dose to allow the INR to be at the lower end of the target range the morning of the procedure. If it is anticipated that a large sheath will be placed in the femoral artery, we may hold warfarin for longer and allow the INR to fall below 2. We suggest this method rather than allowing return of normal clotting status (Grade 2B). (See 'Preprocedural anticoagulant management' above.)

In most cases, we do not bridge with heparin even if the INR falls below 2. Exceptions include those with very high thrombotic risk.

Patients who are taking direct-acting oral anticoagulant – For patients receiving a direct-acting oral anticoagulant (DOAC; also referred to as non-vitamin K oral anticoagulants [NOAC]), we stop the last dose about 24 hours before the procedure in elective cases rather than stopping sooner (Grade 2B).

Intraprocedural anticoagulation – We give intraprocedural heparin to most patients. For patients taking warfarin, we reduce the normal heparin dose if the INR is >2 and reduce it further if it is >2.5. (See 'Intraprocedural anticoagulant management' above.)

We prefer the radial access in most cases, as it decreases the risk of periprocedural bleeding. If the femoral access has been chosen, we encourage the use of micro-puncture technique closure devices. (See 'Access site' above.)

Periprocedural timing – The timing of restarting OAC depends on factors such as risk of thrombosis off anticoagulant, access site used, and the timing of the last dose of anticoagulant prior to the procedure. For patients who did not take their OAC the morning of the PCI, we restart OAC therapy the evening after the procedure in patients without evidence of bleeding, particularly if they have undergone radial artery access. (See 'Postprocedural anticoagulant management' above.)

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