Perspective:

The following are 10 points to remember from this Joint Consensus Document:

1. Atrial fibrillation (AF) confers a substantial risk of mortality and morbidity from stroke and thromboembolism, and this common cardiac arrhythmia represents a major healthcare burden.

2. In AF patients, stroke risk must be assessed using the CHA₂-DS₂-VASc score, and bleeding risk must be assessed using the HAS-BLED score. Risk stratification is a dynamic process, and must be performed at regular intervals (i.e., on a yearly basis).

3. Where adjusted-dose vitamin K antagonist (VKA) is used, good quality anticoagulation control is recommended, with a time in the therapeutic range >70%.

4. When VKA is given in combination with clopidogrel and/or low-dose aspirin, the dose intensity of VKA should be carefully regulated, with a target international normalized ratio (INR) range of 2.0–2.5.

5. Where a non-VKA oral anticoagulant (NOAC) is used in combination with clopidogrel and/or low-dose aspirin, the lower tested dose for stroke prevention in AF (that is, dabigatran 110 mg BID, rivaroxaban 15 mg OD, or apixaban 2.5 mg BID) may be considered.

6. In a patient with AF and stable vascular disease (arbitrarily defined as being free from any acute ischemic event or repeat revascularization for >1 year), the patient should be managed with oral anticoagulation (OAC) alone (i.e., whether NOAC or a VKA).

7. Novel P2Y₁₂ receptor inhibitors (prasugrel and ticagrelor) should not be routinely part of a triple therapy regimen in patients with AF. The use of ticagrelor or prasugrel in combination with OAC may only be considered under certain circumstances (e.g., definite stent thrombosis while on clopidogrel, aspirin, and OAC).

8. In patients with stable coronary artery disease and AF undergoing percutaneous coronary intervention (PCI) at low bleeding risk (HAS-BLED 0–2), triple therapy (OAC, aspirin 75–100 mg daily, clopidogrel 75 mg daily) should be given for a minimum of 4 weeks (and no longer than 6 months) after PCI following which dual therapy with OAC (i.e., whether NOAC or a VKA) and clopidogrel 75 mg/day (or alternatively, aspirin 75–100 mg/day) should be continued for up to 12 months.

9. In the acute ST-segment elevation myocardial infarction (STEMI) setting, a patient with AF and STEMI may be treated with primary PCI, aspirin, clopidogrel, and heparin (unfractionated heparin) or bivalirudin, while glycoprotein (GP) IIb/IIIa inhibitors in bailout situations might be useful in some cases. Given the risk of bleeding with such combination antithrombotic therapies, it may sometimes be prudent to temporarily stop OAC therapy. Regular or even ‘routine’ use of GP IIb/IIIa inhibitors is discouraged, as are the novel P2Y₁₂ inhibitors.

10. Where patients have AF and a prosthetic mechanical heart valve, such patients would be at substantial risk of thromboembolism and/or prosthetic valve thrombosis during interruption of anticoagulation using a VKA. These patients should undergo percutaneous procedures during anticoagulation with VKA with the lowest possible median INR within the therapeutic range based on risk factors and prosthesis thrombogenicity.