The next question is when anticoagulation therapy should be initiated in patients with AFib.  Based on robust data, the European Society of Cardiology (ESC) based their guidelines for an anticoagulant risk assessment scheme on the CHA₂DS₂-VASc score (Figure 5).[2]  The recently updated American Heart Association (AHA) guidelines are also now embracing the broader risk stratification with theCHA₂DS₂-VASc score.[3] Dr Bhatt reviews this scoring system in detail in his presentation (Bhatt, Figure 12).  This system improves on the older CHADS₂ score, particularly for individuals at lower risk of stroke, because an individual with a CHADS₂ risk of “0” still has a risk for ischemic stroke of about 2% per year.  Unfortunately too many clinicians tend to think that that is a trivial risk, but 2% per year is still high.

The other question concerns which anticoagulation approach is preferred.  At the base of the algorithm in Figure 5 are solid blue and red lines pointing to therapy with a NOAC, with dashed lines pointing to the vitamin K antagonists (VKA, warfarin).  This is because based on the data from the randomized clinical trials included in the recent meta-analysis[1] and listed in Figures 2–4, the ESC committee decided that a NOAC is the preferred therapy, with the VKA as a valid alternative.

The AHA guidelines, on the other hand, deviate from this position in that they state that if a patient’s warfarin is well controlled and the patient has access to anticoagulation clinics, and the patient’s preferences have been taken into account, then warfarin may be preferred.[3]  What the AHA is really saying is that all of these agents represent valid choices for the patient and the physician, as covered in our Roundtable Discussion.

A final point concerns antiplatelet prophylaxis.  Despite everything said in these presentations, it seems that it is still necessary to ask how it is possible that patients at risk of systemic embolism are still being treated with aspirin?  Part of this unfortunate practice may stem from a notion that aspirin is both providing some benefit and is “safer.”  Hopefully in our Roundtable Discussion we are able to dispel some of those misconceptions, particularly with regard to using aspirin in older patients, where there are known to be deleterious effects based on changes in the gastric mucosa and prostaglandins in patients aged >75 years.  Personally I believe that doctors have to continue to grapple with and overcome these misconceptions about antiplatelet therapy.