Dr. Allen. I agree that there is concern about the lack of reversibility, but I think it has been completely overplayed. In the pivotal trials, patients who bled on DOAC therapy actually had better outcomes than those that bled on warfarin. This includes intracranial hemorrhage. There was a paper published in Stroke in 2012 that evaluated the subgroup of patients in the RE-LY trial that suffered intracranial hemorrhage. Patients on dabigatran actually fared better despite a lack of a specific reversal agent. When evaluating the available data about reversal of the DOACs, I’m not 100% convinced that we’re significantly impacting outcomes by reversing these agents. We’re certainly running up the bill, but are we treating the patient or treating the providers? As long as the renal function remains intact, the DOACs clear quickly, perhaps more quickly than warfarin can typically be reversed with standard reversal agents.
Dr. Minichiello. Remember that this patient has a history of a GI bleed. We are going to start him on full-dose anticoagulation for stroke prevention for his nonvalvular AF. He’s also on aspirin, and he has stable coronary disease. He does not have any stents in place but he did have a remote non-ST elevation myocardial infarction (MI) a number of years ago. Do we feel that the risk of dual therapy—anticoagulation combined with antiplatelet therapy—outweighs the risks? And how do we approach that risk?
Dr. Barnes. This is an important point to discuss. There has been a lot of discussion in the literature recently. When I start this type of patient on an oral anticoagulant, I try to discontinue the antiplatelet agent because I know how much bleeding risk that brings. The European guidelines (for example, Eur Heart J. 2014;35[45]:3155-3179) have been forward thinking with this for the last couple of years and have highlighted that if there’s an indication for anticoagulation for patients with stable coronary disease, meaning no MI and no stent within the past year, then we should stop the antiplatelet agents after a year in order to reduce the risk of MI. This is based on a lot of older literature where warfarin was compared with aspirin and shown to be protective in coronary patients, but at the risk of bleeding.
It’s important because there have been recent studies that have raised questions, including a recent Swedish article in (Circulation. 2017;136:1183-1192) that suggested discontinuing aspirin led to increased mortality. But it’s important to look at the details. While that was true for most patients, it was not true for the group of patients who were on an oral anticoagulant. Many colleagues ask me questions about that particular paper and its media coverage. I tell them that for our patients on chronic oral anticoagulants, the paper supports the notion that there is not increased mortality when aspirin use is stopped. We know that aspirin plus an anticoagulant leads to increased bleeding, so I try to stop it for patients who have stable CAD but are on long-term anticoagulation.
Dr. Allen. This isn’t a new thought. Back in early 2012, the 9th edition of the American College of Chest Physicians (CHEST) Antithrombotic Guidelines probably gave us the best guidance that we had ever seen to help us address this issue. Since that time the cardiology guidelines have caught up to recommend that we do not need additional antiplatelet therapy for stable CAD, and, in fact, it should be limited even in the setting of acute coronary syndromes and percutaneous coronary intervention (PCI).
Dr. Minichiello. That’s a good point because people are not necessarily clear about when there would be an indication to continue dual therapy and when it is safe to go to monotherapy. Scenarios where benefit of dual therapy may outweigh risk suggested in the CHEST 2012 guidelines include acute coronary syndrome or a recent stent, high-risk mechanical valves, and history of coronary artery bypass surgery.
I think the important thing is to consider each case individually and not to reflexively continue aspirin therapy. Often what we see is once on aspirin—always on aspirin. Being thoughtful about it, we should acknowledge that it likely results in a 2-fold increased risk of bleeding and make sure that we believe that the benefit outweighs the risk.
Dr. Allen. I agree. We probably have better evidence in the CAD population, but what do we do for patients with significant peripheral vascular disease, or those patients with symptomatic carotid stenosis or history of strokes? Some of the European guidance suggests taking a similar approach to CAD, but these are the patients for whom stopping aspirin makes me more nervous.
Dr. Parra. This is a perfect example of where less is more. All too often the reflex is to continue aspirin treatment indefinitely because the patient has a history of acute coronary syndrome or even peripheral arterial disease, when the best thing to do would be to drop the aspirin. It involves an individualized risk assessment and underscores the need to periodically do a risk/benefit assessment in all patients on anticoagulants, whether it’s warfarin or a DOAC.