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2014 AF Treatment Guidelines: 10 Things to Like and Only One to Dislike
John MandrolaMarch 31, 2014
The "2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation" is here. I've read the entire 123 pages. Let's do this report in 10 categories (some with bulleted lists). I'll mix reporting with editorial comment. I'll try to keep it to one to two paragraphs per issue, and look for blatant editorial to be in italics. At the end, I'll offer one criticism.

The writers began strongly—with the obvious, which is often elusive.

1. Guidelines are for guidance. Let's start with this quote from the introduction (emphasis mine): "The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment about care of a particular patient must be made by the clinician and patient in light of all the circumstances presented by that patient." Writing committee chair Dr Craig January (University of Wisconsin, Madison) offered this nugget of self-awareness in the press release: "Because what we say in the guideline can affect how a drug is used, we were careful to be even-handed and evidence-based in presenting new drugs."

These two statements deserve emphasis because patient-centered care is threatened when guidelines morph into scripture. Good on the writers.

2. Nonvalvular AF gets a definition (sort of): From table 3: Nonvalvular AF is that which occurs in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral-valve repair. Hmm?

3. Atrial flutter gets special emphasis: Heart-rhythm doctors are seeing more atrial flutter. The increased incidence of typical flutter, which we painfully call cavotricuspid-isthmus (CTI) dependent, parallels the rise in obesity, sleep apnea, use of AF drugs, and advancing age of the populace. Our efforts in the left atrium—with ablation catheters—have brought us enhanced knowledge of the atypical forms of flutter.

The writers urge care with the flutter/fib diagnosis, specifically calling out the fact that "coarse" AF can be mistaken as atrial flutter—a common error in the real world. Also, efforts to distinguish typical from atypical flutter are important for counseling patients on expectations of ablation. The former is easy to ablate, and the latter is not.

4. Antithrombotic-therapy recommendations: Check this out.The very first class I recommendation: "In patients with AF, antithrombotic therapy should be individualized based on shared decision-making after discussion of the absolute and [relative risks] RRs of stroke and bleeding and the patient's values and preferences. Read that again. The patient-centric nature of that statement is a remarkable and welcome stand for experts to take. Thank you.

Let's do a bulleted list of other notables on stroke-prevention strategies:

Use the CHA2DS2-VASc score rather than the CHADS2 score.

Bleeding scores, such as HAS-BLED, REITE, and HEMORR2HAGES may be helpful in defining risk, but the evidence for using them for specific recommendations was not sufficient.

The non–vitamin K–antagonist anticoagulant (NOAC) drugs—dabigatran etexilate (Pradaxa, Boehringer Ingelheim), rivaroxaban (Xarelto, Bayer/Janssen Pharmaceuticals), and apixaban (Eliquis, Bristol-Myers Squibb/Pfizer)—were added to warfarin as preferred therapy.

Patients who struggle to maintain stable INRs may be considered for NOAC drugs. In my view, INR yo-yoing most often reflects deficits in patient education and/or adherence. Neither of these are necessarily good situations for the use of NOAC drugs.

Bridging strategies with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) came with strong wording to "balance the risks of stroke and bleeding." My take on bridging is that it's no small thing. So I am glad for this language.

In patients with AF who are undergoing stent placement, bare-metal stents could be considered as well as dual antiplatelet therapy (minus aspirin).

5. Little benefit with aspirin: This quote says a lot. "No studies, with the exception of the [Stroke Prevention in Atrial Fibrillation-1] SPAF-1 trial, show benefit for aspirin alone in preventing stroke among patients with AF."

The writers then use data that I quote often in the clinic. The Birmingham Atrial Fibrillation Treatment of the Aged (BAFTA) trial compared warfarin and aspirin in high-risk subjects greater than 75 years old. Those treated with warfarin had fewer strokes and similar rates of bleeding. Most striking: the risk of extracranial bleeding was 1.4% with warfarin and 1.6% with aspirin.

We were also urged to question the common practice of using aspirin in low-risk patients. Did you know "aspirin has not been studied in a low-risk AF population?"

6. Warfarin vs NOAC drugs: What was so notable about the discussion of how and why to choose between agents was what the writers did not say. They did not use the word superior, nor did they recommend one drug over another. Rather, a reader learned the pros, cons, and expectations of each drug. Good. Doctors and patients should be able to evaluate the results of the clinical trials that enrolled more than 50 000 patients and counted easy things to count, such as strokes, bleeds, and deaths.

7. Wait and see on LAA occlusion: Percutaneous left atrial appendage occlusion devices earned a couple of paragraphs, but no formal recommendations were made. Comments regarding surgical closure at the time of concomitant cardiac surgery were interesting. "The current data regarding LAA occlusion at the time of concomitant cardiac surgery reveals a lack of clear consensus because of the inconsistency of techniques used for surgical excision, the highly variable rates of successful LAA occlusion, and the unknown impact LAA occlusion may or may not have upon future thromboembolic events." On the matter of the left atrial appendage, put me down as skeptical on the idea that a focal strategy (LAA occlusion) can treat a systemic disease (stroke).

8. Rate control: There were not many surprises in the recommendations on rate control. Here are four topics worth mentioning:

Acute rate control: Ca-channel blocker vs beta-blocker? The clinical trials of acute rate control were performed in the 1980s and 1990s. These studies had variable end points and small sample sizes and were often from single sites. It is with great pleasure that I offer this quote: "Unless immediate rate control is required or an enteral route of administration is not available, oral administration is appropriate." Regular readers know how this column feels about using IV drugs when oral ones will do.

Be cautious with digoxin. The writers reiterate the pharmacology of digoxin and give mention to recent meta-analyses that suggest a possible signal of harm. Attention to digoxin's narrow therapeutic window is laudable.

Lenient rate-control strategy (less than 110 bpm) may be reasonable: The caveat is that patients remain symptom-free with preserved LV function. Noting the limitations of the RACE-II trial, the writers expressed worry that its findings may not apply well to a broad group of AF patients.

AV-node ablation and pacing earns a class IIa indication. The writers make it clear that this irreversible procedure has both benefits and risks. They also nudge us to think about the benefits of cardiac resynchronization therapy (CRT) pacing for patients who have undergone AV node ablation and have moderate to severe LV systolic dysfunction.

9. Rhythm control: The writers were clear that rhythm-control therapy of AF must be individualized. Four topics struck me as notable.

What's a reversible cause of AF? The writers say this: "Class I: Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended."

Here we have a real dilemma. In past guidelines, this sort of wording implied underlying causes like ectopic atrial tachycardia, hyperthyroidism, acute alcohol ingestion, infection, chronic obstructive pulmonary disease (COPD) exacerbation, or trauma. Okay. I get that. Fix those problems and AF might resolve itself. The interesting caveat now is that we know obesity, sleep apnea, hypertension, and metabolic syndrome are both precipitating and reversible causes of AF.

So, do the writers mean we should treat these problems before initiating rhythm control? Because if they do, there will be a lot fewer AF patients treated with AF drugs and ablation. It's provocative to even think that patients help themselves. But you see where failing in this regard got us with hypertension therapy—eg, drugs (and kidney ablation almost) get used as substitutes for lifestyle changes.

Big changes in AF ablation recommendations: AF ablation has been moved to first-line status for both paroxysmal and persistent AF patients. This welcome change aligns these guidelines with those from Europe. My previous post discusses many of the issues surrounding the decision-making in the initial approach to rhythm control.

Class III harm distinction added for two false beliefs . AF ablation should not be performed in patients who cannot be treated with anticoagulants, and AF ablation should not be done with the sole intent of avoiding anticoagulation. This might seem obvious to electrophysiologists but it is not well-known in the real world. A good add.

Don't forget about the surgical maze option: Both stand-alone and concomitant procedures are mentioned as options. This is a worthy addition because AF surgery offers selected patients reasonable options.