Take control of atrial fibrillation with expert insights and pearls from cardiologist, Dr. James Furgerson, in this jam-packed episode! You’ll learn why atrial fibrillation is such a big deal, how to diagnose it, how to treat it and when to call in for reinforcements. Dr. James Furgerson, MD is a cardiologist from San Antonio, Texas with over 20 years in academics. Buckle up – This episode is going to send your heart racing! You might even skip a beat!
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The power of the relationship between a patient and their primary care provider cannot be overstated! In this case, modifiable risk factors for atrial fibrillation: obesity, obstructive sleep apnea, hypertension and alcohol use disorder – to name a few – can and should be addressed early and often!
Long standing hypertension leads to left ventricular hypertrophy and elevated pressure in the left atrium (Note: it’s probably more complicated than that —listen to #150 HFpEF). This in turn causes dilation of the left atrium which disrupts the physiologic electrical conduction of the heart, setting the stage for atrial fibrillation. Less commonly, atrial fibrillation occurs in the setting of a structurally normal heart.
Symptomatic tachycardia and stroke risk are the major issues seen in patients with atrial fibrillation. Most patients with paroxysmal atrial fibrillation (i.e. suddenly starts and terminates spontaneously or with intervention within 7 days) respond well to rate control alone, typically with a beta-blocker such as metoprolol. Some patients may need two agents.
Other patients, such as those with concomitant heart failure may benefit from early rhythm control strategies, even though antiarrhythmic agents can be more difficult to manage. These patients may also be candidates for early ablation.
On the other end of the spectrum, young, highly-athletic patients may develop paroxysmal atrial fibrillation as a function of exercise-induced cardiac remodeling. These patients may be great candidates for an early ablation strategy for persistent symptoms.
The decision to initiate or defer anticoagulation is a complicated one, best handled through shared decision making via a patient centered approach.
Remember the CHA2DS2VASc score for calculating stroke risk in a patient (see this calculator from MDCalc).
The other side of the coin is bleeding risk which also must be considered and may be more nuanced than stroke risk. One place to start is the HAS-BLED score, an accepted risk calculator cited in the JACC’s ACC/AHA/HRS 2019 Update on Atrial Fibrillation (again, see this calculator from MDCalc).
Generally speaking, if a patient’s bleeding risk is not markedly elevated, a CHA2DS2VASc score ≥ 2 for men or ≥ 3 for women, indicated a patient who would benefit from anticoagulation.
What agent to start? Again, requires shared decision making via a patient centered approach. The non-vitamin K oral anticoagulants (NOACs) are excellent options for non-valvular (afib WITHOUT mod-to-severe mitral stenosis or a mechanical heart valve) but dosing must be done based on renal function. Vitamin-K antagonists (VKAs, warfarin in the U.S.) are the drug-of-choice for valvular atrial fibrillation.
Synchronized cardioversion (a shock delivered in synchrony with the patient’s native QRS complex) can be used to electrically convert a patient in atrial fibrillation to normal sinus rhythm in certain circumstances.
Patients with hypotension/hemodynamic instability, or those with pre-excitation on their EKG are good candidates for cardioversion which should be done without hesitation (i.e. TEE to check for mural thrombus is NOT required for emergency cardioversion).
Acute, ongoing ischemia with new-onset atrial fibrillation and rapid ventricular response – Class 1c recommendation for urgent cardioversion per 2014 ACC/AHA/HRS guideline
Highly symptomatic patients: Consider cardioversion. May defer TEE in patients with a known long-standing history of atrial fibrillation, adherent to chronic anticoagulation.
In some ways, this comprehensive reference discussing the pathophysiology, diagnosis and management of atrial fibrillation in numerous populations was the cornerstone for our discussion. We specifically examined the interplay between heart failure and atrial fibrillation with Dr. Furgerson. He mentioned the preferential use of rhythm control in atrial fibrillation when a patient is thought to develop heart failure secondary to their atrial fibrillation (see page e46 in the above document for more). Additionally, with respect to atrial fibrillation and heart failure in general, there is a IIa recommendation to combine digoxin (a rate and rhythm control agent) with a beta-blocker, if necessary to improve symptoms (see section 7.9).
This is an important update to the aforementioned guideline which we discussed during our show. Dr. Furgerson specifically pointed out the following:
In this 2002 landmark randomized controlled trial of > 4000 patients published in the New England Journal of Medicine, the investigators found no difference in survival benefit when comparing rate versus rhythm control in atrial fibrillation. Specifically, there was no statistically significant difference in 5-year mortality. However, there were statistically significant differences (favoring rate control) regarding rate of hospitalization, incidence of torsades and PEA/bradycardia. Dr. Furgerson discusses that, as a function of AFFIRM the 2014 ACC/AHA/HRS Guideline on Atrial Fibrillation states “routine use of a rhythm control strategy is not warranted for some patients” and that “an initial rate-control strategy is reasonable for many patients.” In Dr. Furgerson’s practice, he prioritizes addressing any reversible/modifiable conditions that may be associated with atrial fibrillation and then attempting a rate-control strategy with a beta blocker or calcium channel blocker.
This 2010 study was briefly discussed by Dr. Furgerson during our show. It was a randomized non-inferiority study of around 600 individuals with permanent or persistent atrial fibrillation, split into a lenient rate control group (<110 bpm) vs. a more strict rate control group (<80 bpm). The goal was to identify differences between the groups with respect to cardiovascular outcomes. To this end, the study focused on a composite CV end-point which included things like CV mortality, CHF, stroke, VTE and development of life-threatening arrhythmias. The researchers found lenient rate control was non-inferior to strict rate control & easier to achieve (not surprisingly!). Furthermore, there was a signal suggestive of fewer complications! Dr. Furgerson uses this study to support a lenient strategy in his patients…but only when the lenient strategy is sufficient to mitigate their symptoms.
While not a major point of discussion during our show PIONEER AF-PCI is an important study as it pertains to anticoagulation in patients with atrial fibrillation and CAD who require PCI. Traditionally, these patients have been placed on dual-antiplatelet therapy (DAPT) and warfarin. Dr. Furgerson, discussed the rise of NOACs and waning use of warfarin. Specifically, the PIONEER AF-PCI study placed patients into three basic groups: a full dose rivaroxaban + P2Y12 inhibitor group x 12 months (group 1), reduced-dose rivaroxaban + DAPT x 1, 6 or 12 months (group 2) or DAPT + warfarin x 1, 6 or 12 months (group 3). While the findings are a bit nuanced, the overall findings suggest greater risk of bleeding in those on warfarin than those not placed on warfarin. Furthermore, those that were spared warfarin did not have more in-stent thrombosis events, nor did they suffer from more strokes, MIs, or greater rates of CV mortality, although the study was limited in its ability to assess the efficacy of these agents on outcomes other than bleeding.
During the episode, we discussed catheter ablation and populations for which it can be beneficial. Dr. Furgerson cited some of the data from this 2018 study as it pertains to the potential benefits of early atrial fibrillation ablation in patients with HFrEF vs. medical therapy. The pathophysiologic underpinning is the thought that patient’s with HFrEF and thus, already compromised cardiac output, are even further compromised when in atrial fibrillation. Thus, the researchers postulated that getting these patients out of atrial fibrillation while reducing their pill burden & polypharmacy, could prove beneficial. The primary outcome was death or hospitalization for heart failure. Those randomized to the early ablation group had significantly fewer heart failure hospitalizations than those placed on medical therapy. It is important to note that this study had significant industry involvement in addition to very specific inclusion & exclusion criteria (ex. EF ≤ 35%, no prior ablation attempts) which impacts the generalizability of these findings.
Dr. Furgerson compared the findings of CASTLE-AF to the 2019 CABANA trial. In this study, there were many more patients enrolled with fewer inclusion criteria, as compared to CASTLE-AF. Therefore, the findings of this study also looking at catheter ablation vs. medical management in atrial fibrillation, are more generalizable in comparison. The primary outcome for this study was also a composite, looking at the incidence of death, disabling CVA, major bleeding or cardiac arrest. No statistically significant difference was found, although there was a high cross-over rate which may impact the results to some degree. During our discussion, this study along with CASTLE-AF frame Dr. Furgerson’s practice to consider referral for early antiarrhythmic use and early ablation in HFrEF patients, but generally not taking this approach with all-comers. Of course, there are other populations that may benefit from early ablation (such as young athletes, discussed in the show) but these folks generally fall outside the scope of either CASTLE-AF or CABANA (average age 68) .
While not discussed specifically, Dr. Furgerson wanted to include this study in the show notes as it pertains to our chat about cardioversion in atrial fibrillation. This study, published in 2019, looked at whether restoration of sinus rhythm by pharmacologic or electrical cardioversion within 48 hours of onset of atrial fibrillation was beneficial for return to sinus rhythm at 30 days. They concluded that a “wait-and-see” approach to cardioversion in new-onset atrial fibrillation was non-inferior to early cardioversion. The results can be explained by a spontaneous conversion to normal sinus rhythm that occurs in patients while receiving rate control.
Listeners will appreciate the significance of early diagnosis and management of atrial fibrillation, to include rate versus rhythm control, control of risk factors and need for anticoagulation.
After listening to this episode listeners will…
Provided in text above.
Dr . Furgerson reports no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.
Furgerson, James. Guest expert. “#159 Atrial Fibrillation”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list. July 8, 2019.
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Hi , just finished medical school and i still wondering what structural heart disease exactly means because we say it all the time but i dont know if all of us mean the same thing. Great episode just to the point!
Great question! I might start here: https://academic.oup.com/eurheartjsupp/article/12/suppl_E/E2/452925
This question and the responses intrigued me the most. References, please, to expand upon Dr. Fugerson's insights: "70:45 Atrial fibrillation during critical illness, after CABG and in hyperthyroidism" What do you do with ETOH, sepsis, PE-induced AF that is transient? CHADS it and treat or is there a more pragmatic approach? THanks Brad
Great question! I'm not sure that I can find you a citation necessarily - I can tell you what I've seen in practice and what I think most would do... ... Generally, favor treating over not treating. Outside of a-fib developing immediately after a cardiac procedure that is self-limiting, a-fib shouldn't really "pop up" in otherwise healthy hearts of those who are septic, develop hyperthyroidism, etc. These people likely have some degree of conductive disease which set them up for a-fib. Thus, you should CHA2DS2VASc / HASBLED them and treat accordingly. Down the road, in the right patient, you could certainly do a 4-week monitor and discuss the risks/benefits of stopping therapy, but that's a joint-decision on a case-by-case basis.