Atrial Fibrillation Treatment & Management: Approach Considerations, Risk-Management Decisions, Management of New-Onset AF (2022)

Long-term management of atrial fibrillation (AF) is focused on reducing the likelihood of AF recurrence, reducing AF-related symptoms, control of ventricular rate, and reducing stroke risk. As discussed previously, AF is often the result of established cardiovascular risk factors. Appropriate management of these risk factors will reduce the likelihood of future episodes of AF and AF-related morbidity and mortality. Anticoagulation with either aspirin or warfarin should be initiated for all individuals with AF, except in those with contraindications. Selection of the appropriate antithrombotic regimen for a given patient should be balanced between the risk of stroke and the risk of bleeding. Antiarrhythmic therapy can aid in maintenance of sinus rhythm in certain patients but requires close monitoring.

Optimal long-term strategies for AF management should be based on a thoroughly integrated consideration of patient-specific factors and likelihood of success. As a rule, younger patients with more severe symptoms and fewer comorbidities tend to derive greater benefit from a long-term focus on rhythm control. Older patients with structural heart disease (eg, left ventricular hypertrophy, prior myocardial infarction, depressed ejection fraction, atrial dilatation) are less likely to remain in sinus rhythm and are more likely to have serious side effects from antiarrhythmic drugs. In this cohort, most clinicians focus on long-term rate control.

Because of the electrophysiologic and structural remodeling caused by AF, many patients with paroxysmal AF will progress to persistent and long-standing persistent AF. The degree to which this reflects the continuing influence of underlying cardiovascular risk factors as opposed to a direct effect of AF is unknown. Regardless, clinicians need to reevaluate their management strategies frequently, as AF burden and comorbidities increase with time.

Anticoagulation

The goal of long-term anticoagulation in AF is to reduce the risk of thromboembolism. Patients in AF have a risk of stroke or peripheral embolism that is approximately five times that of individuals in sinus rhythm. Recommendations for anticoagulation for patients with nonvalvular AF are based on guidelines from a 2014 American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS) task force on the management of patients with AF. [1] Currently approved anticoagulants include warfarin, dabigatran, rivaroxaban, apixaban, and edoxaban.

Warfarin

Anticoagulation therapy with warfarin is significantly more effective than antiplatelet therapy (relative risk of 40%) if the international normalized ratio (INR) is adjusted. The INR goal in AF is usually between 2 and 3, except in patients who are at a significant risk for stroke (eg, patients with artificial valves, those with rheumatic heart disease, and those at a high risk for AF with recurrent prior strokes), in whom the INR should be maintained between 2.5 and 3.5. A lower INR goal (1.8-2) may be considered in elderly patients who are at high risk for a fall.

Anticoagulation clinics have shown more success and a lower complication rate than primary care physicians in controlling patients’ INR. In addition, one study reported that patients who used an Internet-based program for patient self-management of oral anticoagulant therapy achieved a higher mean time in the therapeutic range than patients whose INR was controlled by an established anticoagulation clinic. [72] Similar programs alone or in combination with regular care provided by anticoagulation clinics may improve the mean time that patients are in the therapeutic range and may further reduce the risk of stroke.

As patients with AF age, the relative efficacy of oral anticoagulation appears not to decrease, whereas the efficacy of antiplatelet therapy does appear to decrease. [73] A mutation in coagulation factor IX may cause spontaneous bleeding, even with an INR in the therapeutic range. Adverse effects of warfarin therapy are not limited to bleeding, however; other important side effects include skin necrosis within the first few days of therapy and cholesterol embolization to the skin or visceral organs in the first few weeks of therapy.

Several scoring systems have been developed to estimate risk-benefit for warfarin use in AF (summarized below).

The major adverse effect of anticoagulation therapy with warfarin is bleeding. Factors that increase this risk include the following:

  • History of bleeding (the strongest predictive risk factor)

  • Age older than 75 years

  • Liver or renal disease

  • Malignancy

  • Thrombocytopenia or aspirin use

  • Hypertension

  • Diabetes mellitus

  • Anemia

  • Prior stroke

  • Fall risk

  • Genetic predisposition

  • Supratherapeutic INR

Several risk models have been introduced. The risk model called HEMORR2HAGES assigns points to risk factors, as follows [74] :

Using this scoring, the risks of a major bleeding event per 100 patient-years of warfarin therapy are as follows:

  • 0 points: 1.9%

  • 1 point:2.5%

  • 2 points:5.3%

  • 3 points:8.4%

  • 4 points:10.4%

  • 5 or more points:12.3%

When the bleeding risk outweighs the benefit, avoidance of anticoagulation therapy in AF should be considered. In addition, because of its teratogenic effects, anticoagulation with warfarin is contraindicated in pregnant women, especially in the first trimester.

Dabigatran

Dabigatran (Pradaxa) is a direct oral thrombin inhibitor. The RE-LY study evaluated the efficacy and safety of two different doses of dabigatran relative to warfarin in more than 18,000 patients with AF. Patients were randomized to one of three arms: (1) adjusted-dose warfarin, (2) dabigatran 110 mg twice daily (BID), or (3) dabigatran 150 mg BID. Dabigatran 110 mg was noninferior to warfarin for the primary efficacy endpoint of stroke or systemic embolization, whereas dabigatran 150 mg was significantly more effective than warfarin or dabigatran 110 mg. Major bleeding occurred significantly less often with dabigatran 110 mg than with warfarin; dabigatran 150 mg had similar bleeding to that of warfarin. [75, 76]

A meta-analysis by Uchino and Hernandez evaluated the risk of myocardial infarction or acute coronary syndrome (ACS) with the use of dabigatran. The results suggest the risk of myocardial infarction or ACS was similar when using revised RE-LY trial results. Dabigatran is associated with an increased risk of myocardial infarction or ACS in an extensive range of patients when tested against different controls. [77]

A different meta-analysis involving more than 1000 patients found that major bleeding complications were generally less critical and more manageable in patients being treated with dabigatran than in those on warfarin therapy. For example, in patients treated with dabigatran, the worst major bleeds tended to be gastrointestinal, whereas in patients treated with warfarin, most of the worst bleeds were intracranial and therefore more difficult to treat. In addition, among patients with major bleeds, the dabigatran patients spent less time in intensive care and had a lower mortality rate than did the warfarin patients. [78, 79]

The US Food and Drug Administration (FDA) has approved the 150 mg BID dose—but not the 110 mg BID dose—of dabigatran for the management of patients with AF. The 75 mg BID dose has also been approved for patients with moderate renal failure (creatinine clearance of 15-29 mL/min). Patients with AF who are not candidates for dabigatran include those with prosthetic heart valves or hemodynamically significant valve disease, severe renal failure (creatinine clearance ≤15 mL/min), or advanced liver disease.

Rivaroxaban

Rivaroxaban (Xarelto) was approved by the FDA in November 2011 for nonvalvular AF. [80] It is a highly selective direct factor Xa inhibitor with high oral bioavailability, and with rapid onset of action. Clinical trial data have shown that it allows predictable anticoagulation with no need for dose adjustments and routine coagulation monitoring. [81]

Approval of rivaroxaban was based on the ROCKET-AF multinational, double-blind trial, in which the risk of major bleeding was similar for rivaroxaban and warfarin, but a significantly lower risk of intracranial hemorrhage and fatal bleeding was seen with rivaroxaban when compared with warfarin. [82] The studyincluded over 14,000 patients who were randomized to either rivaroxaban or warfarin; rivaroxaban 20 mg once daily was used for patients with normal renal function and 15 mg once daily for patients with mild renal failure (creatinine clearance of 30-49 mL/min). In the primary analysis of this study, rivaroxaban was found to be noninferior to warfarin for prevention of stroke or systemic embolism in patients with nonvalvular AF. [82] During the approval process, there was concern expressed over the amount of time the warfarin-treated patients spent at the optimal INR during the study (57.8%), which was lower than in other trials with warfarin (eg, RE-LY trial for Dabigatran). [75] Also, the participants of the ROCKET-AF trial had higher mean CHADS2 scores (3.67) when compared to those of the RE-LY trial (2.1).

Apixaban

Another factor Xa inhibitor, apixaban (Eliquis), was approved by the FDA in December 2012. Approval was based on two clinical trials: ARISTOTLE (Apixaban for Reduction in Stroke and Other Thromboembolic Events in AF) and AVERROES (Apixaban Versus Acetylsalicylic Acid [ASA] to Prevent Stroke in AF Patients Who Have Failed or Are Unsuitable for Vitamin K Antagonist Treatment). (Patients with serum creatinine of 2.5 mL/dL or greater were excluded from both apixaban trials.)

The ARISTOTLE trial compared apixaban with warfarin for the prevention of stroke or systemic embolism in 18,201 patients with AF and found that apixaban was superior to warfarin in preventing stroke or systemic embolism, caused less bleeding, and resulted in lower mortality. [83, 84, 85]

The AVERROES trial, which compared apixaban with aspirin in 5599 patients with AF for whom warfarin therapy was considered unsuitable, was stopped early (after 1.1 year) after an interim analysis because apixaban showed a significant reduction in stroke and systemic embolism compared with aspirin. [86] A modest increase of major bleeding was observed with apixaban compared with aspirin. [86]

(Video) Acute Atrial Fibrillation

Edoxaban

Edoxaban (Savaysa) was approved for the prevention of thromboembolism in AF by the FDA in January 2015 on the basis of results from the ENGAGE AF-TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation–Thrombolysis in Myocardial Infarction Study 48) trial. [87] This double-blind, noninferiority trial randomized 21,105 patients with nonvalvular AF to high-dose edoxaban (60 mg daily), low-dose edoxaban (30 mg daily), or warfarin (creatinine clearance up to 30 mL/minwas an exclusion criterion). Mean CHADS2 score for the subjects in this trial was 2.8. In intention-to-treat analyses, both doses of edoxaban were noninferior to warfarin for prevention of the stroke and systemic embolic events; however, there was a trend toward superiority for high-dose edoxaban (embolic risk of 1.57% with high-dose edoxaban compared to 1.8% with warfarin; P = 0.08). [87]

Of note, in participants with a creatinine clearance of 95 mL/min or greater, the hazard ratios (HRs) for developing embolic events were similar between the high-dose edoxaban and the warfarin groups. [87] Consequently, the FDA recommends avoiding edoxaban in patients with a creatinine clearance of 95 mL/min. [88] Both doses of edoxaban were reported to be superior to warfarin for all types of bleeding, except gastrointestinal bleeding wherein low-dose edoxaban was superior (HR: 0.67 (ie, 33% lower risk of bleeding);P< 0.001), whereas high-dose edoxaban was inferior to warfarin (HR: 1.23 [ie, 23% higher risk of bleeding]; P = 0.03).

A meta-analysis of four randomized trials involving 42,411 patients who received newer anticoagulants and 29,272 who received warfarin showed that, in patients with AF, the newer oral anticoagulants dabigatran, rivaroxaban, apixaban, and edoxaban protected against stroke or systemic embolism better than warfarin and had comparable safety profiles. [87, 89, 90, 91]

The newer anticoagulants also significantly reduced the incidence of all-cause mortality and intracranial hemorrhage, but increased gastrointestinal bleeding. Median follow-up periods ranged from 1.8 years to 2.8 years. The risk of stroke or systemic embolic events was reduced by 19% with the newer anticoagulants compared with warfarin; hemorrhagic strokes accounted for a large proportion of the reduction. Compared with warfarin, low-dose new anticoagulant regimens showed similar overall reductions in stroke or systemic embolic events and a more favorable bleeding profile, but significantly more ischemic strokes. [87, 89, 90, 91]

Newer oral anticoagulants versus warfarin

There are several advantages of using the newer oral anticoagulants over warfarin, including the following:

  • Predictable pharmacologic profiles with fewer drug–drug interactions, and dietary effects

  • Lower risk of intracranial bleeding

  • Rapid onset and offset of action, with no need for bridging with parenteral anticoagulant therapy during initiation or after interruption

  • No need for periodic INR testing

  • Superiority to warfarin for reducing the risk of thromboembolic events with dabigatran 150 mg BID and apixaban

Disadvantages of the newer oral anticoagulants include the following:

  • Requires strict compliance, because missing even a single dose could result in a period without anticoagulation

  • No FDA-approved reversal agents for rivaroxaban, apixaban, and edoxaban (currently under clinical trials) [92, 93]

  • Limited safety profile data for patients with severe kidney failure

  • No data for their use in the presence of mechanical heart valves (dabigatran was associated with increased risk of thromboembolic complications in patients with mechanical heart valves in the RE-ALIGN trial) or valvular AF, due to hemodynamically significant mitral stenosis

  • No data for their use in pregnant or lactating women, in children, or in patients with a recent stroke (≤7-14 days), reversible causes of AF, severe increase in blood pressure, and significant liver disease

  • Lack of reliable blood tests to ascertain therapeutic effect or toxicity

Reversal of anticoagulation

In the presence of acute major bleeding, emergent reversal of anticoagulation is required. Fresh frozen plasma is often utilized to reverse the effects of warfarin, but it takes 6-24 hours to achieve compete reversal. In more emergent settings, prothrombin complex concentrates (PCCs) can be used, because they provide complete reversal of anticoagulation in 15-20 minutes. [94]

For patients taking newer oral anticoagulants, several reversal agents have been developed; however, it should be noted that these newer anticoagulants have short half-lives (5-17 hours), and reversal is rarely indicated. Idarucizumab (Praxbind) is a monoclonal antibody fragment which binds with high affinity to dabigatran. Its efficacy was studied in the RE-VERSE AD trial (Reversal Effects of Idarucizumab on Active Dabigatran) in which 90 patients who were taking dabigatran and presented with serious bleeding or had a need for an urgent invasive procedure (< 8 hours) were given two doses of idarucizumab 15 minutes apart. As measured by laboratory testing, idarucizumab completely normalized coagulation parameters in 90% of patients within the first 10-30 minutes. Five thrombotic events and 18 deaths were reported, but there was no control group to compare the relative risk of thrombosis and death. [92]

Andexanet alfa targets and sequesters factor Xa inhibitors (rivaraoxaban, apixaban, edoxaban). This agent is currently under clinical trials and is not FDA approved. [93, 95]

Recommendations from the American Academy of Neurology (AAN)

In 2014, the AAN released level B and C recommendations on the prevention of stroke in patients with nonvalvular AF. The level B recommendations included the following [96, 97] :

  • Patients with nonvalvular AF should be informed that the potential benefit of antithrombotic treatment in reducing stroke risk must be weighed against an increased risk for major bleeding from such therapy.

  • Patients with nonvalvular AF and a history of transient ischemic attack (TIA) or stroke should routinely be offered anticoagulation therapy.

    (Video) Management of New Onset Atrial Fibrillation | Rate vs Rhythm Control

  • Dabigatran, rivaroxaban, or apixaban, which are associated with a lower risk of intracranial hemorrhage than warfarin, should be administered to patients with a higher intracranial bleeding risk.

  • Dabigatran, rivaroxaban, or apixaban should also be administered to patients who refuse or are unable to undergo frequent periodic testing of their INR.

  • Oral anticoagulants should routinely be offered to elderly patients (aged >75 years) with nonvalvular AF who do not have a history of recent, unprovoked bleeding or intracranial hemorrhage.

  • Patients with nonvalvular AF who have dementia or who suffer occasional falls can be offered oral anticoagulation, but patients or their families/caregivers should be informed that the risk-benefit ratio of such therapy is uncertain in patients who have moderate to severe dementia or who suffer very frequent falls.

  • In developing countries, where newer anticoagulants may be unavailable or too expensive, the guidelines state that in patients who have a moderate stroke risk, the use of the antiplatelet agent triflusal 600 mg/day in combination with moderate anticoagulation (INR 1.25-2.0) with acenocoumarol is probably more effective in reducing stroke risk than is the use of acenocoumarol alone at the higher INR (2.0-3.0).

  • A risk-stratification scheme should be used by clinicians to help them decide which patients with nonvalvular AF would particularly benefit from anticoagulation therapy, but it should not be the definitive means of making such decisions.

Postoperative and postdischarge anticoagulation therapy

Anticoagulation prior to and during an elective surgery may be continued or stopped depending on the patient’s risk of bleeding and risk of thromboembolism. If the risk of thromboembolism is high (stratified by the CHA2DS2-Vasc score) and the risk of bleeding is low, anticoagulation should be continued with the INR in the low therapeutic range. However, a high risk of bleeding during the procedure should prompt discontinuation of warfarin for 3-5 days prior to surgery. These patients should then be treated with heparin prior to and following the operation to allow discontinuation of anticoagulation if bleeding occurs.Newer anticoagulants can generally be discontinued 1-2 days before the surgery and do not require bridging with heparin or low molecular-weight heparin (LMWH).

In general, patients who develop AF only postoperatively do not need anticoagulation. Administration of preoperative and postoperative beta-blockers is usually sufficient, as postoperative AF is usually paroxysmal and tends to terminate spontaneously. The Colchicine for the Prevention of the Postpericardiotomy Syndrome (COPPS) AF Substudy found that the administering of colchicine appears to be safe and efficacious in the reduction of postoperative AF, which could potentially halve the complication and reduce the time a patient stays in the hospital. [98]

Research has shown that the administration of colchicine in patients who underwent pulmonary vein isolation helped to prevent early recurrences of paroxysmal AF. [99, 100] This process appeared to be mediated through a postablation reduction in inflammation.

A large cohort study in Denmark compared the bleeding risk of anticoagulants prescribed upon hospital discharge for AF: During mean follow-up (3.3 years), 11.4% of patients experienced a nonfatal or fatal bleeding episode. [101] The highest incidence for bleeding was observed for dual therapy with warfarin and clopidogrel and for triple therapy with warfarin, aspirin, and clopidogrel (3-fold higher risk) compared with single agent use. [101]

Omega-3 fatty acids

Several small trials have suggested that treatment for paroxysmal AF with prescription omega-3 fatty acids may provide a safe and effective treatment option. However, no benefit has been found to date. [102, 103]

Angiotensin-converting enzyme (ACE) inhibitors and ACE-receptor blockers (ARB)

Trials examining the incidence of AF in patients with heart failure who are treated with ACE inhibitors or ARBs have demonstrated a potential beneficial effect on AF recurrence. This recurrence is thought to be mediated by blocking the rennin-angiotensin-aldosterone system and the downstream effects on atrial mechanical and electrical remodeling. [104, 105, 106]

A study by Yusuf et al examined the effects of irbesartan in patients with permanent AF or at least two episodes of paroxysmal AF in the previous 6 months. [107] Irbesartan did not demonstrate a benefit in patients with AF who were already receiving an ACE inhibitor or patients in sinus rhythm. No reduction in cardiovascular death, stroke, or myocardial infarction was noted in the patient population studied.

Rate control

As discussed previously, several trials have validated the noninferiority of an initial rate-control strategy. Many clinicians believe, however, that an attempt at a rhythm-control strategy should be made in most patients. Older patients with comorbid cardiovascular disease have a lower likelihood of successful long-term rhythm control, and thus, these patients are often managed using a rate-control strategy. Some patients managed initially with a rhythm-control strategy will progress to recurrent or persistent AF. Clinicians often switch to a rate-control strategy as the AF burden increases.

Effectiveness of rate control should be assessed both at rest and with exertion, especially in patients who experience primarily exertional AF-related symptoms. Twenty-four hour Holter monitoring or exercise-treadmill testing can be helpful in evaluating heart rate variability.

Adequate rate control was previously defined as a heart rate of 60-80 bpm at rest and 90-115 bpm with moderate exercise. However, the ACC/AHA/HRS guidelines on the management of AF now advise that there is no benefit in achieving strict heart rate control (< 80 bpm at rest, < 110 bpm after a 6-minute walk) relative to more lenient rate control (< 110 bpm at rest). Strict rate control in patients with stable ventricular function is no longer recommended. [1]

AV nodal blocking medications are the cornerstone of rate control in long-standing AF. In the absence of an accessory pathway, oral beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin are effective. Generally, coadministration of beta-blockers and calcium channel blockers is reserved for patients in whom adequate rate control cannot be achieved with a single agent.

Digoxin can be effective in sedentary patients (especially in those with heart failure) but requires close monitoring of drug levels, serum electrolytes (potassium, magnesium), and renal function. Combinations of rate-control medications (eg, beta-blocker and digoxin) may be superior to individual agents in some patients.

Amiodarone may contribute to ventricular rate control. However, antiarrhythmic agents may organize AF to a potentially life-threatening atrial flutter with 1:1 AV conduction. Particularly with class IC agents, maintenance of effective AV nodal rate control is essential in most patients. Therefore, administration of a beta-blocker or calcium channel blocker is recommended before class IC drugs are initiated.

In the presence of tachycardia-mediated cardiomyopathy or inadequate ventricular rate control despite drug therapy, AV nodal ablation and permanent pacemaker implantation may be considered.

Rhythm control

Maintenance of sinus rhythm requires treatment of cardiovascular risk factors and any underlying disorder (eg, hyperthyroidism, sleep apnea) that may have triggered AF. As mentioned previously, several antiarrhythmic drugs (flecainide, propafenone, dofetilide, amiodarone) have an established efficacy in the pharmacologic conversion of AF to sinus rhythm. The noncardiac adverse effects and contraindications of each drug should be checked prior to administration.

Amiodarone, as a part of a strategy to achieve sinus rhythm, appears to be safe and effective in patients with persistent AF, according to Doyle and Ho. However, in their study, intolerable adverse effects were more common with amiodarone than with placebo or rate-control drugs. [108] Nevertheless, in patients with cardiac disease such as coronary artery disease or systolic or diastolic heart failure, amiodarone becomes the drug of choice because of its decreased proarrhythmic effects compared with other antiarrhythmic drugs. [71]

Amiodarone was also found to be more effective at maintaining sinus rhythm than other drugs in the Canadian Trial of Atrial Fibrillation (CTAF) and the Sotalol Amiodarone Atrial Fibrillation Efficacy Trial (SAFE-T). [109, 110]

Dronedarone is structurally similar to amiodarone, but it lacks amiodarone's iodine moieties. Although the lack of iodine moieties reduces the incidence of adverse events, dronedarone is less effective for rhythm control than amiodarone. [111] Dronedarone has been found to be associated with increased mortality in patients with permanent AF. The randomized, double-blind, phase III Permanent Atrial fibriLLation Outcome Study Using Dronedarone on Top of Standard Therapy (PALLAS) trial was halted following a preliminary review that revealed that dronedarone was associated with a 2-fold rise in risk of death. [112] Two-fold increases in two other endpoints, stroke and hospitalization for heart failure, were also noted when compared with placebo.

The FDA advises healthcare professionals not to prescribe dronedarone to patients with permanent AF. A separate study by Connolly et al also found that dronedarone increased rates of heart failure, stroke, and death from cardiovascular causes in patients with permanent AF who were at risk for major vascular events; the authors of that study suggested that dronedarone should not be used in this group of patients. [113] The 2014 ACC/AHA/HRS guidelines for the management of AF advise against using dronedarone for patients with New York Heart Association (NYHA) class III and IV heart failure or for patients who have had an episode of decompensated heart failure in the past 4 weeks. [1]

Several distinct agents, most notably sotalol, are used for the long-term maintenance of sinus rhythm. Sotalol is efficacious, but as with other class III drugs, it requires close monitoring of the QT interval and serum electrolyte levels. Sotalol is associated with the risk of QT interval prolongation and torsade de pointes. The proarrhythmic effect of sotalol is increased in patients with congestive heart failure (unlike dofetilide and amiodarone), so it is generally contraindicated in such patients or in those with a prolonged QT interval. Hypokalemia should be corrected and monitored prior to administration of sotalol because it may also prolong the QT interval. Sotalol can be used in patients with coronary artery disease. [71]

(Video) Management of atrial fibrillation- for USMLE Step 2 CK

In a study of 99 consecutive patients with persistent AF, atrial flutter, or both, patients whose AF responded to chemical cardioversion with dofetilide were particularly vulnerable to proarrhythmias. [114, 115] Of the 99 patients, 46 had successful cardioversion after an average of 2.2 doses of dofetilide, and 53 required electrical cardioversion after an average of 4.7 doses. Of the 21 patients who chemically converted with only one dose of dofetilide, 15 developed QT prolongation and had to either adjust their dose or discontinue treatment. In contrast, only one patient in the electrical conversion group had to discontinue treatment because of QT prolongation. In all, 2% of the patients in the electrical conversion group and 17% of those in the dofetilide-sensitive group had to discontinue treatment because of QT prolongation (P = 0.007). [114, 115]

Class III agents (sotalol, amiodarone) also have some beta-blocking effect and should be used with caution in patients with a history of bradycardia.

Class Ic drugs (flecainide, propafenone) increased the mortality risk in patients with coronary artery disease during the Cardiac Arrhythmia Suppression Trial (CAST) and therefore should not be used in these patients. [116]

Class Ic drugs increased the mortality risk in patients with coronary artery disease during the Cardiac Arrhythmia Suppression Trial (CAST) and therefore should not be used in these patients. [110]

Ablation (catheter based, surgical, or hybrid) for AF can also be performed for achieving rhythm-control. The ACC/AHA/HRS guidelines recommend catheter ablation in the following settings [1] :

  • It is useful for patients with symptomatic paroxysmal AF who are intolerant of, or whose condition is refractory to, at least one class I or III antiarrhythmic medication when a rhythm-control strategy is desired (class I, level of evidence [LOE]: A).

  • It is reasonable as a treatment for certain patients with symptomatic persistent AF who are intolerant of, or whose condition is refractory to, at least one class I or III antiarrhythmic medication (class IIa, LOE: A).

  • It is a reasonable initial strategy for rhythm control prior to using antiarrhythmic drug therapy for patients with recurrent symptomatic paroxysmal AF (class IIa, LOE: B).

Surgical ablation of AF is also an option for patients with AF undergoing other cardiac surgery and for those patients in whom pharmacologic and catheter-based procedures are ineffective or contraindicated. AF ablation may be superior to AV nodal ablation and biventricular pacing in heart failure patients but is technically difficult and demanding, and the widespread applicability of ablation in this population of patients is uncertain.

In the first randomized clinical trial comparing the efficacy and safety of catheter ablation versus minimally invasive surgical ablation during a 12-month follow-up, Boersma et al found that patients with AF who had a dilated left atrium and hypertension or who failed prior AF catheter ablation, surgical ablation was superior in achieving freedom from left atrial arrhythmias after 12 months of follow-up; however, the procedural adverse event rate was found to be significantly higher with surgical ablation than for catheter ablation, primarily postoperative pneumothorax, major bleeding, and an increased need for permanent pacing. [117]

Go to Catheter Ablation for complete information on this topic.

New medical and device-based rhythm-control therapies are being explored actively. Experimental and clinical data suggest that renin-angiotensin system (RAS) antagonists and HMG-CoA-reductase inhibitors (statins) may decrease the incidence of AF and increase the likelihood of successful cardioversion. [118, 119, 120, 121] Device-based therapies under investigation include single- and dual-site atrial pacemakers to prevent AF, as well as atrial defibrillators to rapidly restore sinus rhythm. Invasive (surgical and catheter-based) therapies to compartmentalize the atria and localize focal triggers (in the pulmonary veins) are being evaluated and refined.

Electrical cardioversion

Patients who are hemodynamically unstable, who have severe dyspnea or chest pain with AF, or who have preexcited AF should undergo urgent cardioversion. [71] In stable patients with symptomatic new-onset AF, the rate-control strategy may be considered first to control the ventricular rate. If rate-control treatment does not elicit a response or if echocardiography does not reveal any valvular or functional abnormality of the heart, cardioversion is indicated.

Direct current (DC) cardioversion is the delivery of electrical current that is synchronized to the QRS complexes; it can be delivered in monophasic or biphasic waveforms. The required energy for cardioversion is usually 100-200 J (sometimes higher energy is required) for monophasic waveforms and less for biphasic waveforms. The patient should be sedated. In patients with AF of relatively short duration in whom the left atrium is not significantly large, the success rate of cardioversion exceeds 75% (ie, the size of the left atrium and the duration of AF inversely correlate with the success rate of cardioversion).

Embolization is the most important complication of cardioversion. Accordingly, thrombus in the heart should be ruled out with transesophageal echocardiography (TEE), or anticoagulation should be provided for 3-4 weeks before cardioversion is performed. Stunning of the atria and stasis can occur after cardioversion, and this can lead to thrombus formation even though the patient is in sinus rhythm. Therefore, the patient should receive anticoagulants for at least 4 weeks following the procedure.

Other complications of electrical cardioversion may include pulmonary edema, hypotension, myocardial dysfunction, and skin burns, which may be avoided with the use of steroid cream and proper technique. Electrical cardioversion is also associated with some ST- and T-wave changes on electrocardiography (ECG) and may elevate levels of serum cardiac biomarkers. Synchronization prevents serious ventricular arrhythmias.

Placement of pads or paddle positions include anterior-lateral (ventricular apex and right infraclavicular) and anterior-posterior (sternum and left scapular), with at least one study suggesting increased efficacy with the anterior-posterior (AP) method.

Biphasic waveforms are proved to convert AF at lower energies and higher rates than monophasic waveforms. Strategies include dose escalation (70, 120, 150, 170 J for biphasic or 100, 200, 300, 360 J for monophasic) versus beginning with single high energy/highest success rate for single shock delivered. Patients who are stable and/or awake and can tolerate sedation should be pretreated, with typical regimens involving midazolam, fentanyl, and propofol.

Cardioversion of patients with implanted pacemakers and defibrillator devices is safe when appropriate precautions are taken. Keeping the cardioversion pads in an AP orientation ensures that the shocks are not directly over the generator. Alteration in pacer-programmed data has been reported, as well as heart block and elevated enzymes if the current is conducted through a pacer lead.

Pharmacologic cardioversion

Although pharmacologic cardioversion may be used as the first-line strategy, it is used mainly if DC cardioversion fails or, in some cases, as a precardioversion strategy.

Out-of-hospital self-administration of either flecainide 300 mg or propafenone 600 mg (weight-based dosages if >70 kg) was determined to be successful in terminating AF in 94% of episodes (mean time to symptom resolution of 133 minutes) by Alboni et al. The investigators studied outpatient treatment of AF with a “pill-in-the-pocket” approach in 268 patients with little or no structural heart disease presenting to the emergency department with symptomatic AF. [122]

Pretreatment with amiodarone, flecainide, ibutilide, propafenone, or sotalol has been shown to increase the success rate of DC cardioversion. [4] This strategy is also recommended when DC cardioversion fails and prior to repeat DC cardioversion. [4] Intravenous amiodarone is typically given as a 150-mg bolus over 10-15 minutes, followed by a continuous infusion of 1 mg/min for 6 hours and then 0.5 mg/min.

Hemodynamically unstable patients (eg, those with hypotension) may not tolerate antiarrhythmic drugs, and the adverse effects and contraindications of each antiarrhythmic drug should be considered carefully before administration. Because of possible proarrhythmic adverse effects of antiarrhythmic drugs, these patients should be monitored for at least 24 hours, requiring hospitalization in most cases.

TheFDA mandates inpatient monitoring for dofetilide initiation. Patients who start sotalol usually require inpatient monitoring (for torsade de pointes), although patients with no heart disease, with a QT interval less than 450 msec, and with normal electrolyte levels should be started on outpatient medications.

Special considerations

Postoperative AF is common, and perioperative beta-blockers are recommended in all patients undergoing cardiac surgery unless contraindicated. [123] Preoperative administration of amiodarone and sotalol may reduce the incidence of AF in patients undergoing cardiac surgery. As such, these agents may be used as prophylactic therapy in those at high risk for postoperative AF.

Postoperative AF was reduced by treatment with landiolol hydrochloride. [124] Amelioration of ischemia, an anti-inflammatory effect, and inhibition of sympathetic hypertonia by landiolol presumably reduced the occurrence of AF. Hypotension or bradycardia did not develop in any of the patients, indicating the safety of this beta-blocker. These findings suggest that landiolol hydrochloride could be useful in the perioperative management of patients undergoing cardiac surgery. [124]

Retrospective data suggest that atrial-based pacing (AAI, DDD modes) reduces the risk of developing AF and increases the interval between episodes in patients with sick sinus syndrome. [125]

(Video) Management of Atrial Fibrillation in critically ill patients

FAQs

What is the recommended approach to treatment of atrial fibrillation? ›

Cardioversion may be recommended for some people with atrial fibrillation. It involves giving the heart a controlled electric shock to try to restore a normal rhythm. Cardioversion is usually carried out in hospital so the heart can be carefully monitored.

What are the stages of AF? ›

The three main types of atrial fibrillation (A-fib) are: paroxysmal, persistent, and long-term persistent.

What is AF FVR? ›

By Jenna Fletcher on March 22, 2017. A-fib with RVR is the common term for atrial fibrillation with rapid ventricular response. A common disorder that involves a rapid heart rate, it requires medical attention and, in many cases, hospitalization.

What is AF a risk factor for? ›

Atrial fibrillation (A-fib) is an irregular and often very rapid heart rhythm (arrhythmia) that can lead to blood clots in the heart. A-fib increases the risk of stroke, heart failure and other heart-related complications.

What is the main cause of atrial fibrillation? ›

The basic cause of AFib is disorganized signals that make your heart's two upper chambers (the atria) squeeze very fast and out of sync. They contract so quickly that the heart walls quiver, or fibrillate. Damage to your heart's electrical system can cause AFib.

Which three drugs are commonly used for atrial fibrillation? ›

Three types of medications can be used to restore your normal heart rate: Beta-blockers such as atenolol (Tenormin), carvedilol (Coreg), and propranolol (Inderal) Calcium channel blockers such as diltiazem (Cardizem) and verapamil (Verelan) Digoxin (Lanoxin)

Is AF life threatening? ›

Atrial fibrillation is not usually life threatening, but it can be uncomfortable and often requires treatment. Treatment may involve: medicines to prevent a stroke (people with atrial fibrillation are more at risk of having a stroke) medicines to control the heart rate or rhythm.

What happens if AF is left untreated? ›

Heart failure

If your atrial fibrillation is persistent, it may start to weaken your heart. In extreme cases, it can lead to heart failure, as your heart is unable to pump blood around your body efficiently.

What foods should be avoided with atrial fibrillation? ›

7 Foods to Avoid When You Have Atrial Fibrillation
  • Alcohol. Alcohol tops the list of items to avoid on an atrial fibrillation diet. ...
  • Caffeine. ...
  • Grapefruit. ...
  • Cranberry Juice. ...
  • Asparagus and Leafy Green Vegetables. ...
  • Processed and Salty Foods. ...
  • Gluten.

What is the best position to sleep if you have AFib? ›

A left lateral recumbent position increases the dimensions of the left atrium and the right pulmonary veins and thereby increases local myocardial stress (Wieslander et al., 2019).

What is the first drug of choice for atrial fibrillation? ›

Amiodarone as a first-choice drug for restoring sinus rhythm in patients with atrial fibrillation: a randomized, controlled study.

Can stress cause atrial fibrillation? ›

Stress can contribute to heart rhythm disorders (arrhythmias) such as atrial fibrillation. Some studies suggest that stress and mental health issues may cause your atrial fibrillation symptoms to worsen.

What is the biggest risk factor for atrial fibrillation? ›

What are the risk factors for AFib? The risk for AFib increases with age. High blood pressure, the risk for which also increases with advancing age, accounts for about 1 in 5 cases of AFib.

Who is most at risk for AFib? ›

Typically people who have one or more of the following conditions are at higher risk for AFib:
  • Advanced age: The number of adults developing AFib increases markedly with older age. ...
  • High blood pressure: Longstanding, uncontrolled high blood pressure can increase your risk for AFib.
31 Jul 2016

How can you reduce the risk of atrial fibrillation? ›

The basics include not smoking, following a heart-healthy Mediterranean-style diet (high in plant-based foods, fruits and vegetables, and low in saturated fats), being physically active and keeping to a normal weight (as indicated on a body-mass index chart).

What foods cause AFib? ›

Certain foods, such as caffeine or alcohol, have the potential to trigger AFib. A diet that promotes heart health may help manage and reduce the symptoms of this condition.
...
Foods to eat for AFib.
Frequentlyvegetables whole grains olive oil fruits legumes
Less frequentlyfish chicken and turkey nuts and seeds eggs dairy
1 more row
30 Jun 2020

Can you live a normal life with AFib? ›

With proper treatment, individuals with atrial fibrillation can live normal and active lives. Atrial fibrillation, commonly referred to as AF or a-Fib, is the most commonly occurring arrhythmia, or heart rhythm problem. AF is characterized by an abnormal or irregular heart rhythm that causes a rapid heart rate.

Does sleeping position affect AFib? ›

Your sleeping position could be part of the problem if you have paroxysmal AFib. One study found that people who slept on their left sides reported more symptoms. This position may put more stress on your heart.

What are 5 medications that lower your heart rate? ›

Several drugs are available to slow the rate of heart.
...
List of drugs that slow the heart rate
  • metoprolol (Lopressor)
  • metoprolol succinate (Toprol-KL)
  • labetalol (Trandate), short-acting, 3-6 hours.
  • nadolol (Corgard)
  • nadolol (Coreg)
  • atenolol (Tenormin)
  • nebivolol (Bystolic)
  • acebutolol (Sectral), short-acting, 3-4 hours.

Which beta blocker is best for atrial fibrillation? ›

Bisoprolol* or metoprolol succinate are first-choice beta-blockers for patients with atrial fibrillation as they are prescribed once-daily and do not require dose adjustment in patients with renal impairment. Bisoprolol is preferred as it is more cardioselective than metoprolol and may cause more bradycardia.

What type of pacemaker is used for atrial fibrillation? ›

A patient who has a history of AF and needs a pacemaker for bradycardia should receive a physiological pacemaker (dual chamber or atrial) rather than a single-chamber ventricular pacemaker.

Is AFib a heart disease Yes or no? ›

Atrial fibrillation (AF) is a common heart rhythm condition that can cause stroke and heart failure. Read about AF symptoms, causes, risk factors and common triggers. You can also learn about treatment and find ways to manage your condition.

How long do people live with AFib? ›

Overall survival of patients with lone atrial fibrillation was 92% and 68% at 15 and 30 years, respectively, similar to the 86% and 57% rates for the age- and sex-matched Minnesota population (P=0.12, log-rank test; Figure 3A). Of the 76 patients with lone atrial fibrillation, 27 died during the 30-year follow-up.

How long can you stay in AFib? ›

Paroxysmal Afib lasts less than one week and usually stops on its own without treatment. (Paroxysmal is pronounced par-ək-ˈsiz-məl.) Persistent Afib lasts more than one week and needs treatment. Long-standing persistent Afib lasts more than a year and is sometimes difficult to treat.

Can AF cause heart failure? ›

Treatment and improving lifestyle is important because untreated AF can increase the risk of stroke, heart failure and other heart-related problems.

Does AFib damage the heart? ›

Answer :Atrial fibrillation can result in permanent heart damage, although that's fairly uncommon. The situation in which atrial fibrillation can cause permanent heart damage is if a patient develop atrial fibrillation and the heart rate ends up being very very rapid for a long period of time.

Is walking good for AFib? ›

In fact, walking can prove quite beneficial to the health and longevity of a person living with AFib. Why? Aside from its long-term health benefits, such as lower blood pressure and resting heart rate and improved mental well-being, walking can help reduce the onset of AFib symptoms.

Does drinking water help with AFib? ›

Stay Hydrated. If you're thirsty and your pee is a dark yellow color, you're probably dehydrated. That means you're more likely to have an AFib episode. Experts recommend that men drink about 15.5 cups of fluid per day.

Why does AFib happen at night? ›

A: It's not uncommon for atrial fibrillation (AFib) to occur at night. The nerves that control your heart rate typically are in sleep mode, and that's when your resting heart rate drops. Under these conditions, pacemaker activity from areas other than the normal pacemaker in the heart can trigger the onset of AFib.

Which side sleep is good for heart? ›

If you sleep on your right side, the pressure of your body smashes up against the blood vessels that return to your ticker, but “sleeping on your left side with your right side not squished is supposed to potentially increase blood flow back to your heart.” And anything you can do to help your most important organ pump ...

What a good night's sleep can do for your heart? ›

Good-quality sleep gives your heart the much-needed rest by reducing its work and lowering the blood pressure and heart rate at night. On the other hand, lack of sleep increases insulin resistance, a risk factor for the development of type-2 diabetes and heart disease.

Can lack of sleep cause atrial fibrillation? ›

Poor sleep is an independent risk factor for atrial fibrillation (AF), according to results of a new study. This suggests that patients with sleep apnea, insomnia, and others should be considered for AF screening as well.

What is the best drug for arrhythmia? ›

Beta blockers may stop the arrhythmia occurring but, more often, are useful for slowing down the heart rate during the arrhythmia without actually terminating it. Calcium channel blockers such as verapamil and diltiazem work in a similar way. Digoxin is also commonly prescribed for AF to help control the rate.

How do you feel when you have atrial fibrillation? ›

When you have atrial fibrillation, you might notice a skipped heartbeat, and then feel a thud or thump, followed by your heart racing for an extended amount of time. Or you might feel heart palpitations or fluttering or jumping of your heart. Or you might experience sweating or chest pain, mimicking a heart attack.

Can atrial fibrillation go away? ›

Paroxysmal atrial fibrillation is one of the types that starts suddenly and goes away own on its own. However, patients should still be monitored and treated. Usually, atrial fibrillation is permanent, and medicines or other nonsurgical treatments can't restore a completely normal heart rhythm.

How do you reverse AFib naturally? ›

Natural and Alternative Treatments for AFib
  1. Avoid stimulants.
  2. Get your nutrients.
  3. Stay hydrated.
  4. Supplements.
  5. Cut out gluten.
  6. Exercise and stress relief.
  7. Q&A.

Is age a risk factor for AFib? ›

Yes. Your risk of developing atrial fibrillation, a common heart rhythm disorder, increases as you become older. Atrial fibrillation is much more common in older adults. Atrial fibrillation can occur at any age, but when it develops in younger people, it's usually associated with other heart conditions.

What are the complications of atrial fibrillation? ›

If you have atrial fibrillation (Afib), your heart has episodes when it beats irregularly. The condition can cause troubling symptoms and serious medical complications, including blood clots that can lead to stroke and heart failure. Afib is a type of arrhythmia, or abnormal heart rhythm.

How do you stop AFib without medication? ›

You may be able to keep your heart pumping smoothly for a long time if you:
  1. manage your blood pressure.
  2. manage your cholesterol levels.
  3. eat a heart-healthy diet.
  4. exercise for 20 minutes most days of the week.
  5. quit smoking if you smoke.
  6. maintain a healthy weight.
  7. get enough sleep.
  8. drink alcohol in moderation.

How does caffeine affect atrial fibrillation? ›

Research suggests that caffeine isn't a cause of abnormal heart rhythms or atrial fibrillation, and drinking four to five cups of tea or coffee a day shouldn't increase your risk of developing coronary heart disease either. However, the effect of caffeine will vary between people.

What is the first drug of choice for atrial fibrillation? ›

Amiodarone as a first-choice drug for restoring sinus rhythm in patients with atrial fibrillation: a randomized, controlled study.

What is the safest medication for AFib? ›

Blood thinners (Aspirin and Heparin) can thin the blood and lower the risk of serious complications. Heart rate controlling medicines, such as beta-blockers that include Coreg (Carvedilol) and Lopressor and Toprol (Metoprolol), is the best way to treat AFib.

How long do you have to be in AFib before cardioversion? ›

Current guidelines support the well-established clinical practice that patients who present with atrial fibrillation (AF) of less than 48 hours duration should be considered for cardioversion, even in the absence of pre-existing anticoagulation.

How do you treat atrial fibrillation in the elderly? ›

What's the Treatment for AFib in Older Adults?
  1. Anticoagulation therapy. Experts suggest that older people with AFib take treatments to prevent blood clots. ...
  2. Percutaneous left atrial appendage closure. ...
  3. Antiarrhythmic drugs. ...
  4. Catheter ablation.
8 Jul 2022

What are 5 medications that lower your heart rate? ›

Several drugs are available to slow the rate of heart.
...
List of drugs that slow the heart rate
  • metoprolol (Lopressor)
  • metoprolol succinate (Toprol-KL)
  • labetalol (Trandate), short-acting, 3-6 hours.
  • nadolol (Corgard)
  • nadolol (Coreg)
  • atenolol (Tenormin)
  • nebivolol (Bystolic)
  • acebutolol (Sectral), short-acting, 3-4 hours.

What is the best position to sleep if you have AFib? ›

A left lateral recumbent position increases the dimensions of the left atrium and the right pulmonary veins and thereby increases local myocardial stress (Wieslander et al., 2019).

What drug prevents complications of atrial fibrillation? ›

Several antiarrhythmic drugs are commonly used to prevent atrial fibrillation recurrence, such as quinidine, flecainide, propafenone, sotalol, and dofetilide. Other antiarrhythmic agents, such as amiodarone, are used in an off-label fashion with great clinical efficacy.

Is a pacemaker better than ablation? ›

Catheter ablation of atrial fibrillation (AFib) is a safer, and more effective treatment for patients with tachycardia-bradycardia syndrome (TBS) than pacemaker implantation, according to a study published in Frontiers in Cardiovascular Medicine.

How do you stop atrial fibrillation fast? ›

At a minimum, these strategies may help you relax and cope with the episode until it stops.
  1. Engage in deep, mindful breathing. ...
  2. Get some exercise. ...
  3. Valsalva maneuver. ...
  4. Practice yoga. ...
  5. Put some cold water on your face. ...
  6. Contact a health professional.

How long can you live with AFib? ›

Overall survival of patients with lone atrial fibrillation was 92% and 68% at 15 and 30 years, respectively, similar to the 86% and 57% rates for the age- and sex-matched Minnesota population (P=0.12, log-rank test; Figure 3A). Of the 76 patients with lone atrial fibrillation, 27 died during the 30-year follow-up.

Do they shock your heart for A-fib? ›

Electrical cardioversion can help treat several different abnormal heart rhythms. It is commonly used to treat atrial fibrillation (AFib). With this condition, the atria of the heart quiver instead of beating the right way. Symptoms of AFib may include shortness of breath, fatigue, and a very fast heartbeat.

Can atrial fibrillation be caused by anxiety? ›

Stress can contribute to heart rhythm disorders (arrhythmias) such as atrial fibrillation. Some studies suggest that stress and mental health issues may cause your atrial fibrillation symptoms to worsen.

How long are you in the hospital after cardiac ablation? ›

What happens during catheter ablation

catheter ablation
Ablation describes any technique used to target and eliminate abnormal electrical signals from your heart. During cardiac ablation, a cardiologist (a doctor who specializes in heart conditions) uses hot or cold energy to create tiny scars in heart tissue, targeting the areas of your heart causing the arrhythmia.
https://my.clevelandclinic.org › health › 23047-heart-ablation
? A cardiologist performs catheter ablation in the hospital. You will need to stay at the hospital for six to eight hours after the procedure. Depending on your condition, you may go home that day or spend the night at the hospital.

Are there any new treatments for AFib? ›

Now, there is a solution for those patients. MU Health Care offers a left atrial appendage (LAA) closure procedure. It's a minimally invasive surgery that drastically reduces the chance of strokes for patients with nonvalvular AFib.

Is exercise good for AFib patients? ›

“And for people with AFib, regular exercise can help keep the condition in check,” Dr. Khan says. Researchers have found that among people who have atrial fibrillation, those who are most fit have the fewest AFib episodes. People with the lowest levels of fitness, by contrast, have more frequent episodes.

Can you live with AFib without treatment? ›

Paroxysmal AFib is episodes of symptoms that come and go and often get better without treatment. Persistent AFib is a constant abnormal heart rhythm that doesn't improve until you treat it. Permanent AFib is an abnormal heart rhythm that doesn't go away.

Videos

1. Paradigm Shift in Contemporary Atrial Fibrillation Management 2022
(APSC Asian Pacific Society of Cardiology)
2. Atrial Fibrillation Treatment- Medications
(Atrium Health)
3. Atrial Fibrillation: An Approach to Diagnosis and Management in the Emergency Department - EMplify
(EBMedicine)
4. WEBINAR: Anticoagulation in Atrial Fibrillation: "A Holistic Approach"
(SADEC)
5. Afib: Cardioversion for AF
(Canadian Cardiovascular Society)
6. Anticoagulation in Atrial Fibrillation - 3 Situations for Anticoagulation in AF & its Principles
(Last Second Medicine)

Top Articles

Latest Posts

Article information

Author: Barbera Armstrong

Last Updated: 08/27/2022

Views: 5506

Rating: 4.9 / 5 (59 voted)

Reviews: 82% of readers found this page helpful

Author information

Name: Barbera Armstrong

Birthday: 1992-09-12

Address: Suite 993 99852 Daugherty Causeway, Ritchiehaven, VT 49630

Phone: +5026838435397

Job: National Engineer

Hobby: Listening to music, Board games, Photography, Ice skating, LARPing, Kite flying, Rugby

Introduction: My name is Barbera Armstrong, I am a lovely, delightful, cooperative, funny, enchanting, vivacious, tender person who loves writing and wants to share my knowledge and understanding with you.