You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1 Cicely Anne Dye -- 2272 2023-03-19 21:20:35 |
2 Reference format revised. Lindsay Dong -1 word(s) 2271 2023-03-20 08:06:24 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Dye, C.A.; Skeete, J.; Khan, A.; Dunleavy, M.; Dietrich, M.; Volgman, A.S.; Sharma, P.; Huang, H. Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation. Encyclopedia. Available online: https://encyclopedia.pub/entry/42328 (accessed on 21 December 2025).
Dye CA, Skeete J, Khan A, Dunleavy M, Dietrich M, Volgman AS, et al. Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation. Encyclopedia. Available at: https://encyclopedia.pub/entry/42328. Accessed December 21, 2025.
Dye, Cicely Anne, Jamario Skeete, Asad Khan, Michael Dunleavy, Michael Dietrich, Annabelle Santos Volgman, Parikshit Sharma, Henry Huang. "Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation" Encyclopedia, https://encyclopedia.pub/entry/42328 (accessed December 21, 2025).
Dye, C.A., Skeete, J., Khan, A., Dunleavy, M., Dietrich, M., Volgman, A.S., Sharma, P., & Huang, H. (2023, March 19). Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation. In Encyclopedia. https://encyclopedia.pub/entry/42328
Dye, Cicely Anne, et al. "Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation." Encyclopedia. Web. 19 March, 2023.
Clinical Impact of Anti-Arrhythmic Medications in Atrial Fibrillation
Edit
This entry is adapted from the peer-reviewed paper 10.3390/pharma2010008

Atrial fibrillation has been described as a global epidemic with a three-fold increase in prevalence in the last 50 years. As the prevalence of atrial fibrillation continues to grow, multiple landmark trials have been designed to determine the best method to treat atrial fibrillation. Initial trials have stated that rate control was not inferior to rhythm control, however, as the efficacy of rhythm control of atrial fibrillation has improved, a benefit in rhythm control has been shown. Because of this trend towards increased rhythm control, more patients have been placed on anti-arrhythmic medications. 

atrial fibrillation anti-arrhythmics arrhythmias

1. Introduction

The increasing global burden of atrial fibrillation (AF) continues to be a major cause for concern due to the significant morbidity, mortality, and astounding economic impact attributable to this highly prevalent condition. To counter this surge in prevalence noted over the last five decades, there has been a valiant effort to identify the most effective strategies to prevent and manage AF [1]. While historically, the standard practice favored approaches aimed at controlling heart rates while in AF (rate control) over the pharmacologic restoration and maintenance of sinus rhythm (rhythm control) based on the findings of early clinical trials before catheter ablation techniques were available. In recent years, with improvements in technology and clinical outcome from catheter ablation, there has been a paradigm shift toward rhythm control [1][2].
Initial trials such as Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study (RACE) and Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM), have demonstrated rate control to be non-inferior to rhythm control [3][4]. In this context, providers often avoided the use of anti-arrhythmic drugs (AADs), which are often less well tolerated, require closer monitoring, and may be associated with several drug-to-drug interactions when compared to rate control agents. However, as the efficacy of rhythm control strategies for AF has improved with the introduction of catheter ablation in the last two decades [5][6][7][8][9][10], such as the Early Treatment of Atrial Fibrillation for Stroke Prevention Trial, Atrial Fibrillation Network (EAST-AFNET) has shown a possible benefit of earlier more aggressive pursuance of rhythm control [11][12][13][14][15]. This benefit of rhythm control has been most pronounced in certain populations, such as those with heart failure with reduced ejection fraction (HFrEF), leading to an update in the current clinical guidelines [16][17][18]. This update to the consensus guidelines for the management of AF has led to an increase in rhythm control in patients with AF, including the increased use of AADs alone or in conjunction with catheter ablations.
Although clinically available choices for AADs for the treatment of AF have remained mostly unchanged in recent decades, the role of AADs has come to the forefront with an increased focus on rhythm control, and their use is now becoming more commonplace, particularly in select populations. At the same time, it is essential for prescribers of these agents to perform close patient monitoring, similar to those utilized in landmark trials, to mitigate complications associated with drug toxicities in real-world practice.

2. The Impact of Atrial Fibrillation on Clinical Co-Morbidities

Several conditions accompany AF, many of which play a direct role in the pathogenesis and future development of AF. These co-morbidities include heart failure, hypertrophic cardiomyopathy, channelopathies, cardiac amyloidosis, human immunodeficiency virus (HIV), and malignancy.

2.1. Heart Failure with Preserved and Reduced Ejection Fraction

Of these co-morbidities, heart failure has the greatest correlation with AF. This association has, been recognized for over seven decades, with Paul Dudley White (1886–1973) once declaring, “Since auricula fibrillation so often complicates very serious heart disease, its occurrence may precipitate heart failure or even death, unless successful therapy is instituted.” Approximately 24% of patients diagnosed with congestive heart failure (CHF) had a prior diagnosis of AF or were found to have AF at the time of CHF diagnosis. The converse is also true, in which AF is strongly associated with a history of CHF or future development of CHF.

2.2. Hypertrophic Cardiomyopathy

Another condition associated with AF is hypertrophic cardiomyopathy (HCM). AF has been found to occur in 18–22% of patients with hypertrophic cardiomyopathy. Patients with AF in this group also have increased mortality [19][20][21]. AF risk increases with age, as well as how long a patient has had HCM [22]. The incidence of AF in persons with HCM is around 2% per year and is 6 times more likely than in the age-matched general population [21][22].

2.3. Cardiac Amyloidosis

AF is commonly present in persons with cardiac amyloidosis, with a prevalence of up to 70% in patients with transthyretin cardiac amyloidosis. In this population, AF is associated with a higher risk of thromboembolism than persons with AF who do not have concomitant cardiac amyloidosis [23]. Comparatively, AF appears to be less strongly associated with sarcoidosis, with a prevalence of AF of 18% in patients with sarcoidosis and cardiac involvement [24].

2.4. Channelopathies

AF has increased prevalence among patients with channelopathies. AF was documented in approximately 2% of patients with long QT syndrome who are younger than 50 years old, which is much higher than the expected 0.1% in the general population [25]. Among the total population of patients with Brugada Syndrome, the prevalence of AF has been estimated to be between 9 and 38% [26][27][28][29][30][31].

2.5. Human Immunodeficiency Virus (HIV)

There is limited research into the association between HIV and AF. One systematic review recently showed the prevalence of AF and atrial flutter (AFL) to be between 2.0% and 5.13%, with an incidence rate of 3.6 per 1000 person-years. They also demonstrated that low CD4+ counts and high viral loads were predictive of AF or AFL [32].

2.6. Malignancies and Chemotherapeutics

In the Women’s Health Study, a new diagnosis of AF is associated with a higher risk for cancer in the Women’s Health Study. The incidence of cancer was 1.4 per 100 person-years after AF diagnosis, compared to 0.8 per 100 person-years in those without AF [33]. In the first 3 months after diagnosis of AF, the incidence of a new cancer diagnosis was 3 times higher. While this risk decreased after that, it remained significantly elevated compared to subjects without AF beyond one year of new AF diagnosis in that same study. While some of the increased risks may be due to bleeding after the initiation of anticoagulation or additional observation after the new diagnosis. Cancer therapies have also been associated with an increased risk of AF.

3. Clinical Impact of Recent Trials on the Utilization of Anti-Arrhythmic Drugs

3.1. Rate Control versus Rhythm Control

The current guidelines in AF management reflect the findings of several key trials which were conducted to compare rhythm versus rate control. Initial findings in these studies did not suggest a benefit to rhythm control over rate control [17]. However, the findings of more recent randomized control trials (RTCs) have suggested the benefit of an early rhythm strategy, particularly in select patients, such as those with HFrEF [34][35][36][37][38][39][40][41][42][43].
The first randomized study to compare therapeutic strategies of rate control to rhythm control for AF was the Pharmacological intervention in Atrial Fibrillation (PIAF) study [35]. Specifically, the study looked at differences in symptoms related to AF between these treatment approaches. This landmark observational study consisted of 252 (125 in the rhythm control group and 127 in the rate control group) patients aged 18 to 75 years with a documented AF duration between 7 and 360 days and study participants were followed for 12 months. Notably, patients with New York Heart Association (NYHA) Class IV functional status, treatment with amiodarone within the 6 months of enrolment, and an average heart rate (HR) < 50 beats per minute (BPM) were excluded from this trial. Diltiazem was the first-line therapy for the rate control group, whereas amiodarone was the first-line therapy for the rhythm control group. Key endpoints assessed during each follow-up visit were changes in symptoms of palpitations, dyspnea, or dizziness compared to baseline. After a 52-week period of follow-up, there was no significant difference in terms of symptomatic improvement between the two groups (p = 0.317). At the end of the study, 56% of patients in the rhythm group were in sinus rhythm compared to only 10% in the rate control group (p < 0.001). Furthermore, those patients treated with a rhythm control strategy showed an improved exercise tolerance (measured by the 6 Minute walk test) by the end of the study (p = 0.008). Patients treated with amiodarone were more likely to have side effects (47% vs. 64%; p = 0.011). Notably, the most common side effects of amiodarone were corneal depositions followed by thyroid problems and photosensitivity. Treatment was more likely to be stopped in the amiodarone group due to side effects (p = 0.036). Finally, there was a significant difference in hospitalizations driven primarily by rhythm-specific circumstances such as electrical cardioversion or amiodarone-associated related side effects (p = 0.001).
Another key landmark study is the Rate Control versus Electrical Cardioversion for persistent atrial fibrillation (RACE) study. This was the first study to evaluate the synergistic effects of AADs on the efficacy of synchronized direct current cardioversions for the purpose of rhythm control [4]. The RACE study randomized 522 patients with persistent atrial fibrillation to a rate control strategy or a rhythm control strategy. Patients in the rhythm control strategy were cardioverted and then treated with sotalol, flecainide, and amiodarone. Rate control was achieved with the administration of digitalis, a non-dihydropyridine calcium-channel blocker, and beta-blocker, alone or in combination. The target resting heart rate in the rate control arm was less than 100 beats per minute. There was no significant difference between the two groups with regards to age, sex, LVEF, valvular disease, history of coronary artery disease (CAD) myocardial infraction (MI) or indexed left atrial (LA) volume. The primary end point was a composite of death from cardiovascular causes, heart failure, thromboembolic complications, bleeding, implantation of a pacemaker, and severe adverse effects of drugs. After a mean follow-up of 2.3 years, the primary end point occurred in 44 of the 256 patients in the rate-control group (17.2%) and in 60 of the 266 patients in the rhythm-control group (22.6%) [HR 0.73 (90% CI 0.53 to 1.01; p = 0.11). Severe adverse effects of anti-arrhythmic drugs occurred mainly in the rhythm-control group: Seven patients had sick sinus syndrome or atrioventricular block, three had torsade de pointes or ventricular fibrillation, one had rapid, hemodynamically significant atrioventricular conduction during flutter, and one had drug-induced heart failure.

3.2. Rhythm Control for Quality of Life

The Japanese Rhythm Management Trial for Atrial Fibrillation (J-RHYTHM) built upon prior studies by including those patients who were underrepresented in prior studies including patients who were younger and without risk factors for stroke, those who had paroxysmal AF, and those who had symptoms that were considered severe [38]. Another novel aspect of this trial was that in addition to the end points of morbidity and mortality, the study also emphasized patient-reported experience and perception of AF-specific disability. A total of 823 patients with PAF were followed for a mean period of 578 days. The primary endpoint occurred in 64 patients (15.3%) assigned to rhythm control and in 89 patients (22.0%) to rate control (p = 0.0128). This was driven by the patients’ desire to move to the alternate treatment strategy because of physical/psychological disability caused by their current treatment regimen. There were no significant differences between the groups in the total occurrences of mortality, embolism, major bleeding, and heart failure. Patients in the rhythm control group did show significant improvement in AF-specific quality of life scores compared to patients in the rate control group.

3.3. Catheter Ablation Used Alone or in Conjunction with AAD

The introduction of catheter ablation as an option for rhythm control has greatly impacted the use of AAD in atrial fibrillation. Catheter ablation has been shown to be more efficacious than AAD use, with a 70% arrhythmia-free survival compared to rates of 50% in most efficacious AAD in paroxysmal atrial fibrillation [44].
EAST-AFNET included patients who also underwent an AF ablation. A total of 1395 were assigned to an early rhythm control strategy, of which 270 underwent catheter ablation. There were no significant clinical or demographic differences between the two groups at baseline. The primary outcome was a composite of death from any cause, stroke, or prespecified serious adverse events arising from complications of rhythm-control therapy. The trial was stopped early due to an early demonstrated benefit in the rhythm control group [HR 0.79 (95% CI 0.66 to 0.95); p = 0.005] [45].

4. Prescribing Considerations for Anti-Arrhythmic Drugs

The use of anti-arrhythmic drugs (AADs) continues to see increased use in the management of atrial fibrillation. This aligns with not only the increasing prevalence that has been noted in atrial fibrillation but an increased emphasis on rhythm control in the last decades.
While there are several AADs of various levels of efficacy in achieving rhythm control in AF, numerous factors influence which drug is used in which clinical situation. For instance, certain co-morbidities, such as structural heart disease, renal impairment, or underlying lung or thyroid disease may limit which agent is used. Additionally, special attention to drug-to-drug interactions and the need for dose adjustment should be noted.
For instance, congestive heart failure (CHF) poses a particular challenge for the use of AADs in the management of atrial fibrillation. This is largely because the CHF may function to act as a pro-arrhythmic state, which can be worsened by several AADs, leading to poor clinical outcomes. Specifically, CHF may lead to impaired calcium handling, up-regulation of adrenergic receptors, and impaired function of voltage-dependent potassium channels, which may potentiate the pro-arrhythmic state of many AADs [46][47][48][49][50][51][52][53]. Furthermore, based on the inferences from landmark studies such as the Cardiac Arrhythmia Suppression Trial (CAST), which included post-myocardial infarction patients with high PVC burden in the era prior to wide-spread percutaneous coronary revascularization, class Ic agents such as flecainide were associated with increased mortality, this agent is contraindicated in the setting of CHF or coronary artery disease [47][48][49][50].
Another key consideration is the impact of co-morbidities on the pharmacokinetic properties of the various AADs. Notably, renal impairment may lead to decreased clearance of select AADs, such as the case for flecainide, sotalol, dofetilide, and dronedarone, prompting the need for dose adjustment in mild cases of kidney disease or avoidance in more advanced stages of chronic kidney disease [54].

References

  1. Lévy, S.; Steinbeck, G.; Santini, L.; Nabauer, M.; Maceda, D.P.; Kantharia, B.K.; Saksena, S.; Cappato, R. Management of atrial fibrillation: Two decades of progress–a scientific statement from the European Cardiac Arrhythmia Society. J. Interv. Card. Electrophysiol. 2022, 65, 287–326.
  2. Fuster, V.; Rydén, L.E.; Cannom, D.S.; Crijns, H.J.; Curtis, A.B.; Ellenbogen, K.A.; Halperin, J.L.; Le Heuzey, J.-Y.; Kay, G.N.; Lowe, J.E.; et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation. Circulation 2006, 114, e257–e354.
  3. Wyse, D.G.; Waldo, A.L.; DiMarco, J.P.; Domanski, M.J.; Rosenberg, Y.; Schron, E.B.; Kellen, J.C.; Greene, H.L.; Mickel, M.C.; E Dalquist, J.; et al. A Comparison of Rate Control and Rhythm Control in Patients with Atrial Fibrillation. N. Engl. J. Med. 2002, 347, 1825–1833.
  4. Van Gelder, I.C.; Hagens, V.E.; Kingma, J.H.; Bosker, H.A.; Kamp, O.; Kingma, T.; Crijns, H.J.G.M. Rate control versus electrical cardioversion for atrial fibrillation: A randomised comparison of two treatment strategies concerning morbidity, mortality, quality of life and cost-benefit–the RACE study design. Neth. Heart J. 2002, 10, 118.
  5. Haïssaguerre, M.; Jaïs, P.; Shah, D.C.; Takahashi, A.; Hocini, M.; Quiniou, G.; Garrigue, S.; Le Mouroux, A.; Le Métayer, P.; Clémenty, J. Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins. N. Engl. J. Med. 1998, 339, 659–666.
  6. Kreidieh, O.; Varley, A.L.; Romero, J.; Singh, D.; Silverstein, J.; Thosani, A.; Varosy, P.; Hebsur, S.; Godfrey, B.E.; Schrappe, G.; et al. Practice Patterns of Operators Participating in the Real-World Experience of Catheter Ablation for Treatment of Symptomatic Paroxysmal and Persistent Atrial Fibrillation (REAL-AF) Registry. J. Interv. Card. Electrophysiol. 2022, 65, 429–440.
  7. Packer, D.L.; Mark, D.B.; Robb, R.A.; Monahan, K.H.; Bahnson, T.D.; Poole, J.E.; Noseworthy, P.A.; Rosenberg, Y.D.; Jeffries, N.; Mitchell, L.B.; et al. Effect of Catheter Ablation vs Antiarrhythmic Drug Therapy on Mortality, Stroke, Bleeding, and Cardiac Arrest Among Patients With Atrial Fibrillation: The CABANA Randomized Clinical Trial. JAMA. 2019, 321, 1261–1274.
  8. Kuck, K.-H.; Brugada, J.; Fürnkranz, A.; Metzner, A.; Ouyang, F.; Chun, K.J.; Elvan, A.; Arentz, T.; Bestehorn, K.; Pocock, S.J.; et al. Cryoballoon or Radiofrequency Ablation for Paroxysmal Atrial Fibrillation. N. Engl. J. Med. 2016, 374, 2235–2245.
  9. Deshpande, R.; AlKhadra, Y.; Singanallur, P.; Botchway, A.; Labedi, M. Outcomes of catheter ablation versus antiarrhythmic therapy in patients with atrial fibrillation: A systematic review and meta-analysis. J. Interv. Card. Electrophysiol. 2022, 65, 773–802.
  10. Kirchhof, P.; Camm, A.J.; Goette, A.; Brandes, A.; Eckardt, L.; Elvan, A.; Fetsch, T.; van Gelder, I.C.; Haase, D.; Haegeli, L.M.; et al. Early Rhythm-Control Therapy in Patients with Atrial Fibrillation. N. Engl. J. Med. 2020, 383, 1305–1316.
  11. Turagam, M.K.; Musikantow, D.; Whang, W.; Koruth, J.S.; Miller, M.A.; Langan, M.N.; Sofi, A.; Choudry, S.; Dukkipati, S.R.; Reddy, V.Y. Assessment of Catheter Ablation or Antiarrhythmic Drugs for First-line Therapy of Atrial Fibrillation: A Meta-analysis of Randomized Clinical Trials. JAMA Cardiol. 2021, 6, 697–705.
  12. Andrade, J.G.; Wells, G.A.; Deyell, M.W.; Bennett, M.; Essebag, V.; Champagne, J.; Roux, J.-F.; Yung, D.; Skanes, A.; Khaykin, Y.; et al. Cryoablation or Drug Therapy for Initial Treatment of Atrial Fibrillation. N. Engl. J. Med. 2021, 384, 305–315.
  13. Baysal, E.; Okşul, M.; Burak, C.; Yalin, K.; Soysal, A.U.; Yalman, H.; Bozyel, S.; Guler, T.E.; Tanboga, H.I.; Aksu, T. Decreasing time between first diagnosis of paroxysmal atrial fibrillation and cryoballoon ablation positively affects long-term consequences. J. Interv. Card. Electrophysiol. 2022, 65, 365–372.
  14. Andrade, J.G.; Deyell, M.W. AF ablation: You cannot escape the responsibility of tomorrow by evading it today. J. Interv. Card. Electrophysiol. 2022, 65, 341–342.
  15. Andrade, J.G.; Deyell, M.W.; Macle, L.; Wells, G.A.; Bennett, M.; Essebag, V.; Champagne, J.; Roux, J.-F.; Yung, D.; Skanes, A.; et al. Progression of Atrial Fibrillation after Cryoablation or Drug Therapy. N. Engl. J. Med. 2023, 388, 105–116.
  16. January, C.T.; Wann, L.S.; Calkins, H.; Chen, L.Y.; Cigarroa, J.E.; Cleveland, J.C., Jr.; Ellinor, P.T., Jr.; Ezekowitz, M.D.; Field, M.E.; Furie, K.L.; et al. AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons. Circulation 2019, 140, e125–e151.
  17. Hindricks, G.; Potpara, T.; Dagres, N.; Arbelo, E.; Bax, J.J.; Blomström-Lundqvist, C.; Boriani, G.; Castella, M.; Dan, G.-A.; Dilaveris, P.E.; et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur. Heart J. 2021, 42, 373–498.
  18. Şaylık, F.; Çınar, T.; Akbulut, T.; Hayıroğlu, M. Comparison of catheter ablation and medical therapy for atrial fibrillation in heart failure patients: A meta-analysis of randomized controlled trials. Hear. Lung 2022, 57, 69–74.
  19. Siontis, K.C.; Geske, J.B.; Ong, K.; Nishimura, R.A.; Ommen, S.R.; Gersh, B.J. Atrial Fibrillation in Hypertrophic Cardiomyopathy: Prevalence, Clinical Correlations, and Mortality in a Large High-Risk Population. J. Am. Hear. Assoc. 2014, 3, e001002.
  20. Olivotto, I.; Cecchi, F.; Casey, S.A.; Dolara, A.; Traverse, J.H.; Maron, B.J. Impact of Atrial Fibrillation on the Clinical Course of Hypertrophic Cardiomyopathy. Circulation 2001, 104, 2517–2524.
  21. A Marston, N.; Han, L.; Olivotto, I.; Day, S.M.; Ashley, E.A.; Michels, M.; Pereira, A.C.; Ingles, J.; Semsarian, C.; Jacoby, D.; et al. Clinical characteristics and outcomes in childhood-onset hypertrophic cardiomyopathy. Eur. Hear J. 2021, 42, 1988–1996.
  22. Maron, B.J.; Desai, M.Y.; Nishimura, R.A.; Spirito, P.; Rakowski, H.; Towbin, J.A.; Dearani, J.A.; Rowin, E.J.; Maron, M.S.; Sherrid, M.V. Management of Hypertrophic Cardiomyopathy. J. Am. Coll. Cardiol. 2022, 79, 390–414.
  23. Lioncino, M.; Monda, E.; Palmiero, G.; Caiazza, M.; Vetrano, E.; Rubino, M.; Esposito, A.; Salerno, G.; Dongiglio, F.; D’Onofrio, B.; et al. Cardiovascular Involvement in Transthyretin Cardiac Amyloidosis. Hear Fail. Clin. 2021, 18, 73–87.
  24. Viles-Gonzalez, J.F.; Pastori, L.; Fischer, A.; Wisnivesky, J.P.; Goldman, M.G.; Mehta, D. Supraventricular Arrhythmias in Patients with Cardiac Sarcoidosis. Chest 2013, 143, 1085–1090.
  25. Johnson, J.N.; Tester, D.J.; Perry, J.; Salisbury, B.A.; Reed, C.R.; Ackerman, M.J. Prevalence of early-onset atrial fibrillation in congenital long QT syndrome. Hear. Rhythm. 2008, 5, 704–709.
  26. Itoh, H.; Shimizu, M.; Ino, H.; Okeie, K.; Yamaguchi, M.; Fujino, N.; Mabuchi, H. Hokuriku Brugada Study Group Arrhythmias in Patients with Brugada-Type Electrocardiographic Findings. Jpn. Circ. J. 2001, 65, 483–486.
  27. Morita, H.; Kusano-Fukushima, K.; Nagase, S.; Fujimoto, Y.; Hisamatsu, K.; Fujio, H.; Haraoka, K.; Kobayashi, M.; Morita, S.T.; Nakamura, K.; et al. Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome. J. Am. Coll. Cardiol. 2002, 40, 1437–1444.
  28. Bordachar, P.; Reuter, S.; Garrigue, S.; Caï, X.; Hocini, M.; Jaïs, P.; Haïssaguerre, M.; Clementy, J. Incidence, clinical implications and prognosis of atrial arrhythmias in brugada syndrome. Eur. Hear. J. 2004, 25, 879–884.
  29. Letsas, K.P.; Sideris, A.; Efremidis, M.; Pappas, L.K.; Gavrielatos, G.; Filippatos, G.S.; Kardaras, F. Prevalence of paroxysmal atrial fibrillation in Brugada syndrome: A case series and a review of the literature. J. Cardiovasc. Med. 2007, 8, 803–806.
  30. Vlachos, K.; Mascia, G.; Martin, C.A.; Bazoukis, G.; Frontera, A.; Cheniti, G.; Letsas, K.P.; Efremidis, M.; Georgopoulos, S.; Gkalapis, C.; et al. Atrial fibrillation in Brugada syndrome: Current perspectives. J. Cardiovasc. Electrophysiol. 2020, 31, 975–984.
  31. Bigi, M.A.B.; Aslani, A.; Shahrzad, S. Clinical predictors of atrial fibrillation in Brugada syndrome. Europace 2007, 9, 947–950.
  32. Park, D.Y.; An, S.; Romero, M.E.; Kaur, A.; Ravi, V.; Huang, H.D.; Vij, A. Incidence and risk factors of atrial fibrillation and atrial arrhythmias in people living with HIV: A systematic review and meta-analysis. J. Interv. Card. Electrophysiol. 2022, 65, 183–191.
  33. Conen, D.; Wong, J.A.; Sandhu, R.K.; Cook, N.R.; Lee, I.-M.; Buring, J.E.; Albert, C. Risk of Malignant Cancer Among Women With New-Onset Atrial Fibrillation. JAMA Cardiol. 2016, 1, 389–396.
  34. Hohnloser, S.H.; Crijns, H.J.; van Eickels, M.; Gaudin, C.; Page, R.L.; Torp-Pedersen, C.; Connolly, S.J. Effect of Dronedarone on Cardiovascular Events in Atrial Fibrillation. N. Engl. J. Med. 2009, 360, 668–678.
  35. Hohnloser, S.H.; Kuck, K.-H.; Lilienthal, J. Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial Fibrillation (PIAF): A randomised trial. Lancet 2000, 356, 1789–1794.
  36. Van Gelder, I.C.; Hagens, V.E.; Bosker, H.A.; Kingma, J.H.; Kamp, O.; Kingma, T.; Said, S.A.; Darmanata, J.I.; Timmermans, A.J.; Tijssen, J.G.; et al. A Comparison of Rate Control and Rhythm Control in Patients with Recurrent Persistent Atrial Fibrillation. N. Engl. J. Med. 2002, 347, 1834–1840.
  37. Carlsson, J.; Miketic, S.; Windeler, J.; Cuneo, A.; Haun, S.; Micus, S.; Walter, S.; Tebbe, U. Randomized trial of rate-control versus rhythm-control in persistent atrial fibrillation. J. Am. Coll. Cardiol. 2003, 41, 1690–1696.
  38. Ogawa, S.; Yamashita, T.; Yamazaki, T.; Aizawa, Y.; Atarashi, H.; Inoue, H.; Ohe, T.; Ohtsu, H.; Okumura, K.; Katoh, T.; et al. Optimal Treatment Strategy for Patients with Paroxysmal Atrial Fibrillation J-RHYTHM Study. Circ. J. 2009, 73, 242–248.
  39. Fosbol, E.L.; Holmes, D.N.; Piccini, J.P.; Thomas, L.; Reiffel, J.A.; Mills, R.M.; Kowey, P.; Mahaffey, K.; Gersh, B.J.; Peterson, E.D.; et al. Provider Specialty and Atrial Fibrillation Treatment Strategies in United States Community Practice: Findings From the ORBIT-AF Registry. J. Am. Hear. Assoc. 2013, 2, e000110.
  40. Thrall, G.; Lane, D.; Carroll, D.; Lip, G.Y. Quality of Life in Patients with Atrial Fibrillation: A Systematic Review. Am. J. Med. 2006, 119, 448.e1–448.e19.
  41. Dorian, P.; Jung, W.; Newman, D.; Paquette, M.; Wood, K.; Ayers, G.M.; Camm, J.; Akhtar, M.; Luderitz, B. The impairment of health-related quality of life in patients with intermittent atrial fibrillation: Implications for the assessment of investigational therapy. J. Am. Coll. Cardiol. 2000, 36, 1303–1309.
  42. Berg, M.V.D.; Hassink, R.; Tuinenburg, A.; Van Sonderen, E.; Lefrandt, J.; De Kam, P.; Van Gelder, I.; Smit, A.; Sanderman, R.; Crijns, H. Quality of life in patients with paroxysmal atrial fibrillation and its predictors: Importance of the autonomic nervous system. Eur. Hear J. 2001, 22, 247–253.
  43. Camm, A.J.; Naccarelli, G.V.; Mittal, S.; Crijns, H.J.; Hohnloser, S.H.; Ma, C.-S.; Natale, A.; Turakhia, M.P.; Kirchhof, P. The Increasing Role of Rhythm Control in Patients with Atrial Fibrillation. J. Am. Coll. Cardiol. 2022, 79, 1932–1948.
  44. Duytschaever, M.; Demolder, A.; Phlips, T.; Sarkozy, A.; El Haddad, M.; Taghji, P.; Knecht, S.; Tavernier, R.; Vandekerckhove, Y.; De Potter, T. PulmOnary vein isolation With vs. without continued antiarrhythmic Drug trEatment in subjects with Recurrent Atrial Fibrillation (POWDER AF): Results from a multicentre randomized trial. Eur. Hear. J. 2017, 39, 1429–1437.
  45. Fang, M.C.; Stafford, R.S.; Ruskin, J.N.; Singer, D.E. National Trends in Antiarrhythmic and Antithrombotic Medication Use in Atrial Fibrillation. Arch. Intern. Med. 2004, 164, 55–60.
  46. Wang, Y.; Hill, J.A. Electrophysiological remodeling in heart failure. J. Mol. Cell. Cardiol. 2010, 48, 619–632.
  47. Ginsburg, K.S.; Weber, C.R.; Bers, D.M. Cardiac Na+-Ca2+exchanger: Dynamics of Ca2+-dependent activation and deactivation in intact myocytes. J. Physiol. 2013, 591, 2067–2086.
  48. Luo, M.; Anderson, M.E. Mechanisms of Altered Ca2+ Handling in Heart Failure. Circ. Res. 2013, 113, 690–708.
  49. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators Preliminary Report: Effect of Encainide and Flecainide on Mortality in a Randomized Trial of Arrhythmia Suppression after Myocardial Infarction. N. Engl. J. Med. 1989, 321, 406–412.
  50. Burnham, T.S.; May, H.T.; Bair, T.L.; Anderson, J.A.; Crandall, B.G.; Cutler, M.J.; Day, J.D.; Freedman, R.A.; Knowlton, K.U.; Muhlestein, J.B.; et al. Long-term outcomes in patients treated with flecainide for atrial fibrillation with stable coronary artery disease. Am. Hear J. 2021, 243, 127–139.
  51. Ashraf, H.; Ko, N.K.; Ladia, V.; Agasthi, P.; Prendiville, T.; O’Herlihy, F.; Pujari, S.H.; Mulpuru, S.K.; Scott, L.; Sorajja, D. Use of Flecainide in Stable Coronary Artery Disease: An Analysis of Its Safety in Both Nonobstructive and Obstructive Coronary Artery Disease. Am. J. Cardiovasc. Drugs 2021, 21, 563–572.
  52. Cay, S.; Kara, M.; Ozcan, F.; Ozeke, O.; Aksu, T.; Aras, D.; Topaloglu, S. Propafenone use in coronary artery disease patients undergoing atrial fibrillation ablation. J. Interv. Card. Electrophysiol. 2022, 65, 381–389.
  53. Naccarelli, G.V.; Burkman, G.M.; Hussain, S.K. Do class IC antiarrhythmics drugs need to be cast aside in atrial fibrillation patients with minimal coronary artery disease? J. Interv. Card. Electrophysiol. 2022, 65, 347–348.
  54. Washam, J.B.; Holmes, D.N.; Thomas, L.E.; Pokorney, S.D.; Hylek, E.M.; Fonarow, G.C.; Mahaffey, K.W.; Gersh, B.J.; Kowey, P.R.; Ansell, J.E.; et al. Pharmacotherapy for Atrial Fibrillation in Patients with Chronic Kidney Disease: Insights From ORBIT-AF. J. Am. Hear Assoc. 2018, 7, e008928.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Cardiac & Cardiovascular Systems
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Cicely Anne Dye , Jamario Skeete , Asad Khan ,
Michael Dunleavy
,
Michael Dietrich
, Annabelle Santos Volgman , Parikshit Sharma , Henry Huang
View Times: 655
Revisions: 2 times (View History)
Update Date: 20 Mar 2023
Table of Contents
    Notice
    You are not a member of the advisory board for this topic. If you want to update advisory board member profile, please contact office@encyclopedia.pub.
    OK
    Confirm
    Only members of the Encyclopedia advisory board for this topic are allowed to note entries. Would you like to become an advisory board member of the Encyclopedia?
    Yes
    No
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    There is no comment~
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    ${ selectedItem.replyTextCharacter }/${ selectedItem.replyMaxCharacter }
    Submit
    Cancel
    Confirm
    Are you sure to Delete?
    Yes No
    Academic Video Service
    Feedback