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Cardiac adrenergic control and atrial fibrillation
Open accessAbstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia, and it causes substantial mortality. The autonomic nervous system, and particularly the adrenergic/cholinergic balance, has a profound influence on the occurrence of AF. Adrenergic stimulation from catecholamines can cause AF in patients. In human atrium, catecholamines can affect each of the electrophysiological mechanisms of AF initiation and/or maintenance. Catecholamines may produce membrane potential oscillations characteristic of afterdepolarisations, by increasing Ca(2+) current, [Ca(2+)](i) and consequent Na(+)-Ca(2+) exchange, and may also enhance automaticity. Catecholamines might affect reentry, by altering excitability or conduction, rather than action potential terminal repolarisation or refractory period. However, which arrhythmia mechanisms predominate is unclear, and likely depends on cardiac pathology and adrenergic tone. Heart failure (HF), a major cause of AF, causes adrenergic activation and adaptational changes, remodelling, of atrial electrophysiology, Ca(2+) homeostasis, and adrenergic responses. Chronic AF also remodels these, but differently to HF. Myocardial infarction and AF cause neural remodelling that also may promote AF. beta-Adrenoceptor antagonists (beta-blockers) are used in the treatment of AF, mainly to control the ventricular rate, by slowing atrioventricular conduction. beta-Blockers also reduce the incidence of AF, particularly in HF or after cardiac surgery, when adrenergic tone is high. Furthermore, the chronic treatment of patients with beta-blockers remodels the atria, with a potentially antiarrhythmic increase in the refractory period. Therefore, the suppression of AF by beta-blocker treatment may involve an attenuation of arrhythmic activity that is caused by increased [Ca(2+)](i), coupled with effects of adaptation to the treatment. An improved understanding of the involvement of the adrenergic system and its control in basic mechanisms of AF under differing cardiac pathologies might lead to better treatments.
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“Investigating the mechanistic underpinning of this age-dependant risk, Hoogsteen et al 24 discuss AF being triggered by adrenergic surges occurring during exercise in younger athletes, 25 whereas older athletes typically experience vagally induced AF after exercise, normally from secondary autonomic dysfunction.26”
From Risk of atrial fibrillation in athletes: a systematic review and meta-analysis (2021) · cites this paper as [25]
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“badrenergic stimulation by catecholamines is known to elevate intracellular calcium through an increase in ICaL and sarcoplasmic reticular Ca2þ content, and the main antiarrhythmic effect of b-blockers is thought to be the suppression of proarrhythmic Ca2þ-dependent afterdepolarizations (46,47).”
BackgroundWang, K., Chang, D., Chu, Z., Yang, Y.-Z., Gao, L.-J., Zhang, S.-L., Xia, Y.-L., Dong, Y.-X., Yin, X.-M., Cong, P.-X., et al. (2013) · TheScientificWorldJournal · doi:10.1155/2013/569564 · Cited by 19
“Increased vagal tone is associated with a shortened atrial effective refractory period and increased dispersion [3, 17], whereas sympathetic stimulation may lead to afterdepolarization and triggered firing [18], which facilitate the initiation and maintenance of AF.”
Agra-Bermejo, R., Cacho-Antonio, C., Rozados-Luís, A., Couselo-Seijas, M., Fernandez, A. L., Martínez-Cereijo, J., Bravo, S., González-Juanatey, J., & Eiras, S. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00620 · Cited by 18
“The combination of HF and AF disease increments the death probability (Middlekauff et al., 1991), in part, due to the fact that the high adrenergic activity contributes to its progression (Workman, 2010).”
BackgroundCouffignal, C., Amour, J., Ait-Hamou, N., Cholley, B., Fellahi, J., Duval, X., Beauregard, Y. C. D., Nataf, P., Dilly, M., Provenchère, S., et al. (2019) · Anesthesiology · doi:10.1097/aln.0000000000003064 · Cited by 18
Atrial Fibrillation in Decompensated Heart Failure: Associated Factors and In-Hospital Outcome
Mendes, F. D. S. N. S., Atié, J., Garcia, M. I., Gripp, E. D. A., de Sousa, A. D., Feijó, L. A., & Xavier, S. (2014) · Arquivos Brasileiros de Cardiologia · doi:10.5935/abc.20140123 · Cited by 18
Optimising risk factors for atrial fibrillation post-cardiac surgery
Goulden, C. J., Hagana, A., Ulucay, E., Zaman, S., Ahmed, A., & Harky, A. (2021) · Perfusion · doi:10.1177/02676591211019319 · Cited by 17
Role of protein phosphatase inhibitor-1 in cardiac beta adrenergic pathway
Weber, S., Meyer-Roxlau, S., & El‐Armouche, A. (2016) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2016.09.007 · Cited by 22
Dexmedetomidine does not reduce atrial fibrillation after lung cancer surgery.
Ai, D., Xu, G., Feng, L., Yu, J., Banchs, J., Vaporciyan, A., & Cata, J. (2015) · Journal of Cardiothoracic and Vascular Anesthesia · doi:10.1053/j.jvca.2014.05.013 · Cited by 16
Fitzgerald, P. J. (2013) · Medical Hypotheses · doi:10.1016/j.mehy.2013.01.018 · Cited by 18
“The above data tend to support the NE disease hypothesis in relation to AF, with the fact that beta blockers are a standard treatment for the disease being strong evidence by itself [35].”
BackgroundGaffey, A. E., Rosman, L., Lampert, R. J., Yaggi, H. K., Haskell, S. G., Brandt, C., Enriquez, A. D., Mazzella, A. J., Skanderson, M., & Burg, M. M. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.123.030331 · Cited by 22
“55 61 Other data from the UK Biobank showed that genetically predicted insomnia is associated with a 13% higher risk of AF, and risk for 8 other cardiovascular diseases.”
Ni, H., Morotti, S., Zhang, X., Dobrev, D., & Grandi, E. (2022) · bioRxiv · doi:10.1093/cvr/cvad118 · Cited by 15
Bond, R., Choisy, S., Bryant, S., Hancox, J., & James, A. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu192 · Cited by 15
“On the other hand, the effects of noradrenaline on K+ channel currents are likely to contribute changes in membrane excitability and repolarization.(1,2) The inwardly rectifying background K+ current (IK1) and the steady-state outward K+ current (IKss) have been reported to be inhibited by a1- and b-adrenoceptor agoni…”
BackgroundInfluentialLiu, X., Ren, L., Yu, S.-D., Li, G., He, P.-K., Yang, Q.-M., Wei, X.-H., Thai, P. N., Wu, L., & Huo, Y. (2023) · Philosophical Transactions of the Royal Society of London. Biological Sciences · doi:10.1098/rstb.2022.0163 · Cited by 14
“The proarrhythmic effects of ISO are principally mediated by activation of a β-adrenergic receptor, resulting in increased ICa,L and elevation of [Ca ]i [19].”
BackgroundPlasma Catecholamine Levels on the Morning of Surgery Predict Post-Operative Atrial Fibrillation
Anderson, E. J., Efird, J., Kiser, A. C., Crane, P. B., O'Neal, W. T., Ferguson, T., Alwair, H., Carter, K., Williams, J. M., Gehi, A., et al. (2017) · JACC Clinical Electrophysiology · doi:10.1016/j.jacep.2017.01.014 · Cited by 14
“However, the net effect of this process depends on the catecholamine type and the density and sensitivity of the adrenoceptors they activate, with sometimes opposing effects on electromechanical function (as was observed with the inverse relationship between NE and DA with POAF in our study) (7).”
Factors influencing post-coronary artery bypass grafting atrial fibrillation episodes
Mariscalco, G., Musumeci, F., & Banach, M. (2013) · Kardiologia Polska · doi:10.5603/kp.2013.0291 · Cited by 12
“Operative trauma increases sympathetic activity, which is mediated by b-adrenoceptors and increases heart rate and contractile forces, enhancing excitability and automaticity [95, 96].”
BackgroundInfluentialAntoun, I., Layton, G., Abdelrazik, A., Eldesouky, M., Davies, H., Barakat, O., Mahfoud, A., Koya, A., Lau, E., Zakkar, M., et al. (2025) · Cardiovascular Electrophysiology · doi:10.1111/jce.70063 · Cited by 11
“Catecholamines, such as epinephrine and norepinephrine, enhance automaticity and triggered activity via activation of β ‐ adrenergic receptors, shortening both the action potential duration and the refractory periods, thereby increasing susceptibility to AF [19].”
Risk factors for new-onset atrial fibrillation during critical illness: A Delphi study
Bedford, J. P., Garside, T., Darbyshire, J., Betts, T., Young, J. D., & Watkinson, P. (2021) · Journal of the Intensive Care Society · doi:10.1177/17511437211022132 · Cited by 11
“Adrenergic stimulation from catecholamines and bronchodilators induces after-depolarisations, enhances automaticity and may promote atrial re-entry circuits.(82) Further to phosphodiesterase inhibition, aminophylline is an antagonist at the adenosine A1.”
BackgroundThe Incidence of Atrial Fibrillation after On-Pump Versus Off-Pump Coronary Artery Bypass Grafting.
Arslan, G., Erol, G., Kartal, H., Demirdaş, E., & Bolcal, C. (2021) · Heart Surgery Forum · doi:10.1532/hsf.3873 · Cited by 10
Morning hypertension is a risk factor of macrovascular events following cerebral infarction
Wu, Q., Qu, J., Yin, Y., Wang, A., Cheng, W., Duan, R., & Zhang, B. (2018) · Medicine · doi:10.1097/md.0000000000012013 · Cited by 9
Molecular Basis of Atrial Fibrillation Initiation and Maintenance
Beneke, K., & Molina, C. E. (2021) · Hearts · doi:10.3390/hearts2010014 · Cited by 9
“Two types of abnormal depolarizations have been characterized: delayed (DADs) and early (EADs) afterdepolarizations [10].”
BackgroundTang, B., He, K., Liu, S., Wu, Z., & Yang, C.-W. (2025) · Comput. Methods Programs Biomed. · doi:10.1016/j.cmpb.2025.108696 · Cited by 8
Colman, M., Saxena, P., Kettlewell, S., & Workman, A. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.01211 · Cited by 8
“, 2018), are modified by autonomic control (e.g., Chen and Tan, 2007; Workman, 2010), and can remodel in the long-term presence of AF (e.”
BackgroundSelf-citationLackermair, K., Clauss, S., Voigt, T., Klier, I., Summo, C., Hildebrand, B., Nickel, T., Estner, H., Kääb, S., Wakili, R., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0184337 · Cited by 8
Polimorfismos beta1-adrenérgico associados com Fibrilação Atrial na Insuficiência Cardíaca Sistólica
Nascimento, B. C., Pereira, S. B., Ribeiro, G. S., & Mesquita, E. (2012) · doi:10.1590/s0066-782x2012005000037 · Cited by 8
Dorey, T. W., Liu, Y., Jansen, H. J., Bohne, L. J., Mackasey, M., Atkinson, L., Prasai, S., Belke, D. D., Hassanabad, A. F., Fedak, P. W. M., et al. (2023) · Circulation Arrhythmia and Electrophysiology · doi:10.1161/circep.123.012199 · Cited by 10
Verkerk, A., & Wilders, R. (2023) · Biomedicines · doi:10.3390/biomedicines11092447 · Cited by 7
Pyridostigmine enhances atrial tachyarrhythmias in aging spontaneously hypertensive rats
Sayin, H., Scridon, A., Oréa, V., Chapuis, B., Chevalier, P., Barrés, C., & Julien, C. (2015) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.12458 · Cited by 7
Identification of necroptosis-related diagnostic biomarkers in coronary heart disease
You, H., & Han, W. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e30269 · Cited by 7
“Besides, investigations have illustrated that catecholamines can generate membrane potential oscillations characteristic of post-depolarization by enhancing Ca 2 + currents and consequent sodium-calcium ion exchange, which may be related to the development of atrial fibrillation [70].”
BackgroundArzt, M., Drzymalski, M. A., Ripfel, S., Meindl, S., Biedermann, A., Durczok, M., Keller, K., Mustroph, J., Katz, S., Tafelmeier, M., et al. (2022) · Antioxidants · doi:10.3390/antiox11020331 · Cited by 6
Grégoire-Lacoste, F., Jacquemet, V., & Vinet, A. (2014) · Mathematical Biosciences · doi:10.1016/j.mbs.2014.01.010 · Cited by 6
Workman, A., & Rankin, A. (2010) · Heart Rhythm · doi:10.1016/j.hrthm.2010.04.004 · Cited by 6
Self-citationAtrial fibrillation, electroconvulsive therapy, stroke risk, and anticoagulation
Kapadia, M., Jagadish, P., Hutchinson, M., & Lee, H. (2023) · Egyptian Heart Journal · doi:10.1186/s43044-023-00409-7 · Cited by 5
“Furthermore, increased circulating catecholamines are thought to promote AF through a mechanism of increased magnitude of open L-type calcium channels as well as excessive intracellular calcium [24].”
BackgroundThe Role of Major Biomarkers of Stress in Atrial Fibrillation: A Literature Review
Rafaqat, S., Rafaqat, S., & Rafaqat, S. (2023) · Journal of Innovations in Cardiac Rhythm Management · doi:10.19102/icrm.2023.14025 · Cited by 7
Altered Excitation-Contraction Coupling in Human Chronic Atrial Fibrillation.
Grandi, E., Workman, A. J., & Pandit, S. V. (2012) · Europe PMC (PubMed Central) · doi:10.4022/jafib.495 · Cited by 4
“The increased ICaL and IKur, with lack of effect on other repolarizing currents, results in no net effect of β-stimulation on atrial APD90, as predicted by our model (16), consistent with 5 of 6 reports in human atrial cells or tissues (87).”
BackgroundResultSelf-citationLi, W., Liu, Y., & Gu, X.-H. (2024) · Drug Design, Development and Therapy · doi:10.2147/dddt.s474818 · Cited by 4
Godoy-Marín, H., Jiménez-Sábado, V., Tarifa, C., Ginel, A., dos Santos, J. D., Bentzen, B., Hove-Madsen, L., & Ciruela, F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043668 · Cited by 4
Kharche, S., Stary, T., Biktasheva, I., Workman, A., Rankin, A., Holden, A., & Zhang, H.-G. (2013) · doi:10.1016/j.jelectrocard.2013.05.026 · Cited by 4
Self-citation54 – Pharmacologic Bases of Antiarrhythmic Therapy
Tamargo, J., & Delpón, E. (2013) · Elsevier eBooks · doi:10.1016/b978-1-4557-2856-5.00054-6 · Cited by 4
Hardi, H., Barinda, A. J., Vidya, A. P., Utama, K. E., & Mahata, L. E. (2026) · Cardiovascular Toxicology · doi:10.1007/s12012-025-10087-3 · Cited by 3
“Of note, corticosteroids in septic shock can reduce the duration of vasopressor therapy [ 50, 51], and vasopressors may induce atrial fibrillation by enhancing automaticity [ 52 ].”
"Lone Atrial Fibrillation" is a Four Letter Word.
Reiffel, J. A. (2025) · American Journal of Medicine · doi:10.1016/j.amjmed.2025.07.004 · Cited by 3
Burashnikov, A. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1447542 · Cited by 3
Pierre, M., Djemai, M., Pouliot, V., Poulin, H., Gollob, M. H., & Chahine, M. (2024) · Heart Rhythm · doi:10.1016/j.hrthm.2024.09.013 · Cited by 3
Colman, M., Varela, M., MacLeod, R. S., Hancox, J. C., & Aslanidi, O. (2024) · Journal of Physiology · doi:10.1113/jp285740 · Cited by 3
“…Ca 2 + influx to load the SR while maintaining a similar APD to control, through an increase in the current densities/maximal flux rates (Heijman et al., 2011; Workman, 2010) of I CaL , the SR Ca 2 + uptake pump ( J up ), and the potassium channels I Kur and I Ks (Supporting information, Text S1).”
BackgroundLong Non-coding RNA Involved in the Pathophysiology of Atrial Fibrillation
Zhong, Z., Li, X., Gao, L., Wu, X. O., Ye, Y., Zhang, X., Zeng, Q., Zhou, C., Lu, X., Wei, Y. Q., et al. (2023) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-023-07491-8 · Cited by 4
“Several studies have shown that excessive adrenergic activation contributes to impaired atrial neural activity, ultimately leading to the initiation and progression of AF [129, 130].”
Kervadec, A., Kezos, J. N., Ni, H., Yu, M. S., Marchant, J., Spiering, S., Kannan, S., Kwon, C., Andersen, P., Bodmer, R., et al. (2023) · Disease Models & Mechanisms · doi:10.1242/dmm.049962 · Cited by 7
“Additional factors such as conductance heterogeneity due to atrial fibrosis (Dzeshka et al., 2015; Xintarakou et al., 2020) and sympathetic stresses (Workman, 2010) have been tightly linked with the onset and maintenance of AF, and are often categorized as ‘ AF-associated risk factors ’ .”
Kervadec, A., Kezos, J. N., Ni, H.-B., Yu, M. S., Spiering, S., Kannan, S., Andersen, P., Grandi, E., Ocorr, K., & Colas, A. (2022) · bioRxiv · doi:10.1101/2022.09.23.509238 · Cited by 3
“Additional factors such as conductance heterogeneity due to atrial fibrosis (Dzeshka et al., 2015; Xintarakou et al., 2020) as well as sympathetic stresses (Workman, 2010) have been tightly linked with the onset and maintenance of AF, and are often categorized as “AF-associated risk factors”.”
BackgroundA frequent gene polymorphism affecting the heart-rate response to carvedilol.
Eschenhagen, T. (2013) · Pharmacogenomics (London) · doi:10.2217/pgs.12.198 · Cited by 3
Atrial Fibrillation Following Electroconvulsive Therapy
Baroni, M., Albaba, D., Ngo, A., & Livingston, R. (2024) · Journal of Ect · doi:10.1097/yct.0000000000001029 · Cited by 3
Metadata
- Authors
- Workman, A. J.
- Affiliations
- British Heart Foundation (GB)
- Corresponding author
- Workman, Antony J.
- ORCID
- Workman, Antony J.
- Venue
- Naunyn-Schmiedeberg's Archives of Pharmacology
- Published
- 2009-12-04
- Volume
- 381
- Issue
- 3
- Pages
- 235-249
- ISSN
- 0028-1298 (ISSN-L)
- 1432-1912
- PMC
- PMC2855383
- OpenAlex
- W2012942841
- Cited by
- 143
- References
- 170
- Citations by year
- 2026: 10 · 2025: 5 · 2024: 10 · 2023: 15 · 2022: 6 · 2021: 8 · 2020: 10 · 2019: 8 · 2018: 2 · 2017: 6 · 2016: 4 · 2015: 7 · 2014: 11 · 2013: 17 · 2012: 10
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Naunyn-Schmiedeberg s Archives of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- British Heart Foundation (BS/06/003, BS/06/003/20338)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Atrial Fibrillation Management and Outcomes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Arrhythmias and Treatments
- Keywords
- atrial fibrillation, adrenergic system, catecholamines, autonomic nervous system, beta-blockers, heart failure, atrial remodeling, calcium homeostasis, afterdepolarizations, automaticity, reentry, atrial electrophysiology, cardiac surgery
- MeSH terms
- Action Potentials, Adrenergic beta-Antagonists, Animals, Atrial Fibrillation, Catecholamines, Humans, Receptors, Adrenergic, Species Specificity, Calcium Signaling
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