The DOI matches its Crossref record; 161 of the 170 references it cites were found in a registry or an index.
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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Cites
Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins.
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“The majority of atrial premature beats that trigger (initiate) AF originate from focal (focussed) ectopic (away from the sinoatrial (SA) node) electrical activity in or near the PVs.”
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“Furthermore, α-stimulation may increase inositol (1,4,5)-trisphosphate (InsP 3 ), and InsP 3 can cause Ca 2+ i release, particularly in atrium, in which InsP 3 receptors are prevalent (Bers 2002).”
InfluentialFuster, 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. (2006) · Circulation · doi:10.1161/circulationaha.106.177292 · Cited by 2,805
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“However, the plateau elevation has the potential to promote afterdepolarisations, either by increasing APD in the voltage range at which ICaL can reactivate and thus cause EADs (Bers 2008), or by its association with increased Cai loading and DADs.”
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“Moreover, AF substantially increases the risk of stroke, heart failure (HF), and death (Fuster et al. 2006).”
Flagged first, then by citations
9 of the 170 references couldn’t be matched to a known paper.
Research works printed but not linked: 7
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Sorted by citations
Items 101–125 of 125
Pro-arrhythmic role of adrenergic spatial densities in the human atria: An in-silico study
Magtibay, K., Massé, S., Nanthakumar, K., & Umapathy, K. (2023) · PLoS ONE · doi:10.1371/journal.pone.0290676 · Cited by 2
Catheter Ablation for Atrial Fibrillation: The Tailored Approach
Sciarra, L., Palamà, Z., & Nesti, M. (2019) · Biomedical Journal of Scientific & Technical Research · doi:10.26717/bjstr.2019.18.003217 · Cited by 2
“Indeed, the suppression of AF by β-blocker treatment may involve an attenuation of arrhythmic activity that is caused by increased [Ca2+]i, coupled with effects of adaptation to the treatment [11].”
BackgroundReversible atrial fibrillation following Crotalinae envenomation
Quan, D., & Zurcher, K. (2017) · Journal of Venomous Animals and Toxins including Tropical Diseases · doi:10.1186/s40409-017-0108-9 · Cited by 2
“Through several proposed electrophysiological mechanisms in the atrium, catecholamines have been shown to affect AF initiation and/or maintenance [22].”
BackgroundYakimova, E. V., Svintsova, L. I., Rebrova, T. Y., Muslimova, E. F., Jaffarova, O. Y., & Afanasyev, S. (2026) · Siberian Journal of Clinical and Experimental Medicine · doi:10.29001/2073-8552-2026-41-1-132-139 · Cited by 1
Effects of spatially dense adrenergic stimulation to rotor behaviour in simulated atrial sheets
Magtibay, K., Massé, S., Nanthakumar, K., & Umapathy, K. (2024) · Comput. Biol. Medicine · doi:10.1016/j.compbiomed.2024.109195 · Cited by 1
Neurohumoral Control of Heart Rate
Graceli, J., Pedrosa, D. F., & Gava, Á. (2012) · InTech eBooks · doi:10.5772/33755 · Cited by 1
“In this field, the autonomic nervous system plays an important role to normal cardiovascular control and changes in autonomic balance has been related to several cardiovascular disorders, such as cardiac arrhythmias and hypertension (Workman, 2010; Pagani and Lucini, 2001).”
Background54 – Pharmacological Bases of Antiarrhythmic Therapy
Tamargo, J., & Delpón, E. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-44733-1.00054-7 · Cited by 1
Development of a New Model for Simulating the Electrical Action Potentials of Human Atrial Myocytes
Colman, M. (2014) · doi:10.1007/978-3-319-01643-6_3 · Cited by 1
Saleeb-Mousa, J., Kalla, M., Herring, N., O'Shea, C., Coney, A., Brain, K., & Holmes, A. P. (2026) · Journal of Physiology · doi:10.1113/jp290871
Huang, X.-Y., Zheng, M.-Y., Zhu, Z., Zhang, Y.-H., & Chen, K.-Y. (2026) · Scientific Reports · doi:10.1038/s41598-026-51249-9
“This cellular disturbanceis thought to promote delayed afterdepolarizations and triggered activity, serving as the initiating focal source for the arrhythmia 10 .”
Identification and validation of five hypoxia- and immune-related hub targets in atrial fibrillation
Weng, J., Huang, D.-D., Wu, Q.-L., Chen, Z.-L., Chen, J.-Z., & Pang, Z. (2026) · Journal of Cardiothoracic Surgery · doi:10.1186/s13019-026-04369-2
“In patients with AF, the activity of the sympathetic nervous system (SNS) is enhanced, and the released norepinephrine stimulates β-adrenergic receptors (β-AR), leading to an increase in cAMP in atrial myocytes [43–45].”
Wei, Z., Wang, F., Wang, S., Lu, R., Li, P. L., Liu, L., Xuan, K., Mao, Z., Wu, Y., & Zhu, X. (2026) · International Journal of Surgery · doi:10.1097/js9.0000000000005211
Grosu, L.-B., Diaconu, C., & Gavril, L. G. (2026) · Medicina · doi:10.3390/medicina62020261
“Women tend to have more proinflammatory myocardium genes, which contribute to a higher prevalence of autoimmune responses, than men, and consequently a higher risk of autoimmune diseases [25,26].”
Huang, Z., Li, W., Xie, W., Gu, X.-H., & Li, H. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1478961
Electrophysiological Changes in Simulated Atrial Sheets Due to Sympathetic Hyperactivity
Magtibay, K., Abderrahman, Y., Massé, S., Nanthakumar, K., & Umapathy, K. (2024) · Annual International Conference of the IEEE Engineering in Medicine and Biology Society · doi:10.1109/embc53108.2024.10782586
“We showed in our previous work that spatially dense adrenergic stimulation could drastically shorten the duration of APs [5], which may be due to excess intracellular Ca 2+ [10].”
Saxena, P., Myles, R., Smith, G. L., & Workman, A. (2022) · Pflügers Archiv: European Journal of Physiology · doi:10.1007/s00424-022-02746-z
Self-citationPost Paddle Boarding Atrial Fibrillation in an Aging Athlete
Faris, M., Goebel, J., & Sherertz, R. (2022) · Cureus · doi:10.7759/cureus.22577
“During exercise, high heart rates are associated with catecholamine release which stimulates the heart by binding to cardiac surface α, β1, β2, and β3 receptors [11].”
BackgroundFushtey, I., Podluzhnyi, S., & Sid', E. (2020) · doi:10.31071/promedosvity2020.04.044
Epigenetics of muscle disorders
Oltra, E. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823928-5.00023-2
Gomes, J. A. (2020) · Springer eBooks · doi:10.1007/978-3-030-45066-3_22 · Cited by 9
Schneider, B. (2020) · Sex and Cardiac Electrophysiology · doi:10.1016/b978-0-12-817728-0.00035-8
37 – CaV1.2 and β-Adrenergic Regulation of Cardiac Function
Leroy, J., & Fischmeister, R. (2014) · doi:10.1016/b978-1-4557-2856-5.00037-6
Atrial Arrhythmogenic Substrates: The Role of Structure and Molecular Remodeling
Ambrosi, C. (2011) · doi:10.7936/k7jq0z1g
“We also explored the gender dependence of relative expression levels for adrenergic receptors as an increased level of adrenergic activity can be associated with the onset of atrial fibrillation (Workman 2010).”
BackgroundIon Channels as New Drug Targets in Atrial Fibrillation
Ravens, U. (2011) · Springer eBooks · doi:10.1007/978-3-642-17575-6_33
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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