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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Hoogsteen et al discuss atrial fibrillation being triggered by adrenergic surges during exercise in younger athletes, whereas older athletes typically experience vagally induced atrial fibrillation after exercise, normally from secondary autonomic dysfunction.
“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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InfluentialArrhythmogenic Substrate of the Pulmonary Veins Assessed by High-Resolution Optical Mapping
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InfluentialAdrenergic modulation of ultrarapid delayed rectifier K+ current in human atrial myocytes.
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Electrophysiological Study of Human Heart Muscle
Trautwein, W., Kassebaum, D. G., Nelson, R., & Hecht, H. (1962) · Circulation Research · doi:10.1161/01.res.10.3.306 · Cited by 139 · cited 2× · see citing works
“Right atrial (RA) pectinate muscles sometimes featured a “single pacemaker”, and adrenaline transiently decreased, then markedly increased, its rate (Trautwein et al. 1962).”
Miyauchi, Y., Zhou, S., Okuyama, Y., Miyauchi, M., Hayashi, H., Hamabe, A., Fishbein, M., Mandel, W., Chen, L. S., Chen, P.-S., et al. (2003) · Circulation · doi:10.1161/01.cir.0000080327.32573.7c · Cited by 135 · cited 1× · see citing works
“This may have resulted from injury of atrial nerves passing through the ventricle (Miyauchi et al. 2003).”
Chou, C.-C., Nihei, M., Zhou, S., Tan, A. Y., Kawase, A., Macias, E. S., Fishbein, M., Lin, S.-F., & Chen, P.-S. (2005) · Circulation · doi:10.1161/circulationaha.104.498758 · Cited by 134 · cited 2× · see citing works
“Focal ectopic beats that were preceded by rises in [Ca 2+ ] i were produced by perfusing canine atria with ryanodine plus ISO, but ISO alone was not studied (Chou et al. 2005).”
Calcium Handling Abnormalities in Atrial Fibrillation as a Target for Innovative Therapeutics
Dobrev, D., & Nattel, S. (2008) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e318171924d · Cited by 132 · cited 1× · see citing works
“differs between atrium and ventricle ( Dobrev and Nattel 2008 ).”
Heath, B., & Terrar, D. (2000) · Journal of Physiology · doi:10.1111/j.1469-7793.2000.t01-2-00391.x · Cited by 132 · see citing works
Chamberlain, P., Jennings, K., Paul, F., Cordell, J., Berry, A., Holmes, S., Park, J., Chambers, J., Sennitt, M. V., Stock, M. J., et al. (1999) · International Journal of Obesity · doi:10.1038/sj.ijo.0801039 · Cited by 127 · cited 1× · see citing works
“and activate cell surface adrenoceptors, including the α, β1, β2 and β3 subtypes, all of which are present in human atrium (Mary-Rabine et al. 1978; Hedberg et al. 1985; Chamberlain et al. 1999).”
Chen, Y.-J., Chen, S.-A., Chen, Y.-C., Yeh, H., Chang, M., & Lin, C.-I. (2002) · Basic Research in Cardiology · doi:10.1007/s395-002-8384-6 · Cited by 126 · cited 1× · see citing works
“Pacemaker activity was found in rabbit PV isolated cells, which was enhanced by ISO (Chen et al. 2002).”
Stambler, B., Fenelon, G., Shepard, R., Clemo, H., & Guiraudon, C. (2003) · Cardiovascular Electrophysiology · doi:10.1046/j.1540-8167.2003.02519.x · Cited by 123 · cited 5× · see citing works
“Nevertheless, CHF-induced atrial arrhythmic activity may involve RyRs, since it was abolished by RyR blockade in dogs (Stambler et al. 2003; Yeh et al. 2008).”
InfluentialEvidence for Increased Atrial Sympathetic Innervation in Persistent Human Atrial Fibrillation
Gould, P. A., Yii, M. Y., McLean, C., Finch, S., Marshall, T., Lambert, G. W., & Kaye, D. M. (2006) · Pacing and Clinical Electrophysiology · doi:10.1111/j.1540-8159.2006.00447.x · Cited by 115 · cited 2× · see citing works
“Comparable changes were associated with chronic AF in humans, including hyperinnervation and increased tissue noradrenaline (Gould et al. 2006).”
Michel, M. C., Pingsmann, A., Beckeringh, J., Zerkowski, H., Doetsch, N., & Brodde, O. (1988) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.1988.tb11576.x · Cited by 115 · cited 1× · see citing works
“Nevertheless, human atrial βreceptors , perhaps predominantly β 1 , were upregulated by β-blocker therapy (Hedberg et al. 1985; Michel et al. 1988), possibly related to a reduction in adrenergic nerve activity (Raine et al. 1977).”
Properties of human atrial ICa at physiological temperatures and relevance to action potential.
Li, G.-R., & Nattel, S. (1997) · American Journal of Physiology · doi:10.1152/ajpheart.1997.272.1.h227 · Cited by 113 · cited 2× · see citing works
“However, the action potential plateau, phase 2, was markedly elevated by adrenergic stimulation in several reports, reflected by increased APD50 (Kecskemeti et al. 1985; Li and Nattel 1997; Redpath et al. 2006).”
Hoppe, U. C., & Beuckelmann, D. J. (1998) · Cardiovascular Research · doi:10.1016/s0008-6363(98)00047-9 · Cited by 104 · see citing works
Barbuti, A., Terragni, B., Brioschi, C., & DiFrancesco, D. (2007) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2006.09.018 · Cited by 104 · cited 2× · see citing works
“In rabbit SA node, β-stimulation increased If, associated with a positive shift in its activation voltage (Barbuti et al. 2007), and accelerated the deactivation of IKr and IKS (Lei et al.”
Cha, T., Ehrlich, J., Zhang, L.-M., Chartier, D., Leung, T., & Nattel, S. (2005) · Circulation · doi:10.1161/01.cir.0000155240.05251.d0 · Cited by 101 · cited 2× · see citing works
“In dogs, chronic rapid atrial rate also decreased APD 90 in isolated PVs (Chen et al. 2000; 14/32 Cha et al. 2005), and either enhanced (Chen et al. 2000) or did not enhance (Cha et al. 2005) the ability of PVs to produce arrhythmic activity.”
What role does modulation of the ryanodine receptor play in cardiac inotropy and arrhythmogenesis?
Eisner, D., Kashimura, T., O'Neill, S., Venetucci, L., & Trafford, A. (2009) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2008.12.005 · Cited by 100 · cited 17×
“β-Stimulation could elevate CaSR content and [Ca ]i sufficiently to cause propagating waves of CICR, which may increase Ca extrusion via INa/Ca sufficiently to produce DADs (Eisner et al. 2009).”
InfluentialTriggered activity and atrial fibrillation.
Wit, A. L., & Boyden, P. (2007) · Heart Rhythm · doi:10.1016/j.hrthm.2006.12.021 · Cited by 98 · cited 2× · see citing works
“proportion with an increasing stimulation rate (Wit and Boyden 2007), as demonstrated in canine atria with”
Koumi, S., Backer, C. L., Arentzen, C., & Sato, R. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118358 · Cited by 97 · cited 2×
“Calibrations: 25 mV, 100 ms. Based on data in (Stengl et al. 2006) (i), (Koumi et al. 1995) (ii), (Yeh et al. 1992) (iii), and (Redpath et al. 2006) (iv) with 19/32 permission from Oxford University Press, American Society for Clinical Investigation, S. Karger AG, Basel, and Elsevier, respectively.…”
Na(+)‐Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium.
Zhou, Z.-F., & Lipsius, S. (1993) · Journal of Physiology · doi:10.1113/jphysiol.1993.sp019720 · Cited by 95 · cited 1×
“INa/Ca was increased by ISO in cat atrium (Zhou and Lipsius 1993), but human atrial data are lacking.”
Greiser, M., Halaszovich, C., Frechen, D., Boknı́k, P., Ravens, U., Dobrev, D., Lückhoff, A., & Schotten, U. (2007) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/s00210-007-0174-6 · Cited by 91 · cited 3× · see citing works
“Nevertheless, chronic AF has consistently been shown to be associated with a potentiated effect of ISO to increase human atrial ICaL (Van Wagoner et al. 1999; Skasa et al. 2001; Christ et al. 2004; Greiser et al. 2007).”
Calstabin deficiency, ryanodine receptors, and sudden cardiac death
Lehnart, S. E., Wehrens, X. H. T., & Marks, A. R. (2004) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2004.08.032 · Cited by 91 · cited 2× · see citing works
“It has been suggested (Lehnart et al. 2004) that chronic adrenergic activation in HF may cause hyperphosphorylation of RyRs and a consequent increased diastolic leak of Ca 2+ SR .”
Skasa, M., Jüngling, E., Picht, E., Schöndube, F., & Lückhoff, A. (2001) · Basic Research in Cardiology · doi:10.1007/s003950170065 · Cited by 89 · cited 2× · see citing works
“Nevertheless, chronic AF has consistently been shown to be associated with a potentiated effect of ISO to increase human atrial ICaL (Van Wagoner et al. 1999; Skasa et al. 2001; Christ et al. 2004; Greiser et al. 2007).”
Johnson, N. J., Danilo, P., Wit, A. L., & Rosen, M. R. (1986) · Circulation · doi:10.1161/01.cir.74.5.1168 · Cited by 85 · cited 3× · see citing works
“2007), as demonstrated in canine atria with adrenaline (Johnson et al. 1986).”
Inotropic and electrophysiological effects of histamine on human ventricular heart muscle.
Eckel, L., Gristwood, R., Nawrath, H., Owen, D. A., & Satter, P. (1982) · Journal of Physiology · doi:10.1113/jphysiol.1982.sp014332 · Cited by 82 · cited 1×
“…repolarisation, since in isolated tissues or cells, APD 95 was markedly prolonged by noradrenaline or ISO in three of four available studies (Eckel et al. 1982; Mitchell et al. 1986; Koumi et al. 1995) (Figure 2aii), and by adrenaline in two of three tissues in the other study (Yeh et al.…”
Grammer, J., Zeng, X.-R., Bosch, R., & Kühlkamp, V. (2001) · Basic Research in Cardiology · doi:10.1007/s003950170081 · Cited by 78 · cited 3×
“I CaL did not change, either in amplitude (Workman et al. 2003b; Pau et al. 2003; Redpath et al. 2006; Workman et al. 2006; Pau et al. 2007), activation voltage-dependence (Redpath et al. 2006), single channel gating (Klein et al. 2003) or expression (Grammer et al. 2001).”
Lei, M., Brown, H., & Terrar, D. (2000) · Experimental Physiology · doi:10.1111/j.1469-445x.2000.01915.x · Cited by 75 · cited 1×
“…increased I f , associated with a positive shift in its activation voltage (Barbuti et al. 2007), and accelerated the deactivation of I Kr and I KS (Lei et al. 2000); each potentially accelerating phase 4. β-stimulation also increases SA nodal I CaL and peak [Ca 2+ ] i , potentially enhancing…”
Oral, H., Crawford, T. C., Frederick, M. A., Gadeela, N., Wimmer, A. P., Dey, S., SARRAZIN, J., Kühne, M., Chalfoun, N. T., Wells, D., et al. (2008) · Journal of Cardiovascular Electrophysiology · doi:10.1111/j.1540-8167.2007.01089.x · Cited by 74 · cited 2× · see citing works
“Infusion of isoprenaline (isoproterenol, ISO), a mixed β-receptor agonist, produced AF in 5% of patients with no history of AF, and in 84% of patients with paroxysmal AF, in a dose-dependent manner (Oral et al. 2008).”
Vascular smooth muscle cell migration mediated by thrombin and urokinase receptor.
Noda-Heiny, H., & Sobel, B. (1995) · American Journal of Physiology · doi:10.1152/ajpcell.1995.268.5.c1195 · Cited by 73
Webb, J., & Hollander, P. B. (1956) · Circulation Research · doi:10.1161/01.res.4.3.332 · Cited by 73
Dinanian, S., Boixel, C., Juin, C., Hulot, J., Coulombe, A., Rücker-Martin, C., Bonnet, N., le Grand, B., Slama, M., Mercadier, J., et al. (2008) · European Heart Journal · doi:10.1093/eurheartj/ehn140 · Cited by 72 · cited 2×
“2009), or potentiated (Dinanian et al. 2008) in patients with”
Steeds, R. P., Birchall, A., Smith, M., & Channer, K. (1999) · Heart · doi:10.1136/hrt.82.2.170 · Cited by 70 · cited 2× · see citing works
“A β 1 -blocker also caused a moderate reduction in the incidence of paroxysmal AF (Steeds et al. 1999) or of relapse into AF after electrical or pharmacological cardioversion (Kuhlkamp et al. 2000).”
Activation of calcium currents in cardiac myocytes by empty beta-adrenoceptors.
Mewes, T., Dutz, S., Ravens, U., & Jakobs, K. (1993) · Circulation · doi:10.1161/01.cir.88.6.2916 · Cited by 70 · cited 1×
“For example, a reduction by atenolol of cAMPstimulated I CaL in human atrial cells (Mewes et al. 1993) might suppress arrhythmic activity that involves increased CICR.”
Hedberg, A., Kempf, F., Josephson, M., & Molinoff, P. (1985) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)23687-4 · Cited by 70 · cited 4×
“In human atrium, however, although up to 55% of β-receptors are β 2 (Hedberg et al. 1985), ISO did not affect APD 75 (Redpath et al. 2006). β 2 -stimulation increased human atrial I CaL (Skeberdis et al. 1997) and I f (Lonardo et al. 2005), although the I f increase was greater with β 1 than β 2…”
InfluentialHaghjoo, M., Saravi, M., Hashemi, M. J., Hosseini, S., Givtaj, N., Ghaffarinejad, M. H., Khamooshi, A. J., Emkanjoo, Z., Fazelifar, A. F., Alizadeh, A., et al. (2007) · Heart Rhythm · doi:10.1016/j.hrthm.2007.04.022 · Cited by 66 · cited 2× · see citing works
“Carvedilol was more effective than a β 1 -blocker (Haghjoo et al. 2007), perhaps by decreasing I Kur and I TO (Deng et al. 2007).”
Roth, D. A., Urasawa, K., Helmer, G. A., & Hammond, H. K. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116315 · Cited by 65 · cited 10×
“CHF also increased atrial diastolic [Ca 2+ ] i , the Ca 2+ i transient, and Ca 2+ SR content, associated with " spontaneous Ca 2+ transient events " (Yeh et al. 2008).”
InfluentialThe arrhythmogenic actions of histamine on human atrial fibers.
Levi, R., Malm, J. R., Bowman, F. O., & Rosen, M. R. (1981) · Circulation Research · doi:10.1161/01.res.49.2.545 · Cited by 61 · cited 1× · see citing works
“A similar effect of adrenergic stimulation was observed in other human studies (Mary-Rabine et al. 1980; Levi et al. 1981), as well as in healthy animal atria (Davis 1975; Ono et al. 1995).”
Štengl, M., Ramakers, C., Donker, D. W., Nabar, A., Rybin, A. V., Spätjens, R. L., van der Nagel, T., Wodzig, W. K. W. H., Sipido, K., Antoons, G., et al. (2006) · Cardiovascular Research · doi:10.1016/j.cardiores.2006.07.015 · Cited by 61 · cited 3×
“Based on data in (Stengl et al. 2006) (i), (Koumi et al.”
Subchronic alpha‐ and beta‐adrenergic regulation of cardiac gap junction protein expression
Salameh, A., Frenzel, C., Boldt, A., Rassler, B., Glawe, I., Schulte, J., Mühlberg, K., Zimmer, H.-G., Pfeiffer, D., & Dhein, S. (2006) · The FASEB Journal · doi:10.1096/fj.05-4871fje · Cited by 60 · cited 1× · see citing works
“outweighed by an opposing increase in Igap (Salameh et al. 2006).”
Klein, G., Schröder, F., Vogler, D., Schaefer, A., Haverich, A., Schieffer, B., Korte, T., & Drexler, H. (2002) · Cardiovascular Research · doi:10.1016/s0735-1097(02)80542-3 · Cited by 60 · cited 2×
“I CaL did not change, either in amplitude (Workman et al. 2003b; Pau et al. 2003; Redpath et al. 2006; Workman et al. 2006; Pau et al. 2007), activation voltage-dependence (Redpath et al. 2006), single channel gating (Klein et al. 2003) or expression (Grammer et al. 2001).”
Alpha and Beta Adrenergic Effects on Human Atrial Specialized Conducting Fibers
Mary-Rabine, L., Hordof, A., Bowman, F. O., Malm, J., Rosen, M., & Perry, N. E. (1978) · Circulation · doi:10.1161/01.cir.57.1.84 · Cited by 60 · cited 1×
“Specialised conducting fibres from human RA were identified by their pacemaker activity after ceasing stimulation, and adrenaline increased phase 4 and automatic rate (Mary-Rabine et al. 1978).”
Kojodjojo, P., Peters, N. S., Davies, D. W., & Kanagaratnam, P. (2007) · Journal of Cardiovascular Electrophysiology · doi:10.1111/j.1540-8167.2007.00723.x · Cited by 57 · cited 2× · see citing works
“dispersion (Kojodjojo et al. 2007), and decreased atrial isolated tissue or cellular ERP (Workman et al.”
Shimizu, W., Tsuchioka, Y., Karakawa, S., Nagata, K., Mukai, J., Yamagata, T., Matsuura, H., Kajiyama, G., & Matsuura, Y. (1994) · British heart journal · doi:10.1136/hrt.71.1.34 · Cited by 57 · cited 3× · see citing works
“%) decrease (Shimizu et al. 1994a) and of no change (Redpath et al. 2006).”
Mechanism of plasma catecholamine increases during coronary artery bypass and valve procedures.
Engelman, R. M., Haag, B., Lemeshow, S., Angelo, A., & Rousou, J. (1983) · Journal of Thoracic and Cardiovascular Surgery · doi:10.1016/s0022-5223(19)39130-5 · Cited by 57 · cited 1×
“Moreover, AF substantially increases the risk of stroke, heart failure (HF) and death (Fuster et al. 2006).”
TRANSMEMBRANE ACTION POTENTIALS AND CONTRACTIONS OF HUMAN ATRIAL MUSCLE.
Sleator, W., & DeGubareff, T. (1964) · American Journal of Physiology · doi:10.1152/ajplegacy.1964.206.5.1000 · Cited by 56
Schackow, T. E., & ten Eick, R. E. (1994) · Journal of Physiology · doi:10.1113/jphysiol.1994.sp020008 · Cited by 52 · cited 1×
“I KATP was increased by ISO in cat ventricle, from ATP i depletion rather than a direct effect (Schackow et al. 1994), but atrial data are lacking.”
Workman, A. J. (2003) · Cardiovascular Research · doi:10.1016/s0008-6363(03)00263-3 · Cited by 51 · cited 10× · see citing works
“That is consistent with a lack of change in APD 50 (Workman et al. 2003b; Redpath et al. 2006).”
InfluentialSelf-citationBartholomeu, J. B., Vanzelli, A., Rolim, N., Ferreira, J., Bechara, L. R. G., Tanaka, L., Rosa, K., Alves, M. M., Medeiros, A., Mattos, K. C., et al. (2008) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2008.05.011 · Cited by 51 · cited 2× · see citing works
“No reports on atrial Ca 2+ i were found, but chronic β1-blockade in mice increased a HF-impaired ventricular Ca 2+ i transient (Bartholomeu et al. 2008).”
Raine, A. E., & Vaughan-Williams, E. (1981) · Circulation Research · doi:10.1161/01.res.48.6.804 · Cited by 48 · cited 1×
“Such " pharmacological remodelling " (Workman et al. 2003b) was originally demonstrated in rabbits (Raine et al. 1981).”
Workman, A., Pau, D., Redpath, C., Marshall, G. E., Russell, J., Norrie, J., Kane, K., & Rankin, A. (2008) · Heart Rhythm · doi:10.1016/j.hrthm.2008.12.028 · Cited by 47 · cited 7× · see citing works
“associated with a reduction in the atrial cellular ERP (Workman et al. 2009).”
InfluentialSelf-citationBerglund, H., Boukter, S., Theodorsson, E., Vallin, H., & Edhag, O. (1990) · British heart journal · doi:10.1136/hrt.64.1.9 · Cited by 47 · cited 2×
“without HF may not change catecholamine levels in patients (Berglund et al. 1990).”
Workman, A., Pau, D., Redpath, C., Marshall, G. E., Russell, J., Kane, K. A., Norrie, J., & Rankin, A. (2006) · Cardiovascular Electrophysiology · doi:10.1111/j.1540-8167.2006.00592.x · Cited by 46 · cited 5× · see citing works
“…β 1 -, β 2 -and α 1 -antagonist, also substantially reduced the incidence of AF/atrial flutter (McMurray et al. 2005). β-blockers reduced the incidence of AF following cardiac surgery (Mathew et al. 2004; Workman et al. 2006), and post-surgery β-blocker withdrawal increased it (Mathew et al. 2004).”
InfluentialSelf-citationComparison of Ca2+-handling properties of canine pulmonary vein and left atrial cardiomyocytes.
Coutu, P., Chartier, D., & Nattel, S. (2006) · American Journal of Physiology. Heart and Circulatory Physiology · doi:10.1152/ajpheart.00730.2005 · Cited by 45 · cited 4× · see citing works
“1995), as reported in atria of other species (Mackenzie et al. 2004; Danson et al. 2005; Coutu et al. 2006).”
InfluentialBosch, R., Schneck, A., Kiehn, J., Zhang, W., Hambrock, A., Eigenberger, B., Rüb, N., Gogel, J., Mewis, C., Seipel, L., et al. (2002) · doi:10.1016/s0008-6363(02)00601-6 · Cited by 44 · cited 1×
“In ventricle, β 3 -stimulation moderately affected APD (Gauthier et al. 1996; Bosch et al. 2002), probably via I KS (Bosch et al. 2002) which may have limited involvement in human atrium.”
Workman, A., Kane, K., & Rankin, A. (2003) · Cardiovascular Research · doi:10.1016/s0008-6363(03)00466-8 · Cited by 42 · cited 10× · see citing works
“That is consistent with a lack of change in APD 50 (Workman et al. 2003b; Redpath et al. 2006).”
InfluentialSelf-citationCharacterization of the Stretch-activated Chloride Channel in Isolated Human Atrial Myocytes
Sato, R., & Koumi, S. (1998) · Journal of Membrane Biology · doi:10.1007/s002329900371 · Cited by 42 · cited 1×
“However, ISO had inconsistent effects on human atrial I Cl , with either an increase (Tsai et al. 2001) or no change (Sakai et al. 1995) in I Cl.cAMP , or no change in I Cl.swell (Sato et al. 1998).”
Chloride conductance in human atrial cells.
Sakai, R., Hagiwara, N., Kasanuki, H., & Hosoda, S. (1995) · Journal of Molecular and Cellular Cardiology · doi:10.1016/s0022-2828(95)92199-0 · Cited by 42 · cited 1×
“However, ISO had inconsistent effects on human atrial I Cl , with either an increase (Tsai et al. 2001) or no change (Sakai et al. 1995) in I Cl.cAMP , or no change in I Cl.swell (Sato et al. 1998).”
Yeh, Y.-H., Ehrlich, J., Qi, X., Hébert, T., Chartier, D., & Nattel, S. (2007) · Cardiovascular Research · doi:10.1016/j.cardiores.2007.01.020 · Cited by 41 · cited 6× · see citing works
“Species differences in effects of adrenergic stimulation on atrial terminal repolarisation should be noted, however, with shortening in dog (Liang et al. 1985; Yeh et al. 2007), and lengthening in guinea pig (Yoshimoto et al.”
InfluentialPau, D., Workman, A., Kane, K., & Rankin, A. (2006) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2006.08.007 · Cited by 41 · cited 5× · see citing works
“This contrasts with an attenuated effect of 5-hydroxytryptamine (5- HT) on I CaL (Pau et al. 2007), despite both acting via cAMP.”
InfluentialSelf-citationParoxysmal atrial fibrillation in sleep.
Coccagna, G., Capucci, A., Bauleo, S., Boriani, G., & Santarelli, A. (1997) · Sleep · doi:10.1093/sleep/20.6.396 · Cited by 41 · cited 2×
“In patients, heart rate variability studies indicated an increased level of adrenergic, relative to cholinergic, activity in the minutes preceding the onset of AF (Dimmer et al. 1998; Coccagna et al. 1997).”
Negative chronotropic effect of endothelin 1 mediated through ETA receptors in guinea pig atria.
Ono, K., Eto, K., Sakamoto, A., Masaki, T., Shibata, K., Sada, T., Hashimoto, K., & Tsujimoto, G. (1995) · Circulation Research · doi:10.1161/01.res.76.2.284 · Cited by 40 · cited 2× · see citing works
“1981), as well as in healthy animal atria (Davis 1975; Ono et al. 1995).”
Redpath, C., Rankin, A., Kane, K., & Workman, A. (2006) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2006.01.012 · Cited by 39 · cited 17×
“In RA isolated cells stimulated at physiological rate, ISO caused action potentials to be interrupted frequently by low amplitude, usually sub-threshold, transient depolarisations, termed " cellular arrhythmic depolarisations " (CADs) (Redpath et al. 2006) (Figure 1b).”
InfluentialSelf-citationLiang, B.-T., Frame, L. H., & Molinoff, P. (1985) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.82.13.4521 · Cited by 39 · cited 4× · see citing works
“Species differences in effects of adrenergic stimulation on atrial terminal repolarisation should be noted, however, with shortening in dog (Liang et al. 1985; Yeh et al. 2007), and lengthening in guinea pig (Yoshimoto et al. 1998) and rat (Webb et al. 1956).”
InfluentialRaine, A. E., & Chubb, I. (1977) · Nature · doi:10.1038/267265a0 · Cited by 37 · cited 1×
“1988), possibly related to a reduction in adrenergic nerve activity (Raine and Chubb 1977).”
Workman, A., Kane, K., & Rankin, A. (1999) · Cardiovascular Research · doi:10.1016/s0008-6363(99)00166-2 · Cited by 36 · cited 2×
“This probably involves an anti-adrenergic effect on I CaL , which is the main inward current in AV node (Workman et al. 1999). βblockers can also prevent AF, convert it to sinus rhythm, or maintain sinus rhythm after it is restored, depending on β-blocker type and cardiac pathology (Lopez-Sendon et…”
Self-citationSwedberg, K. (2007) · doi:10.3410/f.1050385.502285 · Cited by 34 · cited 1×
“For example, in patients with CHF, β 1 -blockade substantially reduced the incidence of AF (Van Veldhuisen et al. 2006).”
Reduced beta-agonist sensitivity in single atrial cells from failing human hearts.
Harding, S. E., Jones, S., O'Gara, P. T., Vescovo, G., & Poole-Wilson, P. (1990) · American Journal of Physiology · doi:10.1152/ajpheart.1990.259.4.h1009 · Cited by 34 · cited 2× · see citing works
“responses to ISO were attenuated (Harding et al. 1990).”
Gelband, H., Rosen, M. R., Myerburg, R., Bush, H. L., Bassett, A. L., & Hoffman, B. F. (1977) · Journal of Electrocardiology · doi:10.1016/s0022-0736(77)80003-4 · Cited by 34 · cited 3×
“was associated with chronic AF in patients (Gould et al. 2006).”
The Effects of Slow Channel Blockers and Beta Blockers on Atrioventricular Nodal Conduction
Prystowsky, E. N. (1988) · The Journal of Clinical Pharmacology · doi:10.1002/j.1552-4604.1988.tb03095.x · Cited by 34 · cited 2× · see citing works
“The mechanism is a slowing of atrioventricular (AV) nodal conduction, associated with increased AV nodal ERP and AH interval (Prystowsky 1988).”
Ryanodine Receptor-Mediated Ca2+ Events in Atrial Myocytes of Patients with Atrial Fibrillation
Liang, X., Xie, H., Zhu, P., Hu, J., Zhao, Q., Wang, C.-S., & Yang, C. (2008) · The Cardiology · doi:10.1159/000119697 · Cited by 33 · cited 2×
“(Liang et al. 2008) in frequency, and increased (Liang et al.”
Stambler, B., Wood, M., & Ellenbogen, K. (1996) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(95)00459-9 · Cited by 33 · cited 2× · see citing works
“thus potentially promoting reentry (Stambler et al. 1996).”
Pau, D., Workman, A., Kane, K. A., & Rankin, A. (2003) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0705553 · Cited by 32 · cited 1×
“I CaL did not change, either in amplitude (Workman et al. 2003b; Pau et al. 2003; Redpath et al. 2006; Workman et al. 2006; Pau et al. 2007), activation voltage-dependence (Redpath et al. 2006), single channel gating (Klein et al. 2003) or expression (Grammer et al. 2001).”
Self-citationStiber, J., Seth, M., & Rosenberg, P. (2009) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e3181aa233f · Cited by 31 · cited 1× · see citing works
“Reports of effects of adrenergic stimulation on other mechanosensitive currents (Stiber et al. 2009) in human atrium could not be found.”
Scherer, D., Kiesecker, C., Kulzer, M., Günth, M., Scholz, E., Kathöfer, S., Thomas, D., Maurer, M., Kreuzer, J., Bauer, A., et al. (2007) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/s00210-007-0167-5 · Cited by 30 · cited 2×
“However, since β3-stimulation can affect IK1 (Scherer et al. 2007), ICaL, and Ca 2+ i (Cheng et al.”
Evidence for presence of Ca2+ channel-gated Ca2+ stores in neonatal human atrial myocytes.
Hatem, S., Sweeten, T., Vetter, V., & Morad, M. (1995) · American Journal of Physiology · doi:10.1152/ajpheart.1995.268.3.h1195 · Cited by 29 · cited 1×
“In human atrial cells, β-stimulation increased the Ca 2+ i transient amplitude (Hatem et al. 1995), as reported in atria of other species (Mackenzie et al. 2004; Danson et al. 2005; Coutu et al. 2006).”
Adrenergic Modulation of Potassium Currents in Isolated Human Atrial Myocytes.
Su, M.-J., Chi, J.-F., & Chu, S.-H. (1994) · Journal of Biomedical Sciences · doi:10.1007/bf02253349 · Cited by 28 · cited 6×
“Altered plateau voltages resulting from changes in I Kur also may affect terminal repolarisation via I Kr and I KS (Wettwer et al. 2004), and adrenergic stimulation increased I Kur in human atrium (Li et al. 1996; Su et al. 1994).”
InfluentialRegional distribution of β1- and β2-adrenoceptors in the failing and nonfailing human heart
Steinfath, M., Lavický, J., Schmitz, W., Scholz, H., Döring, V., & Kalmar, P. (2004) · European Journal of Clinical Pharmacology · doi:10.1007/bf00265923 · Cited by 27 · cited 2×
“An attenuated β-response may involve impaired βreceptor function or signalling, or a reduction in receptor density, as shown in atria of patients with end stage HF (Steinfath et al. 1992) or pigs with CHF (Roth et al. 1993).”
Kaumann, A., & Sanders, L. (1993) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/bf00173215 · Cited by 26 · see citing works
Lonardo, G., Cerbai, E., Casini, S., Giunti, G., Bonacchi, M., Battaglia, F., Fiorani, B., Stefàno, P., Sani, G., & Mugelli, A. (2005) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2004.12.010 · Cited by 24 · cited 3× · see citing works
“…however, although up to 55% of β-receptors are β 2 (Hedberg et al. 1985), ISO did not affect APD 75 (Redpath et al. 2006). β 2 -stimulation increased human atrial I CaL (Skeberdis et al. 1997) and I f (Lonardo et al. 2005), although the I f increase was greater with β 1 than β 2 -stimulation.”
Oostendorp, J., & Kaumann, A. (2000) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/s002109900156 · Cited by 24
Sato, R., & Koumi, S. (1995) · Journal of Membrane Biology · doi:10.1007/bf00207274 · Cited by 24
Danson, E., Zhang, Y.-H., Sears, C., Edwards, A., Casadei, B., & Paterson, D. J. (2005) · Cardiovascular Research · doi:10.1016/j.cardiores.2005.04.034 · Cited by 23 · cited 4× · see citing works
“β-Stimulation also increased atrial diastolic [Ca]i (Danson et al. 2005), and might enhance a diastolic CaSR leak, as shown in rabbit ventricle (Curran et al.”
InfluentialMitchell, M. R., Powell, T., Sturridge, M., Terrar, D., & Twist, V. (1986) · Cardiovascular Research · doi:10.1093/cvr/20.12.869 · Cited by 23 · cited 1×
“…repolarisation, since in isolated tissues or cells, APD 95 was markedly prolonged by noradrenaline or ISO in three of four available studies (Eckel et al. 1982; Mitchell et al. 1986; Koumi et al. 1995) (Figure 2aii), and by adrenaline in two of three tissues in the other study (Yeh et al. 1992).”
Adults with congenital heart disease.
Ho, N. C. (2003) · The Lancet · doi:10.1016/s0140-6736(03)14987-2 · Cited by 22 · cited 1×
“…AF in patients was associated with a decreased atrial ERP and RA conduction velocity, increased ERP dispersion (Kojodjojo et al. 2007) and decreased atrial isolated tissue or cellular ERP (Workman et al. 2001) or APD 90 (Bosch et al. 1999; Workman et al. 2001; Wettwer et al. 2004; Pau et al. 2007).”
Remodelling of human atrial K+ currents but not ion channel expression by chronic β-blockade
Marshall, G. E., Russell, J., Tellez, J. O., Jhund, P., Currie, S., Dempster, J., Boyett, M., Kane, K., Rankin, A., & Workman, A. (2011) · Pflügers Archiv: European Journal of Physiology · doi:10.1007/s00424-011-1061-z · Cited by 21
Self-citationSchaffer, P., Pelzmann, B., Bernhart, E., Lang, P., Løkebø, J. E., Mächler, H., Rigler, B., & Koidl, B. (1998) · Pflügers Archiv · doi:10.1007/s004240050657 · Cited by 20 · cited 1× · see citing works
“I Kr and I KS were relatively small or present in only a minority of cells (Wang et al. 1994; Schaffer et al. 1998), but this might reflect disruption of these currents by the requisite " chunk " method of cell isolation (Yue et al. 1996), and in intact atrial tissue, I Kr blockade may prolong APD…”
Beta-2 adrenergic activation of L-type Ca++ current in cardiac myocytes.
Skeberdis, V. A., Jurevičius, J., & Fischmeister, A. R. (1997) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)37062-4 · Cited by 20 · cited 2× · see citing works
“…however, although up to 55% of β-receptors are β 2 (Hedberg et al. 1985), ISO did not affect APD 75 (Redpath et al. 2006). β 2 -stimulation increased human atrial I CaL (Skeberdis et al. 1997) and I f (Lonardo et al. 2005), although the I f increase was greater with β 1 than β 2 -stimulation.”
Cardiac Responses After Norepinephrine‐Induced Ventricular Hypertrophy in Rats
Brown, L., Sernia, C., Newling, R., & Fletcher, P. (1992) · Journal of Cardiovascular Pharmacology · doi:10.1097/00005344-199208000-00019 · Cited by 20 · cited 2×
“…HF may preferentially downregulate β 1 , in atrium, depending on the cause of HF (Steinfath et al. 1992), and that could result from chronic adrenergic stimulation (Brown et al. 1992). β 3 density was not studied in atrium, although this was increased in ventricle (Moniotte et al. 2001).”
Serotonin, I(f) and human atrial arrhythmia.
Workman, A., & Rankin, A. C. (1998) · Cardiovascular Research · doi:10.1016/s0008-6363(98)00258-2 · Cited by 19 · cited 1× · see citing works
“However, whether such an increase could lead to atrial arrhythmias from AA is uncertain (Workman and Rankin 1998), because of the rather negative activation voltage of If relative to atrial MDP, and the small current size under physiological [K]o.”
Self-citationDeng, C.-Y., Yu, X.-Y., Kuang, S.-J., Zhang, W.-C., Zhou, Z.-L., Zhang, K., Qian, W.-M., Shan, Z., Yang, M., Wu, S.-L., et al. (2007) · Life Science · doi:10.1016/j.lfs.2006.10.012 · Cited by 18 · cited 2×
“Carvedilol was more effective than a β 1 -blocker (Haghjoo et al. 2007), perhaps by decreasing I Kur and I TO (Deng et al. 2007).”
Shimizu, A., Fukatani, M., Tanigawa, M., Kaibara, M., Konoe, A., Isomoto, S., Centurión, O., Yano, K., & Hashiba, K. (1994) · International Journal of Cardiology · doi:10.1016/0167-5273(94)90006-x · Cited by 18 · cited 3×
“%) decrease (Shimizu et al. 1994a) and of no change (Redpath et al. 2006).”
Rasmussen, H. H., ten Eick, R. E., Okita, G. T., Hartz, R. S., & Singer, D. H. (1985) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)24214-8 · Cited by 18 · cited 2×
“However, the hyperpolarisation caused by rewarming of human atrial tissue, considered to be due to I p reactivation, was unaffected by adrenaline (Rasmussen et al. 1985).”
Adults with congenital heart disease.
Celermajer, D. S., & Deanfield, J. (1991) · British medical journal · doi:10.1136/bmj.303.6815.1413 · Cited by 17 · see citing works
ADAPTATIONAL RESPONSES TO PROLONGED β‐ADRENOCEPTOR BLOCKADE IN ADULT RABBITS
Raine, A. E., & Vaughan-Williams, E. (1980) · doi:10.1111/j.1476-5381.1980.tb07926.x · Cited by 17 · cited 1×
“That was confirmed in plasma and tissue samples (Raine et al. 1980).”
Kiss, O., Zima, E., Soós, P., Kékesi, V., Juhász-Nagy, A., & Merkely, B. (2004) · Life Science · doi:10.1016/j.lfs.2003.11.033 · Cited by 13 · cited 2×
“In dogs, adrenaline (Sharifov et al. 2004) or ISO (Kiss et al. 2004; Sharifov et al. 2004) produced AF, and ISO facilitated acetylcholine-induced AF (Sharifov et al. 2004).”
Yoshimoto, K., Hattori, Y., Houzen, H., Kanno, M., & Yasuda, K. (1998) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0702008 · Cited by 13 · cited 1×
“Species differences in effects of adrenergic stimulation on atrial terminal repolarisation should be noted, however, with shortening in dog (Liang et al. 1985; Yeh et al. 2007), and lengthening in guinea pig (Yoshimoto et al. 1998) and rat (Webb et al. 1956).”
Effects of autonomic neurohumors on transmembrane potentials of atrial plateau fibers.
Davis, L. D. (1975) · American Journal of Physiology · doi:10.1152/ajplegacy.1975.229.5.1351 · Cited by 11 · cited 4×
“induced AA in canine atrial fibres (Davis 1975), or AT in a CHF-remodelled atrium that produced spontaneous depo-”
InfluentialArrhythmogenic mechanisms in human atrial and ventricular muscle fibers.
Yeh, T., Vassalle, M., & Lin, C.-I. (1992) · The Cardiology · doi:10.1159/000175004 · Cited by 11 · cited 5×
“Of the six available reports in isolated tissues or cells, five showed no significant effect of adrenaline or ISO on APD 90 (Sleator et al. 1964; Gelband et al. 1977; Kecskemeti et al. 1985; Yeh et al. 1992; Redpath et al. 2006 ).”
InfluentialAdenosine inhibits the L-type calcium current in human atrial myocytes
Pelzmann, B., Schaffer, P., Mächler, H., Rigler, B., & Koidl, B. (1995) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/bf00233249 · Cited by 10 · cited 1×
“Adrenergic stimulation has consistently been shown to increase human atrial I CaL , often more than 2-fold, e.g. (Ouadid et al. 1995; Pelzmann et al. 1995; Li et al. 1997; Van Wagoner et al. 1999; Christ et al. 2004; Redpath et al. 2006; Greiser et al. 2007) (Figure 2b).”
Modulation of cytosolic free calcium concentration by α1-adrenoceptors in rat atrial cells
Jahnel, U., Nawrath, H., Shieh, R., Sharma, V., Williford, D., & Sheu, S. (1992) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/bf00167576 · Cited by 10 · cited 2×
“However, the APD increase could also involve an increase in the Cai transient (Jahnel et al. 1992), although data are lacking in human atrium.”
Tsai, C.-S., Cheng, T.-H., Lin, C.-I., Chen, J.-J., Lee, F., Li, C.-Y., Hong, H.-J., & Loh, S. (2001) · European Journal of Pharmacology · doi:10.1016/s0014-2999(01)01145-1 · Cited by 6 · cited 2×
“However, ISO had inconsistent effects on human atrial ICl, with either an increase (Tsai et al. 2001) or no change (Sakai et al.”
P3-2: Effects of carvedilol on rabbit atrial cell electrophysiology
Cao, F., Huang, C.-X., Wang, T., Li, X., Jiang, H., & Bao, M.-W. (2006) · doi:10.1016/j.hrthm.2006.02.534 · Cited by 4 · cited 1×
“The I TO 17/32 reduction, as found also in atrial cells from rabbits treated with carvedilol (Cao et al. 2006), did not involve altered voltage-dependency, kinetics or channel expression (Marshall et al. 2009).”
公洋, 吉. (1998) · doi:10.11501/3146351 · Cited by 3 · cited 1×
“Species differences in effects of adrenergic stimulation on atrial terminal repolarisation should be noted, however, with shortening in dog (Liang et al. 1985; Yeh et al. 2007), and lengthening in guinea pig (Yoshimoto et al. 1998) and rat (Webb et al. 1956).”
Pharmacological remodelling of human atrial k+ currents by chronic beta-blockade
Marshall, G. E., Rankin, A., Kane, K., & Workman, A. (2006) · doi:10.1093/eurheartj/ehl212 · Cited by 2 · cited 2×
“…patients in sinus rhythm showed that β 1 -blocker treatment for ≥ 7 days was associated with an increased APD 90 and ERP (Workman et al. 2003b; Redpath et al. 2006; Workman et al. 2006) (Figure 3b), and a decreased I TO (Workman et al. 2003b; Marshall et al. 2009) and I K1 (Marshall et al. 2006).”
Self-citationLee, H. (1990) · doi:10.1016/0022-2828(90)91350-g · Cited by 2 · cited 2×
“I Na was reduced by ISO in human atrium (Lee et al. 1990).”
Catheter Ablation of Atrial Fibrillation: For Whom and How?
Katritsis, D. (2008) · Angiology · doi:10.1177/0003319708318581 · Cited by 1 · cited 1× · see citing works
“However, radiofrequency ablation of atrial ganglionated plexi, sites rich in adrenergic and cholinergic neurons, may not be as efficacious as other ablation procedures (Katritsis 2008).”
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
- Christ T Boknik P Wohrl S L-type Ca2+ current downregulation in chronic human atrial fibrillation is associated with increased activity of protein phosphatases Circulation 2004 110 2651 2657 15492323
- Ehrlich JR Nattel S Novel approaches for pharmacological management of atrial fibrillation Drugs 2009 69 757 774 19441867
- Kecskemeti V Kelemen K Solti F Physiological and pharmacological analysis of transmembrane action potentials of human atrial fibers Adv Myocardiol 1985 6 37 47 3887530
- Mary-Rabine L Hordof AJ Danilo P Jr. Mechanisms for impulse initiation in isolated human atrial fibers Circ Res 1980 47 267 277 7397958
- Wang C Zhang YJ Wang YL Effect of dipfluzine on delayed afterdepolarizations and triggered activity induced by isoprenaline in human atrial fibers Acta Pharmaceutica Sinica 2006 41 184 187 16671553
- Workman AJ Rankin AC Serotonin, If and human atrial arrhythmia Cardiovasc Res 1998 40 436 437 10070482
- Workman AJ Kane KA Rankin AC Cellular bases for human atrial fibrillation Heart Rhythm 2008 5 S1 S6 18456193 PMC2639647
Cited by
Sorted by citations
Heijman, J., Voigt, N., Nattel, S., & Dobrev, D. (2014) · Circulation Research · doi:10.1161/circresaha.114.302226 · Cited by 681 · see citing works
“Indeed, sympathetic stimulation provides an important trigger promoting Ca-handling abnormalities and AF initiation.(30)”
BackgroundPost-operative atrial fibrillation: a maze of mechanisms
Maesen, B. A. E., Nijs, J., Maessen, J. G., Allessie, M. A., & Schotten, U. (2011) · EP Europace · doi:10.1093/europace/eur208 · Cited by 456 · see citing works
Human Atrial Action Potential and Ca2+ Model: Sinus Rhythm and Chronic Atrial Fibrillation
Grandi, E., Pandit, S., Voigt, N., Workman, A., Dobrev, D., Jalife, J., & Bers, D. (2011) · Circulation Research · doi:10.1161/circresaha.111.253955 · Cited by 390 · see citing works
Self-citationCaMKII as a Therapeutic Target in Cardiovascular Disease
Gaido, O. E. R., Nkashama, L. J., Schole, K. L., Wang, Q., Umapathi, P., Mesubi, O. O., Konstantinidis, K., Luczak, E. D., & Anderson, M. E. (2022) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-051421-111814 · Cited by 129 · see citing works
“In several animal and human studies of atrial fibrillation and heart failure, there is an increase in several CaMKII upstream signals such as ROS (27, 132, 133), renin-angiotensin-aldosterone system metabolites (134, 135), and catecholamines (136, 137) in atrial tissue or circulating plasma.”
BackgroundMicroRNAs and atrial fibrillation: new fundamentals
Wang, Z., Lu, Y., & Yang, B. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq350 · Cited by 107 · see citing works
Risk of atrial fibrillation in athletes: a systematic review and meta-analysis
Newman, W., Parry-Williams, G., Wiles, J., Edwards, J., Hulbert, S., Kipourou, K., Papadakis, M., Sharma, R., & O'Driscoll, J. (2021) · British Journal of Sports Medicine · doi:10.1136/bjsports-2021-103994 · Cited by 110 · see citing works
Identification of atrial fibrillation associated genes and functional non-coding variants
van Ouwerkerk, A. F., Bosada, F. M., van Duijvenboden, K., Hill, M. C., Montefiori, L. E., Scholman, K. T., Liu, J., de Vries, A. A. F., Boukens, B. J., Ellinor, P. T., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12721-5 · Cited by 94 · see citing works
Ömerovic, E., Citro, R., Bossone, E., Redfors, B., Backs, J., Bruns, B., Ciccarelli, M., Couch, L. S., Dawson, D. K., Grassi, G. M., et al. (2021) · European Journal of Heart Failure · doi:10.1002/ejhf.2400 · Cited by 97 · see citing works
Murad, K., Brubaker, P. H., Fitzgerald, D. M., Morgan, T. M., Goff, D. C., Soliman, E. Z., Eggebeen, J., & Kitzman, D. W. (2012) · Congestive Heart Failure · doi:10.1111/j.1751-7133.2011.00282.x · Cited by 78 · see citing works
The Blinding Period Following Ablation Therapy for Atrial Fibrillation
Gottlieb, L. A., Dekker, L., & Coronel, R. (2021) · JACC. Clinical electrophysiology · doi:10.1016/j.jacep.2021.01.011 · Cited by 80 · see citing works
Rezaei, Y., Peighambari, M. M., Naghshbandi, S., Samiei, N., Ghavidel, A. A., Dehghani, M. R., Haghjoo, M., & Hosseini, S. (2019) · American Journal of Cardiovascular Drugs · doi:10.1007/s40256-019-00365-1 · Cited by 80 · see citing works
Sakamoto, A., Kitakaze, M., Takamoto, S., Namiki, A., Kasanuki, H., & Hosoda, S. (2012) · Circulation Journal · doi:10.1253/circj.cj-11-1332 · Cited by 68
New-Onset Atrial Fibrillation After Cardiac Surgery: Pathophysiology, Prophylaxis, and Treatment.
Lomivorotov, V., Efremov, S., Pokushalov, E., & Karaskov, A. (2016) · Journal of Cardiothoracic and Vascular Anesthesia · doi:10.1053/j.jvca.2015.08.003 · Cited by 66 · see citing works
Benzoni, P., Campostrini, G., Landi, S., Bertini, V., Marchina, E., Iascone, M., Ahlberg, G., Olesen, M., Crescini, E., Mora, C., et al. (2019) · Cardiovascular Research · doi:10.1093/cvr/cvz217 · Cited by 60 · see citing works
CYP2J2 Overexpression Protects against Arrhythmia Susceptibility in Cardiac Hypertrophy
Westphal, C., Spallek, B., Konkel, A., Markó, L., Qadri, F., DeGraff, L. M., Schubert, C., Bradbury, J., Regitz-Zagrosek, V., Falck, J., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0073490 · Cited by 57 · see citing works
“Adrenergic stimulation from catecholamines can cause atrial fibrillation in patients [32].”
BackgroundWorkman, A., Marshall, G. E., Rankin, A., Smith, G. L., & Dempster, J. (2012) · Journal of Physiology · doi:10.1113/jphysiol.2012.235986 · Cited by 55 · see citing works
“…the marked plateau elevation from concurrent ITO subtraction and β-stimulation, each of which increases [Ca2+]i (Sah et al. 2002; Dong et al. 2010; Workman, 2010), with consequent [Ca2+]i loading sufficient to produce DADs and/or abnormal automaticity via spontaneous sarcoplasmic reticular Ca2+…”
BackgroundInfluentialSelf-citationGender Differences in Electrophysiological Gene Expression in Failing and Non-Failing Human Hearts
Ambrosi, C. M., Yamada, K. A., Nerbonne, J. M., & Efimov, I. R. (2013) · PLoS ONE · doi:10.1371/journal.pone.0054635 · Cited by 59 · see citing works
“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 AF [46].”
BackgroundChronic Atrial Fibrillation Alters the Functional Properties of If in the Human Atrium
Stillitano, F., Lonardo, G., Giunti, G., del Lungo, M., Coppini, R., Spinelli, V., Sartiani, L., Poggesi, C., Mugelli, A., & Cerbai, E. (2013) · Cardiovascular Electrophysiology · doi:10.1111/jce.12212 · Cited by 50 · see citing works
de la Fuente, M. G., Barana, A., Gómez, R., Amorós, I., Dolz-Gaitón, P., Sacristán, S., Atienza, F., Pita, A., Pinto, Á., Fernández-Avilés, F., et al. (2013) · Cardiovascular Research · doi:10.1093/cvr/cvs313 · Cited by 50
“These are exciting results considering that the duration of terminal repolarization, which is actually shortened by CAF, is a major determinant of ARP and that it is generally accepted that shortening of ARP favours re-entry.1,2 Importantly, the role of IKs in determining the APD rises in prominence at increasing beat…”
BackgroundInfluentialTsai, W.-C., Chen, Y.-C., Lin, Y.-K., Chen, S.-A., & Chen, Y.-J. (2011) · Circulation: Arrhythmia and Electrophysiology · doi:10.1161/circep.111.961995 · Cited by 49 · see citing works
Chan, W., Yang, K.-P., Chao, T., Huang, C.-C., Huang, P.-H., Chen, Y.-C., Chen, T.-J., Lin, S.-J., Chen, J.-W., & Leu, H. (2014) · International Journal of Cardiology · doi:10.1016/j.ijcard.2014.07.087 · Cited by 48 · see citing works
“reported that newly developed AF was induced by inhaled fluticasone propionate [42].”
BackgroundKettlewell, S., Burton, F., Smith, G. L., & Workman, A. (2013) · Cardiovascular Research · doi:10.1093/cvr/cvt087 · Cited by 46
“phorylation/activation of numerous ion channels and Cai-handling proteins.(14) We used ISO at supra-maximal concentration to ensure”
MethodSelf-citationMechanisms of termination and prevention of atrial fibrillation by drug therapy
Workman, A. J., Smith, G. L., & RANKIN, A. C. (2011) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2011.02.002 · Cited by 44 · see citing works
Self-citationKlinger, R., Thunberg, C. A., White, W., Fontes, M., Waldron, N., Piccini, J., Hughes, G., Podgoreanu, M., Stafford-Smith, M., Newman, M., et al. (2015) · Anesthesia and Analgesia · doi:10.1213/ane.0000000000000873 · Cited by 42 · see citing works
Hanson, B., Child, N., van Duijvenboden, S., Orini, M., Chen, Z., Coronel, R., Rinaldi, C., Gill, J., Gill, J., & Taggart, P. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00414 · Cited by 42
“…and elicit changes in the potassium and calcium channels, both of which are important components of the cardiac action potential, it is possible that oscillations in APD may also occur at this slower frequency (Zipes and Jalife, 1999; Workman, 2010; Taggart et al., 2011; Shen and Zipes, 2014).”
BackgroundBeta-adrenoceptor signaling pathways mediate cardiac pathological remodeling.
Fu, Y.-N., Xiao, H., & Zhang, Y.-Y. (2012) · Frontiers in Bioscience · doi:10.2741/484 · Cited by 38
“Recently, Workman AJ (16) summarized the understanding of the involvement of the adrenergic system and its control in atrial fibrillation.”
BackgroundTargeting Ca2 + Handling Proteins for the Treatment of Heart Failure and Arrhythmias
Njegić, A., Wilson, C., & Cartwright, E. J. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.01068 · Cited by 45 · see citing works
“Unsurprisingly, enhanced adrenergic activity has been identified in arrhythmic conditions, including AF, and results in enhanced automaticity and triggered activity (Workman, 2010; Antzelevitch and Burashnikov, 2011).”
BackgroundHuman Atrial Fibrillation: insights from computational electrophysiological models
Bers, D., & Grandi, E. (2011) · Trends in cardiovascular medicine · doi:10.1016/j.tcm.2012.04.004 · Cited by 34
At the heart of the matter: how mental stress and negative emotions affect atrial fibrillation
Leo, D. G., Ozdemir, H., Lane, D. A., Lip, G. Y. H., Keller, S. S., & Proietti, R. (2023) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2023.1171647 · Cited by 31 · see citing works
“The influence of catecholamines in promoting atrial arrhythmic activity may have a role in the onset of cardiac arrhythmias (122).”
BackgroundCarter‐Storch, R., Dahl, J. S., Christensen, N. L., Pecini, R., Søndergård, E., Øvrehus, K. A., & Møller, J. E. (2019) · Interactive Cardiovascular and Thoracic Surgery · doi:10.1093/icvts/ivz094 · Cited by 34 · see citing works
Yang, S.-S., Han, W., Cao, Y., Dong, G., Zhou, G., Li, W.-M., Gan, R.-T., Chang, H.-Y., & Wang, Z. (2011) · Basic Research in Cardiology · doi:10.1007/s00395-011-0154-3 · Cited by 31 · see citing works
Muhib, S., Fujino, T., Sato, N., & Hasebe, N. (2013) · International Heart Journal · doi:10.1536/ihj.54.297 · Cited by 30 · see citing works
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Takotsubo cardiomyopathy: do the genetics matter?
Limongelli, G., D'Alessandro, R., Masarone, D., Maddaloni, V., Vriz, O., Minisini, R., Citro, R., Calabrò, P., Russo, M., Calabro', R., et al. (2013) · Heart Failure Clinics · doi:10.1016/j.hfc.2012.12.008 · Cited by 29
New drugs vs. old concepts: A fresh look at antiarrhythmics
Thireau, J., Pasquié, J., Martel, E., Guennec, J. L., & Richard, S. (2011) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2011.03.003 · Cited by 32 · see citing works
“1) (Corr et al., 1986; Coumel & Maison-Blanche, 1991; Zipes & Wellens, 1998; Zipes & Rubart, 2006; Workman, 2010).”
Genetics of Takotsubo Syndrome.
Limongelli, G., Masarone, D., Maddaloni, V., Rubino, M., Fratta, F., Cirillo, A., Ludovica, S. B., Pacileo, R., Fusco, A., Coppola, G., et al. (2016) · Heart Failure Clinics · doi:10.1016/j.hfc.2016.06.007 · Cited by 27
A Computer Simulation Study of Anatomy Induced Drift of Spiral Waves in the Human Atrium
Kharche, S., Biktasheva, I., Seemann, G., Zhang, H.-G., & Biktashev, V. N. (2015) · BioMed Research International · doi:10.1155/2015/731386 · Cited by 27
“However, there is experimental evidence that spiral and scroll waves (SWs) play a prominent role in promoting atrial arrhythmia [11, 12] as reflected in recent experimental, computational, and theoretical studies [13–17].”
BackgroundNovel pharmacological approaches for antiarrhythmic therapy
Ravens, U. (2010) · Naunyn-Schmiedeberg's Archives of Pharmacology · doi:10.1007/s00210-009-0487-8 · Cited by 27 · see citing works
“The role of catecholamines in atrial fibrillation and the therapeutic benefits of β-adrenoceptor blocking drugs are summarised by (Workman 2009).”
BackgroundSimopoulos, V., Tagarakis, G., Hatziefthimiou, A., Skoularigis, I., Triposkiadis, F., Trantou, V., Tsilimingas, N., & Aidonidis, I. (2014) · Clinical Research in Cardiology · doi:10.1007/s00392-014-0754-7 · Cited by 27 · see citing works
“However, a combination of EPL with beta-blockers is seemingly in the right direction since EPL’s antiarrhythmic effects have been shown to be reversed by isoproterenol [9], resembling clinical situations of high adrenergic tone as after cardiac surgery accompanying by heart failure [10].”
BackgroundJohnsen, A., Høydal, M., Røsbjørgen, R. N., Stølen, T., & Wisløff, U. (2013) · PLoS ONE · doi:10.1371/journal.pone.0066288 · Cited by 26 · see citing works
“Alterations in Ca homeostasis in HF may be a predisposing factor to atrial arrhythmic activity [26].”
BackgroundHuang, J.-J., Wu, B.-Q., Qin, P., Cheng, Y.-P., Zhang, Z.-Y., & Chen, Y.-M. (2023) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2023.1270452 · Cited by 25 · see citing works
“Catecholamines can in fl uence every electrophysiological mechanism of AF initiation and maintenance in human atria (34).”
Backgroundvan Loon, T., Rijks, J., van Koll, J., Wolffs, J., Cornelussen, R., van Osta, N., Luermans, J., Prinzen, F., Linz, D., van Empel, V. V., et al. (2024) · European Heart Journal · doi:10.1093/eurheartj/ehae718 · Cited by 24
“28 This absence of adrenergic modulation may be further compounded by anaesthesia, beta-blockers, and/or calcium channel blockers used by most patients in our cohort ( Table 1 ), all of which are known to suppress adrenergic responses.”
Mitrić, G., Udy, A., Bandeshe, H., Clement, P., & Boots, R. (2016) · Critical Care · doi:10.1186/s13054-016-1252-2 · Cited by 24
“Both of these mechanisms have been shown to be initiated through adrenergic stimulation with catecholamines [35].”
BackgroundInfluentialAtrial Function in Patients with Breast Cancer After Treatment with Anthracyclines
Yaylali, Y., Sarıçopur, A., Yurtdaş, M., Şenol, H., & Gokoz-Doğu, G. (2016) · Arquivos Brasileiros de Cardiologia · doi:10.5935/abc.20160146 · Cited by 23
Kharche, S., Stary, T., Colman, M., Biktasheva, I., Workman, A., Rankin, A., Holden, A., & Zhang, H.-G. (2014) · Europace · doi:10.1093/europace/euu084 · Cited by 23
“[6] Workman AJ.”
Self-citationCardiovascular Safety Considerations in the Treatment of Neurogenic Orthostatic Hypotension.
Olshansky, B., & Muldowney, J. (2020) · American Journal of Cardiology · doi:10.1016/j.amjcard.2020.01.037 · Cited by 22 · see citing works
Prolonged atrial fibrillation following generalized tonic–clonic seizures
Surges, R., Moskau, S., Viebahn, B., Schoene‐Bake, J., SCHWAB, J. O., & Elger, C. E. (2012) · Seizure · doi:10.1016/j.seizure.2012.05.012 · Cited by 22 · see citing works
Identification of Atrial Fibrillation-Related lncRNA Based on Bioinformatic Analysis
Xie, L., Huang, G.-L., Gao, M., Huang, J.-M., Li, H., Xia, H., Xiang, X., Wu, S.-Z., & Ruan, Y.-J. (2022) · Disease Markers · doi:10.1155/2022/8307975 · Cited by 21
“There is increasing evidence that the mainmechanism of arrhythmia may depend on cardiology and adrenergic stress [30].”
BackgroundRetractedTokmaji, G., McClure, R., Kaneko, T., & Aranki, S. (2013) · Cardiology Research and Practice · doi:10.1155/2013/637482 · Cited by 21 · see citing works
“Myocardial ischemia, atrial cannulation, aortic cross-clamp time, left ventricular venting, hyper and hypovolemic states, damage to the atrium, endotracheal tube insertion, excess inotropic requirements, and electrolyte imbalances are snapshots into the various factors published in the literature as potential predicto…”
BackgroundRemodelling of human atrial K+ currents but not ion channel expression by chronic β-blockade
Marshall, G. E., Russell, J., Tellez, J. O., Jhund, P., Currie, S., Dempster, J., Boyett, M., Kane, K., Rankin, A., & Workman, A. (2011) · Pflügers Archiv: European Journal of Physiology · doi:10.1007/s00424-011-1061-z · Cited by 21
“The mechanisms underlying these atrial antiarrhythmic effects are multifactorial [32, 36], but there is evidence to suggest that long-term treatment with β-blockers can alter atrial cellular electrophysiology by prolonging the action potential duration (APD) and effective refractory period [29, 35] and, therefore, pot…”
InfluentialSelf-citationKettlewell, S., Saxena, P., Dempster, J., Colman, M., Myles, R., Smith, G. L., & Workman, A. (2019) · Journal of Physiology · doi:10.1113/jp277827 · Cited by 20 · see citing works
“To test whether ICaL,D-C window narrowing could suppress or prevent EADs, we induced EADs either by increasing the conductance of an injected ICaL,D-C having a normal window (as produced, for example, by adrenergic stimulation) (Workman, 2010) or, in myocytes then failing to generate EADs, adding the APD-prolonging”
BackgroundSelf-citationKim, S.-J., Zhang, H., Khaliulin, I., Choisy, S., Bond, R., Lin, H., Haou, S. E., Milnes, J., Hancox, J., Suleiman, M., et al. (2012) · Circulation: Arrhythmia and Electrophysiology · doi:10.1161/circep.112.975425 · Cited by 20
“ated with atrial-triggered activity and may involve modulation of Ca handling.(41) Furthermore, glycolytic inhibition”
BackgroundCircadian rhythms of early afterdepolarizations and ventricular arrhythmias in a cardiomyocyte model
Diekman, C. O., & Wei, N. (2020) · bioRxiv · doi:10.1101/2020.09.13.295436 · Cited by 19
“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 · see citing works
“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 · see citing works
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 · see citing works
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 · see citing works
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 · see citing works
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 · see citing works
Fitzgerald, P. J. (2013) · Medical Hypotheses · doi:10.1016/j.mehy.2013.01.018 · Cited by 18 · see citing works
“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 · see citing works
“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 · see citing works
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 · see citing works
“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 · see citing works
“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 · see citing works
“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 · see citing works
“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 · see citing works
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 · see citing works
Molecular Basis of Atrial Fibrillation Initiation and Maintenance
Beneke, K., & Molina, C. (2021) · Hearts · doi:10.3390/hearts2010014 · Cited by 9 · see citing works
“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 · see citing works
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 · see citing works
Verkerk, A., & Wilders, R. (2023) · Biomedicines · doi:10.3390/biomedicines11092447 · Cited by 7 · see citing works
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 · see citing works
Identification of necroptosis-related diagnostic biomarkers in coronary heart disease
You, H., & Han, W.-Q. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e30269 · Cited by 6 · see citing works
“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 · see citing works
Grégoire-Lacoste, F., Jacquemet, V., & Vinet, A. (2014) · Mathematical Biosciences · doi:10.1016/j.mbs.2014.01.010 · Cited by 6 · see citing works
Workman, A., & Rankin, A. (2010) · Heart Rhythm · doi:10.1016/j.hrthm.2010.04.004 · Cited by 6 · see citing works
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 · see citing works
“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 · see citing works
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 · see citing works
“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 · see citing works
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 · see citing works
Hardi, H., Barinda, A. J., Vidya, A. P., Utama, K. E., & Mahata, L. (2026) · Cardiovascular Toxicology · doi:10.1007/s12012-025-10087-3 · Cited by 3 · see citing works
“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 · see citing works
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 · see citing works
“…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 3 · see citing works
“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 6 · see citing works
“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. K. (2024) · Journal of ECT · doi:10.1097/yct.0000000000001029 · Cited by 2
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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