Pharmacological prevention and termination of focal atrial fibrillation
Aims Patients undergo ablation for focal atrial fibrillation (AF) as a result of failure of anti-arrhythmic drugs. Our basic studies have implicated cholinergic and adrenergic neurotransmitter release as the underlying mechanism for focal AF. Therefore, we tested the efficacy of a combination of sod...
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| Veröffentlicht in: | Europace (London, England) England), 2012-03, Vol.14 (3), p.426-430 |
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| creator | Moers, Annerie M.E. Scherlag, Benjamin J. Niu, Guodong Lu, Zhibing Ghias, Muhammad Lazzara, Ralph Jackman, Warren M. Po, Sunny S. |
| description | Aims
Patients undergo ablation for focal atrial fibrillation (AF) as a result of failure of anti-arrhythmic drugs. Our basic studies have implicated cholinergic and adrenergic neurotransmitter release as the underlying mechanism for focal AF. Therefore, we tested the efficacy of a combination of sodium channel-blocking agents with additional vagolytic properties and a β-blocker to terminate and prevent focal AF.
Methods and results
In 18 Na-pentobarbital-anaesthetized dogs, after a right or left thoracotomy, acetylcholine (Ach, 0.5 cc, 100 mM) was injected into a fat pad containing ganglionated plexi (GP) or applied on an atrial appendage (AA) to induce focal firing at the pulmonary veins (PVs) or AA, respectively. Disopyramide (2-4 mg/kg, n= 6) or quinidine (3-6 mg/kg, n= 12) combined with esmolol or propranolol (1 mg/kg, n= 13 and 5, respectively) were slowly injected to terminate (Group I, n= 12) or prevent (Group II, n= 6) Ach-induced sustained focal AF. In another four dogs, only the sodium channel-blocking agents with additional vagolytic properties or only the β-blocker was injected prior to or after the initiation of focal AF. At baseline, the mean duration of AF induced by Ach was 26 ± 4 min. Group I: After drugs, Ach-induced AF duration was 3 ± 1 min (P< 0.001). Group II: Prior to drugs, Ach-induced AF lasted for 19 ± 3 min. With the drug combination the duration of Ach-induced AF, decreased to 6 ± 1/min, P< 0.001. Either quinidine or propranolol alone did not change the duration of Ach-induced AF, mean 25 ± 10 min compared with Ach alone, 28 ± 16 min, P= 0.2.
Conclusions
Type IA (cholinergic antagonist) plus Type II (β-adrenergic antagonist) provides significant prevention and suppression of focal AF arising at PV and non-PV sites. |
| doi_str_mv | 10.1093/europace/eur301 |
| format | Article |
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Patients undergo ablation for focal atrial fibrillation (AF) as a result of failure of anti-arrhythmic drugs. Our basic studies have implicated cholinergic and adrenergic neurotransmitter release as the underlying mechanism for focal AF. Therefore, we tested the efficacy of a combination of sodium channel-blocking agents with additional vagolytic properties and a β-blocker to terminate and prevent focal AF.
Methods and results
In 18 Na-pentobarbital-anaesthetized dogs, after a right or left thoracotomy, acetylcholine (Ach, 0.5 cc, 100 mM) was injected into a fat pad containing ganglionated plexi (GP) or applied on an atrial appendage (AA) to induce focal firing at the pulmonary veins (PVs) or AA, respectively. Disopyramide (2-4 mg/kg, n= 6) or quinidine (3-6 mg/kg, n= 12) combined with esmolol or propranolol (1 mg/kg, n= 13 and 5, respectively) were slowly injected to terminate (Group I, n= 12) or prevent (Group II, n= 6) Ach-induced sustained focal AF. In another four dogs, only the sodium channel-blocking agents with additional vagolytic properties or only the β-blocker was injected prior to or after the initiation of focal AF. At baseline, the mean duration of AF induced by Ach was 26 ± 4 min. Group I: After drugs, Ach-induced AF duration was 3 ± 1 min (P< 0.001). Group II: Prior to drugs, Ach-induced AF lasted for 19 ± 3 min. With the drug combination the duration of Ach-induced AF, decreased to 6 ± 1/min, P< 0.001. Either quinidine or propranolol alone did not change the duration of Ach-induced AF, mean 25 ± 10 min compared with Ach alone, 28 ± 16 min, P= 0.2.
Conclusions
Type IA (cholinergic antagonist) plus Type II (β-adrenergic antagonist) provides significant prevention and suppression of focal AF arising at PV and non-PV sites.</description><identifier>ISSN: 1099-5129</identifier><identifier>EISSN: 1532-2092</identifier><identifier>DOI: 10.1093/europace/eur301</identifier><identifier>PMID: 21933797</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Acetylcholine - administration & dosage ; Adrenergic beta-Antagonists - therapeutic use ; Animals ; Anti-Arrhythmia Agents - therapeutic use ; Atrial Appendage - drug effects ; Atrial Fibrillation - drug therapy ; Atrial Fibrillation - prevention & control ; Disopyramide - therapeutic use ; Dogs ; Drug Therapy, Combination ; Pulmonary Veins - drug effects ; Quinidine - therapeutic use ; Sodium Channel Blockers - therapeutic use</subject><ispartof>Europace (London, England), 2012-03, Vol.14 (3), p.426-430</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2011. For permissions please email: journals.permissions@oup.com. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-acc1ef6bda76a9cfb87ec30d5800e02bf451b6d01f2562ad02ee84f20b41fa393</citedby><cites>FETCH-LOGICAL-c372t-acc1ef6bda76a9cfb87ec30d5800e02bf451b6d01f2562ad02ee84f20b41fa393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,1601,27911,27912</link.rule.ids><linktorsrc>$$Uhttps://dx.doi.org/10.1093/europace/eur301$$EView_record_in_Oxford_University_Press$$FView_record_in_$$GOxford_University_Press</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21933797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moers, Annerie M.E.</creatorcontrib><creatorcontrib>Scherlag, Benjamin J.</creatorcontrib><creatorcontrib>Niu, Guodong</creatorcontrib><creatorcontrib>Lu, Zhibing</creatorcontrib><creatorcontrib>Ghias, Muhammad</creatorcontrib><creatorcontrib>Lazzara, Ralph</creatorcontrib><creatorcontrib>Jackman, Warren M.</creatorcontrib><creatorcontrib>Po, Sunny S.</creatorcontrib><title>Pharmacological prevention and termination of focal atrial fibrillation</title><title>Europace (London, England)</title><addtitle>Europace</addtitle><description>Aims
Patients undergo ablation for focal atrial fibrillation (AF) as a result of failure of anti-arrhythmic drugs. Our basic studies have implicated cholinergic and adrenergic neurotransmitter release as the underlying mechanism for focal AF. Therefore, we tested the efficacy of a combination of sodium channel-blocking agents with additional vagolytic properties and a β-blocker to terminate and prevent focal AF.
Methods and results
In 18 Na-pentobarbital-anaesthetized dogs, after a right or left thoracotomy, acetylcholine (Ach, 0.5 cc, 100 mM) was injected into a fat pad containing ganglionated plexi (GP) or applied on an atrial appendage (AA) to induce focal firing at the pulmonary veins (PVs) or AA, respectively. Disopyramide (2-4 mg/kg, n= 6) or quinidine (3-6 mg/kg, n= 12) combined with esmolol or propranolol (1 mg/kg, n= 13 and 5, respectively) were slowly injected to terminate (Group I, n= 12) or prevent (Group II, n= 6) Ach-induced sustained focal AF. In another four dogs, only the sodium channel-blocking agents with additional vagolytic properties or only the β-blocker was injected prior to or after the initiation of focal AF. At baseline, the mean duration of AF induced by Ach was 26 ± 4 min. Group I: After drugs, Ach-induced AF duration was 3 ± 1 min (P< 0.001). Group II: Prior to drugs, Ach-induced AF lasted for 19 ± 3 min. With the drug combination the duration of Ach-induced AF, decreased to 6 ± 1/min, P< 0.001. Either quinidine or propranolol alone did not change the duration of Ach-induced AF, mean 25 ± 10 min compared with Ach alone, 28 ± 16 min, P= 0.2.
Conclusions
Type IA (cholinergic antagonist) plus Type II (β-adrenergic antagonist) provides significant prevention and suppression of focal AF arising at PV and non-PV sites.</description><subject>Acetylcholine - administration & dosage</subject><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>Animals</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>Atrial Appendage - drug effects</subject><subject>Atrial Fibrillation - drug therapy</subject><subject>Atrial Fibrillation - prevention & control</subject><subject>Disopyramide - therapeutic use</subject><subject>Dogs</subject><subject>Drug Therapy, Combination</subject><subject>Pulmonary Veins - drug effects</subject><subject>Quinidine - therapeutic use</subject><subject>Sodium Channel Blockers - therapeutic use</subject><issn>1099-5129</issn><issn>1532-2092</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1LxDAQxYMo7rp69ia9CULdSbL9yFEWXYUFPeg5pOlEI21Tk1bwv7fd7nr19N4wv3kMj5BLCrcUBF9i712rNI6GAz0ic5pwFjMQ7HjwIEScUCZm5CyETwDImEhOyYxRwXkmsjnZvHwoXyvtKvdutaqi1uM3Np11TaSaMurQ17ZRu9mZyLiRUZ23gxhbeFtVu-U5OTGqCnix1wV5e7h_XT_G2-fN0_puG2uesS5WWlM0aVGqLFVCmyLPUHMokxwAgRVmldAiLYEalqRMlcAQ85VhUKyoUVzwBbmeclvvvnoMnaxt0Dh80aDrgxSM0zwXNB_I5URq70LwaGTrba38j6Qgx_LkoTw5lTdcXO2z-6LG8o8_tDUANxPg-vbftF-YGH4X</recordid><startdate>201203</startdate><enddate>201203</enddate><creator>Moers, Annerie M.E.</creator><creator>Scherlag, Benjamin J.</creator><creator>Niu, Guodong</creator><creator>Lu, Zhibing</creator><creator>Ghias, Muhammad</creator><creator>Lazzara, Ralph</creator><creator>Jackman, Warren M.</creator><creator>Po, Sunny S.</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201203</creationdate><title>Pharmacological prevention and termination of focal atrial fibrillation</title><author>Moers, Annerie M.E. ; Scherlag, Benjamin J. ; Niu, Guodong ; Lu, Zhibing ; Ghias, Muhammad ; Lazzara, Ralph ; Jackman, Warren M. ; Po, Sunny S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-acc1ef6bda76a9cfb87ec30d5800e02bf451b6d01f2562ad02ee84f20b41fa393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetylcholine - administration & dosage</topic><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>Animals</topic><topic>Anti-Arrhythmia Agents - therapeutic use</topic><topic>Atrial Appendage - drug effects</topic><topic>Atrial Fibrillation - drug therapy</topic><topic>Atrial Fibrillation - prevention & control</topic><topic>Disopyramide - therapeutic use</topic><topic>Dogs</topic><topic>Drug Therapy, Combination</topic><topic>Pulmonary Veins - drug effects</topic><topic>Quinidine - therapeutic use</topic><topic>Sodium Channel Blockers - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moers, Annerie M.E.</creatorcontrib><creatorcontrib>Scherlag, Benjamin J.</creatorcontrib><creatorcontrib>Niu, Guodong</creatorcontrib><creatorcontrib>Lu, Zhibing</creatorcontrib><creatorcontrib>Ghias, Muhammad</creatorcontrib><creatorcontrib>Lazzara, Ralph</creatorcontrib><creatorcontrib>Jackman, Warren M.</creatorcontrib><creatorcontrib>Po, Sunny S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Europace (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Moers, Annerie M.E.</au><au>Scherlag, Benjamin J.</au><au>Niu, Guodong</au><au>Lu, Zhibing</au><au>Ghias, Muhammad</au><au>Lazzara, Ralph</au><au>Jackman, Warren M.</au><au>Po, Sunny S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacological prevention and termination of focal atrial fibrillation</atitle><jtitle>Europace (London, England)</jtitle><addtitle>Europace</addtitle><date>2012-03</date><risdate>2012</risdate><volume>14</volume><issue>3</issue><spage>426</spage><epage>430</epage><pages>426-430</pages><issn>1099-5129</issn><eissn>1532-2092</eissn><abstract>Aims
Patients undergo ablation for focal atrial fibrillation (AF) as a result of failure of anti-arrhythmic drugs. Our basic studies have implicated cholinergic and adrenergic neurotransmitter release as the underlying mechanism for focal AF. Therefore, we tested the efficacy of a combination of sodium channel-blocking agents with additional vagolytic properties and a β-blocker to terminate and prevent focal AF.
Methods and results
In 18 Na-pentobarbital-anaesthetized dogs, after a right or left thoracotomy, acetylcholine (Ach, 0.5 cc, 100 mM) was injected into a fat pad containing ganglionated plexi (GP) or applied on an atrial appendage (AA) to induce focal firing at the pulmonary veins (PVs) or AA, respectively. Disopyramide (2-4 mg/kg, n= 6) or quinidine (3-6 mg/kg, n= 12) combined with esmolol or propranolol (1 mg/kg, n= 13 and 5, respectively) were slowly injected to terminate (Group I, n= 12) or prevent (Group II, n= 6) Ach-induced sustained focal AF. In another four dogs, only the sodium channel-blocking agents with additional vagolytic properties or only the β-blocker was injected prior to or after the initiation of focal AF. At baseline, the mean duration of AF induced by Ach was 26 ± 4 min. Group I: After drugs, Ach-induced AF duration was 3 ± 1 min (P< 0.001). Group II: Prior to drugs, Ach-induced AF lasted for 19 ± 3 min. With the drug combination the duration of Ach-induced AF, decreased to 6 ± 1/min, P< 0.001. Either quinidine or propranolol alone did not change the duration of Ach-induced AF, mean 25 ± 10 min compared with Ach alone, 28 ± 16 min, P= 0.2.
Conclusions
Type IA (cholinergic antagonist) plus Type II (β-adrenergic antagonist) provides significant prevention and suppression of focal AF arising at PV and non-PV sites.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>21933797</pmid><doi>10.1093/europace/eur301</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Europace (London, England), 2012-03, Vol.14 (3), p.426-430 |
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| subjects | Acetylcholine - administration & dosage Adrenergic beta-Antagonists - therapeutic use Animals Anti-Arrhythmia Agents - therapeutic use Atrial Appendage - drug effects Atrial Fibrillation - drug therapy Atrial Fibrillation - prevention & control Disopyramide - therapeutic use Dogs Drug Therapy, Combination Pulmonary Veins - drug effects Quinidine - therapeutic use Sodium Channel Blockers - therapeutic use |
| title | Pharmacological prevention and termination of focal atrial fibrillation |
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