Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long-Term Rapid Atrial Stimulation Model
Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short‐term atrial pacing, although the effect of a long‐term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation...
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Veröffentlicht in: | Pacing and clinical electrophysiology 2003-11, Vol.26 (11), p.2072-2082 |
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description | Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short‐term atrial pacing, although the effect of a long‐term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. (PACE 2003; 26:2072–2082) |
doi_str_mv | 10.1046/j.1460-9592.2003.00323.x |
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The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. 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The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. (PACE 2003; 26:2072–2082)</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>atrial fibrillation</subject><subject>Atrial Fibrillation - etiology</subject><subject>Cardiac Pacing, Artificial</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>electrical remodeling</subject><subject>Heart Atria</subject><subject>Heart Conduction System - drug effects</subject><subject>Heart Conduction System - physiology</subject><subject>Heart Rate - drug effects</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Contraction - physiology</subject><subject>Refractory Period, Electrophysiological - drug effects</subject><subject>Refractory Period, Electrophysiological - physiology</subject><subject>verapamil</subject><subject>Verapamil - pharmacology</subject><issn>0147-8389</issn><issn>1540-8159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1v0zAYgC3ExMrgLyCfuCX4K7Fz4FBV3ZjUjrGNbTfLSd52Ls4HdiLaf49DK7hysGxZz2PrfRDClKSUiPzTLqUiJ0mRFSxlhPA0LsbT_Ss0o5kgiaJZ8RrNCBUyUVwV5-htCDtCSE5E9gadR5sxTuQMDY_gTW8a6_D92PceQoCAhxfA1-1L13RbaMEOB9xt8NJBNXhbGYfvoOlqcLbdYttigxemtS3gVddukwfwDb4zva3xPOKRvh9sMzoz2K7F68l7h842xgV4f9ov0PfL5cPiS7L6enW9mK-SKqMFT1itSJnLLC9LpiDOQmhJOWNAmJEbE28F5UrlEkghmKIlF5kRshZxzILUnF-gj8d3e9_9HCEMurGhAudMC90YtIw6k0JEUB3ByncheNjo3tvG-IOmRE_F9U5PxfVUXE_F9Z_ieh_VD6c_xrKB-p94ShyBz0fgl3Vw-O-H9e18sYyn6CdH34YB9n9943_oXHKZ6aebK72-Yd8Yf37Wa_4b6Fmd0Q</recordid><startdate>200311</startdate><enddate>200311</enddate><creator>MORIGUCHI, MASAHIKO</creator><creator>NIWANO, SHINICHI</creator><creator>YOSHIZAWA, NAOTO</creator><creator>KOJIMA, JISHO</creator><creator>INUO, KIMIATSU</creator><creator>IZUMI, TOHRU</creator><general>Blackwell Publishing</general><scope>BSCLL</scope><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>200311</creationdate><title>Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long-Term Rapid Atrial Stimulation Model</title><author>MORIGUCHI, MASAHIKO ; NIWANO, SHINICHI ; YOSHIZAWA, NAOTO ; KOJIMA, JISHO ; INUO, KIMIATSU ; IZUMI, TOHRU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5193-2d80b6756bb28e14701b1322e02a7fabb24138867e094281b345a47d406090d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>atrial fibrillation</topic><topic>Atrial Fibrillation - etiology</topic><topic>Cardiac Pacing, Artificial</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>electrical remodeling</topic><topic>Heart Atria</topic><topic>Heart Conduction System - drug effects</topic><topic>Heart Conduction System - physiology</topic><topic>Heart Rate - drug effects</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Contraction - physiology</topic><topic>Refractory Period, Electrophysiological - drug effects</topic><topic>Refractory Period, Electrophysiological - physiology</topic><topic>verapamil</topic><topic>Verapamil - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MORIGUCHI, MASAHIKO</creatorcontrib><creatorcontrib>NIWANO, SHINICHI</creatorcontrib><creatorcontrib>YOSHIZAWA, NAOTO</creatorcontrib><creatorcontrib>KOJIMA, JISHO</creatorcontrib><creatorcontrib>INUO, KIMIATSU</creatorcontrib><creatorcontrib>IZUMI, TOHRU</creatorcontrib><collection>Istex</collection><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>Pacing and clinical electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MORIGUCHI, MASAHIKO</au><au>NIWANO, SHINICHI</au><au>YOSHIZAWA, NAOTO</au><au>KOJIMA, JISHO</au><au>INUO, KIMIATSU</au><au>IZUMI, TOHRU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long-Term Rapid Atrial Stimulation Model</atitle><jtitle>Pacing and clinical electrophysiology</jtitle><addtitle>Pacing Clin Electrophysiol</addtitle><date>2003-11</date><risdate>2003</risdate><volume>26</volume><issue>11</issue><spage>2072</spage><epage>2082</epage><pages>2072-2082</pages><issn>0147-8389</issn><eissn>1540-8159</eissn><abstract>Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short‐term atrial pacing, although the effect of a long‐term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 ± 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 ± 4 ms in the control group and was larger than that in the verapamil group (31 ± 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (−19 ± 3 vs −5 ± 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged. (PACE 2003; 26:2072–2082)</abstract><cop>350 Main Street , Malden , MA 02148-5018 , U.S.A</cop><pub>Blackwell Publishing</pub><pmid>14622307</pmid><doi>10.1046/j.1460-9592.2003.00323.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis of Variance Animals Anti-Arrhythmia Agents - pharmacology atrial fibrillation Atrial Fibrillation - etiology Cardiac Pacing, Artificial Disease Models, Animal Dogs electrical remodeling Heart Atria Heart Conduction System - drug effects Heart Conduction System - physiology Heart Rate - drug effects Myocardial Contraction - drug effects Myocardial Contraction - physiology Refractory Period, Electrophysiological - drug effects Refractory Period, Electrophysiological - physiology verapamil Verapamil - pharmacology |
title | Verapamil Suppresses the Inhomogeneity of Electrical Remodeling in a Canine Long-Term Rapid Atrial Stimulation Model |
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