Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles
Background Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. Objective The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activat...
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| Veröffentlicht in: | Heart rhythm 2014-04, Vol.11 (4), p.697-706 |
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| creator | Maruyama, Mitsunori, MD, PhD, FHRS Ai, Tomohiko, MD, PhD Chua, Su-Kiat, MD Park, Hyung-Wook, MD, PhD Lee, Young-Soo, MD, PhD Shen, Mark J., MD Chang, Po-Cheng, MD Lin, Shien-Fong, PhD Chen, Peng-Sheng, MD, FHRS |
| description | Background Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. Objective The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. Methods Intracellular calcium (Cai ) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. Results Repeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+ ]o, 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+ ]o , 9 of 10 hearts (90%) in 1.5 mmol/L [K+ ]o , and 7 of 7 hearts (100%) in 1.0 mmol/L [K+ ]o ( P |
| doi_str_mv | 10.1016/j.hrthm.2013.12.032 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3996562</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S154752711301480X</els_id><sourcerecordid>1510103683</sourcerecordid><originalsourceid>FETCH-LOGICAL-c580t-301b4a325ac7dff7102dea1f833bcfed1d381d2da211806aca915fa283c5a3a33</originalsourceid><addsrcrecordid>eNqFks2KFDEUhQtRnHH0CQTJ0k2V-en66YUDMqgjNLhQwV24ldx0pyeVlElVQ_tIPqUpe2zUjZskcM8953K_FMVzRitGWfNqX-3itBsqTpmoGK-o4A-KS1bXTSm6lj1c3qu2rHnLLoonKe0p5euGisfFBV-Jtmub7rL4cXscwx04HCyQMYYhTJiIgwnJuIOERBCE6I4EzIRR4xgcRPsdJhs8Aa9JRDXHiH4ih3xEq-YsIMb20Tp3kuk5Wr8lNoUckF3QB0esN3NaqtaTDfgteh2iMWTEmAuYjaHv7dnVYXpaPDLgEj67v6-KL-_efr65LTcf33-4ebMpVd3RqRSU9SsQvAbVamNaRrlGYKYTolcGNdOiY5pr4Ix1tAEFa1Yb4J1QNQgQ4qq4PvmOcz-gVssA4OQY7QDxKANY-XfF253choMU63VTNzwbvLw3iOHbjGmSg00K8zo8hjlJVmd-VDTdkiVOUhVDShHNOYZRuVCWe_mLslwoS8Zlppy7Xvw54bnnN9YseH0SYN7TwWKUSVn0CrXNvCapg_1PwPU__cpZbxW4Ozxi2oc5-oxAMplyg_y0fLTln7G8_FVHv4qfakjW6w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1510103683</pqid></control><display><type>article</type><title>Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Maruyama, Mitsunori, MD, PhD, FHRS ; Ai, Tomohiko, MD, PhD ; Chua, Su-Kiat, MD ; Park, Hyung-Wook, MD, PhD ; Lee, Young-Soo, MD, PhD ; Shen, Mark J., MD ; Chang, Po-Cheng, MD ; Lin, Shien-Fong, PhD ; Chen, Peng-Sheng, MD, FHRS</creator><creatorcontrib>Maruyama, Mitsunori, MD, PhD, FHRS ; Ai, Tomohiko, MD, PhD ; Chua, Su-Kiat, MD ; Park, Hyung-Wook, MD, PhD ; Lee, Young-Soo, MD, PhD ; Shen, Mark J., MD ; Chang, Po-Cheng, MD ; Lin, Shien-Fong, PhD ; Chen, Peng-Sheng, MD, FHRS</creatorcontrib><description>Background Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. Objective The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. Methods Intracellular calcium (Cai ) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. Results Repeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+ ]o, 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+ ]o , 9 of 10 hearts (90%) in 1.5 mmol/L [K+ ]o , and 7 of 7 hearts (100%) in 1.0 mmol/L [K+ ]o ( P <.001). Optical mapping showed that isoproterenol and hypokalemia enhanced Cai transient duration (Cai TD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small-conductance calcium-activated potassium channel blocker (apamin) failed to prevent recurrent SVF. Conclusion Beta-adrenergic stimulation and concomitant hypokalemia could cause nonischemic activation of IKATP, heterogeneous APD shortening, and prolongation of Cai TD to provoke late phase 3 EAD, triggered activity, and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.</description><identifier>ISSN: 1547-5271</identifier><identifier>EISSN: 1556-3871</identifier><identifier>DOI: 10.1016/j.hrthm.2013.12.032</identifier><identifier>PMID: 24378768</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Afterdepolarization ; Animals ; ATP-sensitive potassium channels ; Calcium - metabolism ; Cardiovascular ; Electrical storm ; Heart Ventricles ; Hypokalemia ; Hypokalemia - complications ; In Vitro Techniques ; Infusions, Intravenous ; Intracellular calcium ; Isoproterenol - administration & dosage ; Rabbits ; Recurrence ; Ventricular fibrillation ; Ventricular Fibrillation - physiopathology</subject><ispartof>Heart rhythm, 2014-04, Vol.11 (4), p.697-706</ispartof><rights>Heart Rhythm Society</rights><rights>2014 Heart Rhythm Society</rights><rights>Copyright © 2014 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</rights><rights>2013 The Heart Rhythm Society. Published by Elsevier Inc. All rights reserved. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-301b4a325ac7dff7102dea1f833bcfed1d381d2da211806aca915fa283c5a3a33</citedby><cites>FETCH-LOGICAL-c580t-301b4a325ac7dff7102dea1f833bcfed1d381d2da211806aca915fa283c5a3a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.hrthm.2013.12.032$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24378768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maruyama, Mitsunori, MD, PhD, FHRS</creatorcontrib><creatorcontrib>Ai, Tomohiko, MD, PhD</creatorcontrib><creatorcontrib>Chua, Su-Kiat, MD</creatorcontrib><creatorcontrib>Park, Hyung-Wook, MD, PhD</creatorcontrib><creatorcontrib>Lee, Young-Soo, MD, PhD</creatorcontrib><creatorcontrib>Shen, Mark J., MD</creatorcontrib><creatorcontrib>Chang, Po-Cheng, MD</creatorcontrib><creatorcontrib>Lin, Shien-Fong, PhD</creatorcontrib><creatorcontrib>Chen, Peng-Sheng, MD, FHRS</creatorcontrib><title>Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles</title><title>Heart rhythm</title><addtitle>Heart Rhythm</addtitle><description>Background Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. Objective The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. Methods Intracellular calcium (Cai ) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. Results Repeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+ ]o, 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+ ]o , 9 of 10 hearts (90%) in 1.5 mmol/L [K+ ]o , and 7 of 7 hearts (100%) in 1.0 mmol/L [K+ ]o ( P <.001). Optical mapping showed that isoproterenol and hypokalemia enhanced Cai transient duration (Cai TD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small-conductance calcium-activated potassium channel blocker (apamin) failed to prevent recurrent SVF. Conclusion Beta-adrenergic stimulation and concomitant hypokalemia could cause nonischemic activation of IKATP, heterogeneous APD shortening, and prolongation of Cai TD to provoke late phase 3 EAD, triggered activity, and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.</description><subject>Afterdepolarization</subject><subject>Animals</subject><subject>ATP-sensitive potassium channels</subject><subject>Calcium - metabolism</subject><subject>Cardiovascular</subject><subject>Electrical storm</subject><subject>Heart Ventricles</subject><subject>Hypokalemia</subject><subject>Hypokalemia - complications</subject><subject>In Vitro Techniques</subject><subject>Infusions, Intravenous</subject><subject>Intracellular calcium</subject><subject>Isoproterenol - administration & dosage</subject><subject>Rabbits</subject><subject>Recurrence</subject><subject>Ventricular fibrillation</subject><subject>Ventricular Fibrillation - physiopathology</subject><issn>1547-5271</issn><issn>1556-3871</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks2KFDEUhQtRnHH0CQTJ0k2V-en66YUDMqgjNLhQwV24ldx0pyeVlElVQ_tIPqUpe2zUjZskcM8953K_FMVzRitGWfNqX-3itBsqTpmoGK-o4A-KS1bXTSm6lj1c3qu2rHnLLoonKe0p5euGisfFBV-Jtmub7rL4cXscwx04HCyQMYYhTJiIgwnJuIOERBCE6I4EzIRR4xgcRPsdJhs8Aa9JRDXHiH4ih3xEq-YsIMb20Tp3kuk5Wr8lNoUckF3QB0esN3NaqtaTDfgteh2iMWTEmAuYjaHv7dnVYXpaPDLgEj67v6-KL-_efr65LTcf33-4ebMpVd3RqRSU9SsQvAbVamNaRrlGYKYTolcGNdOiY5pr4Ix1tAEFa1Yb4J1QNQgQ4qq4PvmOcz-gVssA4OQY7QDxKANY-XfF253choMU63VTNzwbvLw3iOHbjGmSg00K8zo8hjlJVmd-VDTdkiVOUhVDShHNOYZRuVCWe_mLslwoS8Zlppy7Xvw54bnnN9YseH0SYN7TwWKUSVn0CrXNvCapg_1PwPU__cpZbxW4Ozxi2oc5-oxAMplyg_y0fLTln7G8_FVHv4qfakjW6w</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>Maruyama, Mitsunori, MD, PhD, FHRS</creator><creator>Ai, Tomohiko, MD, PhD</creator><creator>Chua, Su-Kiat, MD</creator><creator>Park, Hyung-Wook, MD, PhD</creator><creator>Lee, Young-Soo, MD, PhD</creator><creator>Shen, Mark J., MD</creator><creator>Chang, Po-Cheng, MD</creator><creator>Lin, Shien-Fong, PhD</creator><creator>Chen, Peng-Sheng, MD, FHRS</creator><general>Elsevier Inc</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><scope>5PM</scope></search><sort><creationdate>20140401</creationdate><title>Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles</title><author>Maruyama, Mitsunori, MD, PhD, FHRS ; Ai, Tomohiko, MD, PhD ; Chua, Su-Kiat, MD ; Park, Hyung-Wook, MD, PhD ; Lee, Young-Soo, MD, PhD ; Shen, Mark J., MD ; Chang, Po-Cheng, MD ; Lin, Shien-Fong, PhD ; Chen, Peng-Sheng, MD, FHRS</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-301b4a325ac7dff7102dea1f833bcfed1d381d2da211806aca915fa283c5a3a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Afterdepolarization</topic><topic>Animals</topic><topic>ATP-sensitive potassium channels</topic><topic>Calcium - metabolism</topic><topic>Cardiovascular</topic><topic>Electrical storm</topic><topic>Heart Ventricles</topic><topic>Hypokalemia</topic><topic>Hypokalemia - complications</topic><topic>In Vitro Techniques</topic><topic>Infusions, Intravenous</topic><topic>Intracellular calcium</topic><topic>Isoproterenol - administration & dosage</topic><topic>Rabbits</topic><topic>Recurrence</topic><topic>Ventricular fibrillation</topic><topic>Ventricular Fibrillation - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maruyama, Mitsunori, MD, PhD, FHRS</creatorcontrib><creatorcontrib>Ai, Tomohiko, MD, PhD</creatorcontrib><creatorcontrib>Chua, Su-Kiat, MD</creatorcontrib><creatorcontrib>Park, Hyung-Wook, MD, PhD</creatorcontrib><creatorcontrib>Lee, Young-Soo, MD, PhD</creatorcontrib><creatorcontrib>Shen, Mark J., MD</creatorcontrib><creatorcontrib>Chang, Po-Cheng, MD</creatorcontrib><creatorcontrib>Lin, Shien-Fong, PhD</creatorcontrib><creatorcontrib>Chen, Peng-Sheng, MD, FHRS</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Heart rhythm</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maruyama, Mitsunori, MD, PhD, FHRS</au><au>Ai, Tomohiko, MD, PhD</au><au>Chua, Su-Kiat, MD</au><au>Park, Hyung-Wook, MD, PhD</au><au>Lee, Young-Soo, MD, PhD</au><au>Shen, Mark J., MD</au><au>Chang, Po-Cheng, MD</au><au>Lin, Shien-Fong, PhD</au><au>Chen, Peng-Sheng, MD, FHRS</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles</atitle><jtitle>Heart rhythm</jtitle><addtitle>Heart Rhythm</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>11</volume><issue>4</issue><spage>697</spage><epage>706</epage><pages>697-706</pages><issn>1547-5271</issn><eissn>1556-3871</eissn><abstract>Background Hypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear. Objective The purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia. Methods Intracellular calcium (Cai ) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts. Results Repeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K+ ]o, 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K+ ]o , 9 of 10 hearts (90%) in 1.5 mmol/L [K+ ]o , and 7 of 7 hearts (100%) in 1.0 mmol/L [K+ ]o ( P <.001). Optical mapping showed that isoproterenol and hypokalemia enhanced Cai transient duration (Cai TD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small-conductance calcium-activated potassium channel blocker (apamin) failed to prevent recurrent SVF. Conclusion Beta-adrenergic stimulation and concomitant hypokalemia could cause nonischemic activation of IKATP, heterogeneous APD shortening, and prolongation of Cai TD to provoke late phase 3 EAD, triggered activity, and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24378768</pmid><doi>10.1016/j.hrthm.2013.12.032</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Afterdepolarization Animals ATP-sensitive potassium channels Calcium - metabolism Cardiovascular Electrical storm Heart Ventricles Hypokalemia Hypokalemia - complications In Vitro Techniques Infusions, Intravenous Intracellular calcium Isoproterenol - administration & dosage Rabbits Recurrence Ventricular fibrillation Ventricular Fibrillation - physiopathology |
| title | Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles |
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