Postrepolarization refractoriness in acute ischemia and after antiarrhythmic drug administration: Action potential duration is not always an index of the refractory period
Action potential duration is widely used as a measure of refractory period in ischemia. Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of exc...
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| Veröffentlicht in: | Heart rhythm 2012-06, Vol.9 (6), p.977-982 |
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| creator | Coronel, Ruben, MD, PhD Janse, Michiel J., MD, PhD Opthof, Tobias, PhD Wilde, Arthur A., MD, PhD Taggart, Peter, MD, DSc |
| description | Action potential duration is widely used as a measure of refractory period in ischemia. Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of excitability lags behind full repolarization. The purpose the study was to review this phenomenon of postrepolarization refractoriness during ischemia and after application of various antiarrhythmic drugs. The findings showed that although postrepolarization refractoriness is profoundly proarrhythmic during ischemia, it may protect the heart from reentrant arrhythmias in the absence of depolarization of the resting membrane. An increase in postrepolarization refractoriness induced by sodium-channel–blocking drugs may exert an antifibrillatory action. |
| doi_str_mv | 10.1016/j.hrthm.2012.01.021 |
| format | Article |
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Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of excitability lags behind full repolarization. The purpose the study was to review this phenomenon of postrepolarization refractoriness during ischemia and after application of various antiarrhythmic drugs. The findings showed that although postrepolarization refractoriness is profoundly proarrhythmic during ischemia, it may protect the heart from reentrant arrhythmias in the absence of depolarization of the resting membrane. An increase in postrepolarization refractoriness induced by sodium-channel–blocking drugs may exert an antifibrillatory action.</description><identifier>ISSN: 1547-5271</identifier><identifier>EISSN: 1556-3871</identifier><identifier>DOI: 10.1016/j.hrthm.2012.01.021</identifier><identifier>PMID: 22293142</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Action potential duration ; Action Potentials - drug effects ; Acute Disease ; Anti-Arrhythmia Agents - adverse effects ; Anti-Arrhythmia Agents - therapeutic use ; Antiarrhythmic drugs ; Arrhythmias, Cardiac - drug therapy ; Arrhythmias, Cardiac - physiopathology ; Cardiovascular ; Dispersion of refractoriness ; Dispersion of repolarization ; Electrocardiography - drug effects ; Graded responses ; Heart Conduction System - drug effects ; Heart Conduction System - physiopathology ; Humans ; Ischemia ; Myocardial Ischemia - chemically induced ; Myocardial Ischemia - physiopathology ; Sodium Channel Blockers - adverse effects ; Sodium Channel Blockers - therapeutic use</subject><ispartof>Heart rhythm, 2012-06, Vol.9 (6), p.977-982</ispartof><rights>Heart Rhythm Society</rights><rights>2012 Heart Rhythm Society</rights><rights>Copyright © 2012 Heart Rhythm Society. 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All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-56a62d147c769db4dec88d1422a9b7342a35cc95e092650c83317868f7aa7383</citedby><cites>FETCH-LOGICAL-c414t-56a62d147c769db4dec88d1422a9b7342a35cc95e092650c83317868f7aa7383</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.2012.01.021$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22293142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Coronel, Ruben, MD, PhD</creatorcontrib><creatorcontrib>Janse, Michiel J., MD, PhD</creatorcontrib><creatorcontrib>Opthof, Tobias, PhD</creatorcontrib><creatorcontrib>Wilde, Arthur A., MD, PhD</creatorcontrib><creatorcontrib>Taggart, Peter, MD, DSc</creatorcontrib><title>Postrepolarization refractoriness in acute ischemia and after antiarrhythmic drug administration: Action potential duration is not always an index of the refractory period</title><title>Heart rhythm</title><addtitle>Heart Rhythm</addtitle><description>Action potential duration is widely used as a measure of refractory period in ischemia. Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of excitability lags behind full repolarization. The purpose the study was to review this phenomenon of postrepolarization refractoriness during ischemia and after application of various antiarrhythmic drugs. The findings showed that although postrepolarization refractoriness is profoundly proarrhythmic during ischemia, it may protect the heart from reentrant arrhythmias in the absence of depolarization of the resting membrane. An increase in postrepolarization refractoriness induced by sodium-channel–blocking drugs may exert an antifibrillatory action.</description><subject>Action potential duration</subject><subject>Action Potentials - drug effects</subject><subject>Acute Disease</subject><subject>Anti-Arrhythmia Agents - adverse effects</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>Antiarrhythmic drugs</subject><subject>Arrhythmias, Cardiac - drug therapy</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Cardiovascular</subject><subject>Dispersion of refractoriness</subject><subject>Dispersion of repolarization</subject><subject>Electrocardiography - drug effects</subject><subject>Graded responses</subject><subject>Heart Conduction System - drug effects</subject><subject>Heart Conduction System - physiopathology</subject><subject>Humans</subject><subject>Ischemia</subject><subject>Myocardial Ischemia - chemically induced</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Sodium Channel Blockers - adverse effects</subject><subject>Sodium Channel Blockers - therapeutic use</subject><issn>1547-5271</issn><issn>1556-3871</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUstu1TAQjRCIlsIXICEv2ST4kTgJEkhVRQGpEkh0wc6aa0-IL0kcbKeQ_hI_iXNvAYkNK48155x5nMmyp4wWjDL5Yl_0PvZjwSnjBWUF5exedsqqSuaiqdn9LS7rvOI1O8kehbCnlLeSiofZCee8Fazkp9nPjy5Ej7MbwNtbiNZNxGPnQUfn7YQhEDsR0EtEYoPucbRAYDIEuog-RdGC9_2aGrGaGL98IWBGO9mkelB7Sc71QXV2ETf0QMxyTCVBMrlIYPgOa0haqZTBH8R1JPb4t42VzOitM4-zBx0MAZ_cvWfZ9eWb64t3-dWHt-8vzq9yXbIy5pUEyQ0ra13L1uxKg7pp0p9zaHe1KDmISuu2QtpyWVHdCMHqRjZdDVCLRpxlz4-ys3ffFgxRjWlyHAaY0C1BpeVXpWxoTRNUHKHauxBSw2r2dgS_JtCGk2qvDiapzSRFmUomJdazuwLLbkTzh_PblQR4dQRgmvLGoldBW5w0GutRR2Wc_U-B1__w9ZAs0TB8xRXD3i1-SgtUTIXEUZ-2O9nOhHFKaUM_i19q-71Z</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Coronel, Ruben, MD, PhD</creator><creator>Janse, Michiel J., MD, PhD</creator><creator>Opthof, Tobias, PhD</creator><creator>Wilde, Arthur A., MD, PhD</creator><creator>Taggart, Peter, MD, DSc</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></search><sort><creationdate>20120601</creationdate><title>Postrepolarization refractoriness in acute ischemia and after antiarrhythmic drug administration: Action potential duration is not always an index of the refractory period</title><author>Coronel, Ruben, MD, PhD ; 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Although the end of repolarization closely corresponds to the end of refractoriness in the well-perfused, well-oxygenated myocardium, it is no longer true for the ischemic myocardium, in which the recovery of excitability lags behind full repolarization. The purpose the study was to review this phenomenon of postrepolarization refractoriness during ischemia and after application of various antiarrhythmic drugs. The findings showed that although postrepolarization refractoriness is profoundly proarrhythmic during ischemia, it may protect the heart from reentrant arrhythmias in the absence of depolarization of the resting membrane. An increase in postrepolarization refractoriness induced by sodium-channel–blocking drugs may exert an antifibrillatory action.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22293142</pmid><doi>10.1016/j.hrthm.2012.01.021</doi><tpages>6</tpages></addata></record> |
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| subjects | Action potential duration Action Potentials - drug effects Acute Disease Anti-Arrhythmia Agents - adverse effects Anti-Arrhythmia Agents - therapeutic use Antiarrhythmic drugs Arrhythmias, Cardiac - drug therapy Arrhythmias, Cardiac - physiopathology Cardiovascular Dispersion of refractoriness Dispersion of repolarization Electrocardiography - drug effects Graded responses Heart Conduction System - drug effects Heart Conduction System - physiopathology Humans Ischemia Myocardial Ischemia - chemically induced Myocardial Ischemia - physiopathology Sodium Channel Blockers - adverse effects Sodium Channel Blockers - therapeutic use |
| title | Postrepolarization refractoriness in acute ischemia and after antiarrhythmic drug administration: Action potential duration is not always an index of the refractory period |
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