Cellular bases for human atrial fibrillation
Atrial fibrillation (AF) causes substantial morbidity and mortality. It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully...
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| Veröffentlicht in: | Heart rhythm 2008-06, Vol.5 (6), p.S1-S6 |
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| creator | Workman, Antony J., PhD Kane, Kathleen A., PhD Rankin, Andrew C., MD |
| description | Atrial fibrillation (AF) causes substantial morbidity and mortality. It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully understood and may include increased inward rectifier K+ current and altered Ca2+ handling. Heart failure, a major cause of AF, may involve arrhythmogenic atrial electrical remodeling, but the pattern is unclear in humans. Beta-blocker therapy prolongs atrial cell refractory period; a potentially antiarrhythmic influence, but the ionic and molecular mechanisms are unclear. The search for drugs to suppress AF without causing ventricular arrhythmias has been aided by basic studies of cellular mechanisms of AF. It remains to be seen whether such drugs will improve patient treatment. |
| doi_str_mv | 10.1016/j.hrthm.2008.01.016 |
| format | Article |
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It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully understood and may include increased inward rectifier K+ current and altered Ca2+ handling. Heart failure, a major cause of AF, may involve arrhythmogenic atrial electrical remodeling, but the pattern is unclear in humans. Beta-blocker therapy prolongs atrial cell refractory period; a potentially antiarrhythmic influence, but the ionic and molecular mechanisms are unclear. The search for drugs to suppress AF without causing ventricular arrhythmias has been aided by basic studies of cellular mechanisms of AF. 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It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully understood and may include increased inward rectifier K+ current and altered Ca2+ handling. Heart failure, a major cause of AF, may involve arrhythmogenic atrial electrical remodeling, but the pattern is unclear in humans. Beta-blocker therapy prolongs atrial cell refractory period; a potentially antiarrhythmic influence, but the ionic and molecular mechanisms are unclear. The search for drugs to suppress AF without causing ventricular arrhythmias has been aided by basic studies of cellular mechanisms of AF. It remains to be seen whether such drugs will improve patient treatment.</description><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>Arrhythmias (mechanisms)</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - drug therapy</subject><subject>Atrial Fibrillation - metabolism</subject><subject>Atrial Function</subject><subject>Beta-blocker</subject><subject>Calcium - metabolism</subject><subject>Cardiovascular</subject><subject>Electrical remodeling</subject><subject>Electrophysiological Phenomena</subject><subject>Heart Atria - cytology</subject><subject>Heart failure</subject><subject>Heart Failure - metabolism</subject><subject>Humans</subject><subject>Ion current</subject><subject>Potassium Channels, Inwardly Rectifying - metabolism</subject><subject>Refractory period</subject><subject>Transmembrane action potential</subject><issn>1547-5271</issn><issn>1556-3871</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU2LFDEQDaK4H_oLBOmTJ3tMJZ105-CCDK4KCx7Uc5HOVDsZ05016V7Yf2_aGfy6CAVVkPdeVd5j7BnwDXDQrw6bfZr340Zw3m04lNIP2DkopWvZtfBwnZu2VqKFM3aR84FzYTSXj9kZdI3SYOQ5e7mlEJZgU9XbTLkaYqr2y2inys7J21ANvk8-BDv7OD1hjwYbMj099Uv25frt5-37-ubjuw_bNze1UyDmugM-mFZKKYahdyS0sprMjhoA6XgvjGiVkj1IsNpybvrOOmilGiSZjlwrL9nVUfd26UfaOZrmZAPeJj_adI_Revz7ZfJ7_BrvUGhpdLMKvDgJpPh9oTzj6LMrP7UTxSWjNtA2BVeA8gh0KeacaPi1BDiuLuMBf7qMq8vIoZQurOd_3vebc7K1AF4fAVRcuvOUMDtPk6OdT-Rm3EX_nwVX__Bd8JN3Nnyje8qHuKSpBICAWSDHT2vQa8684yVk1ckfDQ2j9g</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Workman, Antony J., PhD</creator><creator>Kane, Kathleen A., PhD</creator><creator>Rankin, Andrew C., MD</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</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><scope>5PM</scope></search><sort><creationdate>20080601</creationdate><title>Cellular bases for human atrial fibrillation</title><author>Workman, Antony J., PhD ; Kane, Kathleen A., PhD ; Rankin, Andrew C., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-810f973332ffbce265a6e9de4113c0b2927553b131a6a009b8ac1735f3e98ec73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>Arrhythmias (mechanisms)</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - drug therapy</topic><topic>Atrial Fibrillation - metabolism</topic><topic>Atrial Function</topic><topic>Beta-blocker</topic><topic>Calcium - metabolism</topic><topic>Cardiovascular</topic><topic>Electrical remodeling</topic><topic>Electrophysiological Phenomena</topic><topic>Heart Atria - cytology</topic><topic>Heart failure</topic><topic>Heart Failure - metabolism</topic><topic>Humans</topic><topic>Ion current</topic><topic>Potassium Channels, Inwardly Rectifying - metabolism</topic><topic>Refractory period</topic><topic>Transmembrane action potential</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Workman, Antony J., PhD</creatorcontrib><creatorcontrib>Kane, Kathleen A., PhD</creatorcontrib><creatorcontrib>Rankin, Andrew C., MD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Heart rhythm</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Workman, Antony J., PhD</au><au>Kane, Kathleen A., PhD</au><au>Rankin, Andrew C., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cellular bases for human atrial fibrillation</atitle><jtitle>Heart rhythm</jtitle><addtitle>Heart Rhythm</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>5</volume><issue>6</issue><spage>S1</spage><epage>S6</epage><pages>S1-S6</pages><issn>1547-5271</issn><eissn>1556-3871</eissn><abstract>Atrial fibrillation (AF) causes substantial morbidity and mortality. 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| fulltext | fulltext |
| identifier | ISSN: 1547-5271 |
| ispartof | Heart rhythm, 2008-06, Vol.5 (6), p.S1-S6 |
| issn | 1547-5271 1556-3871 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adrenergic beta-Antagonists - pharmacology Adrenergic beta-Antagonists - therapeutic use Arrhythmias (mechanisms) Atrial fibrillation Atrial Fibrillation - drug therapy Atrial Fibrillation - metabolism Atrial Function Beta-blocker Calcium - metabolism Cardiovascular Electrical remodeling Electrophysiological Phenomena Heart Atria - cytology Heart failure Heart Failure - metabolism Humans Ion current Potassium Channels, Inwardly Rectifying - metabolism Refractory period Transmembrane action potential |
| title | Cellular bases for human atrial fibrillation |
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