Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology
Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process...
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| Veröffentlicht in: | The Lancet (British edition) 1989-06, Vol.1 (8650), p.1309-1312 |
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| creator | DEAN, J. N LAB, M. J |
| description | Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process of mechanoelectric feedback. Moreover, when changes in cardiac loading similar to those seen in heart failure are produced experimentally in normal heart, there is a greater tendency to arrhythmogenesis. The intimate relation between changes in mechanical function and arrhythmia in heart failure could account for the lack of effect of most conventional antiarrhythmic drugs on arrhythmogenesis, and the beneficial effect of peripheral vasodilators. This paper argues that mechanically induced changes in electrophysiology are very important in the development of arrhythmia in cardiac failure; there may be no need to implicate other mechanisms, such as relative ischaemia, metabolic changes, or changes in sympathetic tone. |
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N ; LAB, M. J</creator><creatorcontrib>DEAN, J. N ; LAB, M. J</creatorcontrib><description>Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process of mechanoelectric feedback. Moreover, when changes in cardiac loading similar to those seen in heart failure are produced experimentally in normal heart, there is a greater tendency to arrhythmogenesis. The intimate relation between changes in mechanical function and arrhythmia in heart failure could account for the lack of effect of most conventional antiarrhythmic drugs on arrhythmogenesis, and the beneficial effect of peripheral vasodilators. This paper argues that mechanically induced changes in electrophysiology are very important in the development of arrhythmia in cardiac failure; there may be no need to implicate other mechanisms, such as relative ischaemia, metabolic changes, or changes in sympathetic tone.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>PMID: 2566835</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Lancet</publisher><subject>Action Potentials ; Animals ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - physiopathology ; Biological and medical sciences ; Cardiology. Vascular system ; Evaluation Studies as Topic ; Heart ; Heart Failure - complications ; Heart Failure - drug therapy ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Humans ; Medical sciences ; Models, Biological ; Myocardial Contraction ; Stress, Mechanical ; Vasodilator Agents - therapeutic use</subject><ispartof>The Lancet (British edition), 1989-06, Vol.1 (8650), p.1309-1312</ispartof><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6884371$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2566835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DEAN, J. N</creatorcontrib><creatorcontrib>LAB, M. J</creatorcontrib><title>Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology</title><title>The Lancet (British edition)</title><addtitle>Lancet</addtitle><description>Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process of mechanoelectric feedback. Moreover, when changes in cardiac loading similar to those seen in heart failure are produced experimentally in normal heart, there is a greater tendency to arrhythmogenesis. The intimate relation between changes in mechanical function and arrhythmia in heart failure could account for the lack of effect of most conventional antiarrhythmic drugs on arrhythmogenesis, and the beneficial effect of peripheral vasodilators. This paper argues that mechanically induced changes in electrophysiology are very important in the development of arrhythmia in cardiac failure; there may be no need to implicate other mechanisms, such as relative ischaemia, metabolic changes, or changes in sympathetic tone.</description><subject>Action Potentials</subject><subject>Animals</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Evaluation Studies as Topic</subject><subject>Heart</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - physiopathology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Myocardial Contraction</subject><subject>Stress, Mechanical</subject><subject>Vasodilator Agents - therapeutic use</subject><issn>0140-6736</issn><issn>1474-547X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LxDAQhoMo67r6E4QexFsh2Xy13pbFL1jwouKtZGcn20ja1KQ99N_bxeJpYJ7nHZj3jCyZ0CKXQn-dkyVlguZKc3VJrlL6ppQKReWCLNZSqYLLJfncxFiPfd04k7k2q9HEPrPG-SHiQxaDxyzYrEGoTevAeD9O2mEAPGSn1RHTKYYeoY-hq8fkgg_H8ZpcWOMT3sxzRT6eHt-3L_nu7fl1u9nlHVO6z7mVlIIqBaIxem85FlaA1YzpggFAiRa50msKWnCkVu-R2XUBFIExBOArcv93t4vhZ8DUV41LgN6bFsOQKl2UupRSTeLtLA77Bg9VF11j4ljNRUz8buYmTW_aaFpw6V9TRSG4ZvwX_WlpkQ</recordid><startdate>19890610</startdate><enddate>19890610</enddate><creator>DEAN, J. 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Vascular system</topic><topic>Evaluation Studies as Topic</topic><topic>Heart</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - physiopathology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Myocardial Contraction</topic><topic>Stress, Mechanical</topic><topic>Vasodilator Agents - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DEAN, J. N</creatorcontrib><creatorcontrib>LAB, M. 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J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology</atitle><jtitle>The Lancet (British edition)</jtitle><addtitle>Lancet</addtitle><date>1989-06-10</date><risdate>1989</risdate><volume>1</volume><issue>8650</issue><spage>1309</spage><epage>1312</epage><pages>1309-1312</pages><issn>0140-6736</issn><eissn>1474-547X</eissn><coden>LANCAO</coden><abstract>Various mechanisms have been suggested to explain the high prevalence of ventricular arrhythmia in patients with heart failure, but as yet there is no unifying theory. There is growing evidence that changes in myocardial mechanical properties may directly alter cardiac electrophysiology by a process of mechanoelectric feedback. Moreover, when changes in cardiac loading similar to those seen in heart failure are produced experimentally in normal heart, there is a greater tendency to arrhythmogenesis. The intimate relation between changes in mechanical function and arrhythmia in heart failure could account for the lack of effect of most conventional antiarrhythmic drugs on arrhythmogenesis, and the beneficial effect of peripheral vasodilators. This paper argues that mechanically induced changes in electrophysiology are very important in the development of arrhythmia in cardiac failure; there may be no need to implicate other mechanisms, such as relative ischaemia, metabolic changes, or changes in sympathetic tone.</abstract><cop>London</cop><pub>Lancet</pub><pmid>2566835</pmid><tpages>4</tpages></addata></record> |
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| ispartof | The Lancet (British edition), 1989-06, Vol.1 (8650), p.1309-1312 |
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| subjects | Action Potentials Animals Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - physiopathology Biological and medical sciences Cardiology. Vascular system Evaluation Studies as Topic Heart Heart Failure - complications Heart Failure - drug therapy Heart Failure - physiopathology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Humans Medical sciences Models, Biological Myocardial Contraction Stress, Mechanical Vasodilator Agents - therapeutic use |
| title | Arrhythmia in heart failure: role of mechanically induced changes in electrophysiology |
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