dc.contributor.author |
Sánchez-Quintana, Damián |
|
dc.contributor.author |
López Mínguez, José Ramón |
|
dc.contributor.author |
Pizarro, Gonzalo
|
|
dc.contributor.author |
Murillo Haba, Margarita |
|
dc.contributor.author |
Cabrera Rodríguez, José Ángel
|
|
dc.date.accessioned |
2017-02-22T19:13:41Z |
|
dc.date.available |
2017-02-22T19:13:41Z |
|
dc.date.issued |
2012 |
|
dc.identifier.citation |
Sánchez-Quintana, D., Ramon Lopez-Minguez, J., Pizarro, G., Murillo, M., y Angel Cabrera, J. (2012). Triggers and anatomical substrates in the genesis and perpetuation of atrial fibrillation. Current cardiology reviews, 8(4), 310-326. |
spa |
dc.identifier.issn |
1573403X |
|
dc.identifier.uri |
http://hdl.handle.net/11268/6214 |
|
dc.description.abstract |
The definition of atrial fibrillation (AF) as a functional electrical disorder does not reflect the significant underlying structural abnormalities. Atrial and Pulmonary Vein (PV) muscle sleeve microstructural remodeling is present, and establishes a vulnerable substrate for AF maintenance. In spite of an incomplete understanding of the anatomo-functional basis for AF, current evidence demonstrates that this arrhythmia usually requires a trigger for initiation and a vulnerable electrophysiological and/or anatomical substrate for maintenance. It is still unclear whether the trigger mechanisms include focal enhanced automaticity, triggered activity and/or micro re-entry from myocardial tissue. Initiation of AF can be favored by both parasympathetic and sympathetic stimulation, which also seem to play a role in maintaining AF. Finally, evolving clinical evidence demonstrates that inflammation is associated with new-onset and recurrent AF through a mechanism that possibly involves cellular degeneration, apoptosis, and subsequent atrial fibrosis. © 2012 Bentham Science Publishers. |
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dc.description.sponsorship |
Sin financiación |
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dc.language.iso |
eng |
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dc.title |
Triggers and anatomical substrates in the genesis and perpetuation of atrial fibrillation |
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dc.type |
article |
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dc.description.impact |
0.546 SJR (2012) Q2, 2321/6630 Medicine, 139/332 Cardiology and cardiovascular medicine |
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dc.identifier.doi |
10.2174/157340312803760721 |
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dc.rights.accessRights |
closedAccess |
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dc.subject.uem |
Cardiología |
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dc.subject.uem |
Vasos sanguíneos |
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dc.subject.uem |
Aparato respiratorio |
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dc.subject.unesco |
Sistema cardiovascular |
spa |
dc.subject.unesco |
Aparato respiratorio |
spa |
dc.description.filiation |
UEM |
spa |
dc.peerreviewed |
Si |
spa |