書誌事項
- 公開日
- 2000-03
- DOI
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- 10.1146/annurev.physiol.62.1.51
- 公開者
- Annual Reviews
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説明
<jats:p>▪ Abstract Atrial fibrillation (AF) was recognized and studied extensively in the early twentieth century, but many fundamental aspects of the arrhythmia were poorly understood until quite recently. It is now recognized that AF can be initiated by a variety of mechanisms that share the ability to cause extremely rapid, irregular atrial electrical activity. Once initiated, AF causes alterations in atrial electrical properties (electrical remodeling), including both rapid functional changes and slower alterations in ion channel gene expression, which promote the maintenance of AF and facilitate reinitiation of the arrhythmia should it terminate. Electrical remodeling decreases the atrial refractory period in a heterogeneous way, thus decreasing the size and stability of potential functional atrial reentry waves and promoting multiple-circuit reentry. Whatever the initial cause of AF, electrical remodeling is likely to be a final common pathway that ultimately supervenes. Recent advances in understanding ion channel function, regulation, and remodeling at the molecular level have allowed for a much more detailed appreciation of the basic determinants of AF. Improvements in the clinical management of AF will inevitably follow the recent advances in our understanding of its detailed pathophysiology.</jats:p>
収録刊行物
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- Annual Review of Physiology
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Annual Review of Physiology 62 (1), 51-77, 2000-03
Annual Reviews
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詳細情報 詳細情報について
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- CRID
- 1363670319524298240
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- NII論文ID
- 30022153670
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- NII書誌ID
- AA00055449
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- ISSN
- 15451585
- 00664278
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- データソース種別
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- Crossref
- CiNii Articles