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The multidimensional role of calcium in atrial fibrillation pathophysiology: mechanistic insights and therapeutic opportunities

期刊

EUROPEAN HEART JOURNAL
卷 33, 期 15, 页码 1870-+

出版社

OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehs079

关键词

Atrial fibrillation; Cardiac remodelling; Ion channels; Calcium handling; Antiarrhythmic drug therapy; Structural fibrosis

资金

  1. Canadian Institutes of Health Research [MOP 44365, MGP 6957]
  2. Quebec Heart and Stroke Foundation
  3. European Network for Translational Research in Atrial Fibrillation (EUTRAF) [261057]
  4. German Federal Ministry of Education and Research [AF Competence Network] [01Gi0204]
  5. German Federal Ministry of Education and Research [German Center for Cardiovascular Research]
  6. Deutsche Forschungsgemeinschaft [Do 769/1-3]
  7. Fondation Leducq European-North American Atrial Fibrillation Research Alliance (ENAFRA) [07CVD03]

向作者/读者索取更多资源

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and its prevalence is increasing with the ageing of the population. Presently available treatment options are far from optimal and new insights into underlying mechanisms are needed to improve therapy. A variety of recent lines of research are converging to reveal important and relatively underappreciated multidimensional roles of cellular Ca-2 content, distribution, and handling in AF pathophysiology. The objective of the present paper is to review the participation of changes in cell Ca-2 and related processes in the mechanisms that lead to AF initiation and maintenance, and to consider the relevance of new knowledge in this area to therapeutic innovation. We first review the involvement of Ca-2-related functions in the principal arrhythmia mechanisms underlying AF: focal ectopic activity due to afterdepolarizations and re-entrant mechanisms. The detailed molecular pathophysiology of focal ectopic and re-entrant activity is then discussed in relationship to the participation of cell Ca-2 changes and related Ca-2-handling and Ca-2-sensitive signalling systems. We then go on to consider the participation of Ca-2-related functions in electrical and structural remodelling processes leading to the AF substrate. Finally, we consider the implications for development of new arrhythmia management approaches and future research and development.

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