Atrial fibrillation is associated with accumulation of aging-related common type mitochondrial DNA deletion mutation in human atrial tissue

Ling Ping Lai, Chien Chen Tsai, Ming Jai Su, Jiunn Lee Lin, Yih Sharng Chen, Yung Zu Tseng, Shoei K.Stephen Huang

研究成果: 雜誌貢獻文章

43 引文 斯高帕斯(Scopus)

摘要

Study objective: Accumulation of somatic mutations of mitochondrial DNA (mtDNA) contributes to the aging process and progressive organ dysfunction. We investigated the mitochondrial DNA with 4977-base-pair mtDNA deletion mutation (mtDNA4977) in human atrial tissue and correlated the amount of mtDNA4977 to clinical atrial fibrillation (AF). Methods and results: Atrial tissue from the right atrial appendage was obtained in 88 patients during open-heart surgery (22 children/adolescents and 66 adults). The amount of mtDNA4977 was measured using a nested polymerase chain reaction protocol and normalized to wild-type mtDNA. We found that the mtDNA4977 was absent in all 22 pediatric/adolescent patients. In the adult group, the relative amount of mtDNA4977 was significantly higher in patients with AF than in patients without AF (0.55 ± 0.26 vs 0.35 ± 0.29, p < 0.007) [mean ± SD]. The amount of mtDNA4977 was also positively associated with age (r = 0.29, p < 0.01). Left and right atrial pressures, left atrial dimension, hypertension, and cardiac diagnosis did not influence the amount of mtDNA4977 significantly. Further multivariate analysis showed that both aging and AF contributed independently to the accumulation of mtDNA4977. Conclusion: AF is associated with an increase of mtDNA4977. This change is similar to the aging process of atrial tissue and might contribute to atrial dysfunction in AF.
原文英語
頁(從 - 到)539-544
頁數6
期刊Chest
123
發行號2
DOIs
出版狀態已發佈 - 二月 1 2003
對外發佈Yes

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine

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