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Chronic atrial fibrillation associated with somatic mitochondrial DNA mutations in human atrial tissue
  1. Hyung-Wook Park1,
  2. Youngkeun Ahn1,
  3. Myung-Ho Jeong1,
  4. Jeong-Gwan Cho1,
  5. Jong-Chun Park1,
  6. Jung-Chaee Kang1,
  7. Myung-Geun Shin2,
  8. Jong-Hee Shin2,
  9. Soon-Pal Suh2,
  10. Dong-Wook Ryang2,
  11. Nam-Ho Kim3,
  12. Jong-Bum Choi4,
  13. Hye-Ran Kim5
  1. 1Department of Cardiology, Chonnam National University Medical School, Gwangju, South Korea
  2. 2Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, South Korea
  3. 3Departments of Internal Medicine, Wonkwang University Hospital, Iksan, South Korea
  4. 4Department of Thoracic and Cardiovascular Surgery, Wonkwang University Hospital, Iksan, South Korea
  5. 5Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University, Gwangju, South Korea
  1. Correspondence to:
 Dr Myung-Geun Shin
 Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital, 160 Ilsimri, Hwasun-eup, Hwasun-gun, Jeollanam-do, South Korea 519-809; mgshin{at}

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Somatically acquired mitochondrial DNA (mtDNA) mutations have been linked to aging, degenerative diseases, cancer and organ dysfunction. mtDNA alterations were investigated in matched atrial tissues and blood samples from four patients with chronic atrial fibrillation (cAF) and two matched patients without cAF. Nine novel mtDNA mutations were observed in mtDNA control and coding region. Interestingly, two patients with cAF had tissue-specific length heteroplasmic mutations from nucleotide 16184 to 16193 of the polyC tract and CA repeats starting at nucleotide 514. A 9 bp deletion (nucleotides 8271–8279) in the mtDNA COII gene was only found in tissues and blood cells from two patients with cAF. In patients with cAF, mtDNA mutations, including small deletions and tissue-specific length heteroplasmic mutations, occurred in both mtDNA control and coding regions. These findings strongly suggest that mtDNA mutations may play a crucial role in atrial dysfunction in patients with cAF.

Mitochondria are both the power plant of human cells and the target of reactive oxygen species and free radicals. With ageing and excess (ROS) stress, free radicals and (ROS) can overwhelm the antioxidant system and result in damage to cellular constituents such as lipids, proteins and DNA.1 A few papers have reported that mitochondrial DNA (mtDNA) deletion mutation in human atrial tissue is associated with chronic atrial fibrillation (cAF).2,3 However, these studies only checked mtDNA deletion in atrial tissue and did not examine the corresponding blood samples. Therefore, we analysed the mtDNA control region and cytochrome c oxidase (CO) I, COII, COIII, ATPase 6 and cytochrome b (Cytb) genes in matched atrial tissues and blood samples from patients with cAF and in two matched patients with normal sinus rhythm and no history of cAF.


Atrial tissue samples and corresponding blood samples were taken from four patients with cAF and from two matched …

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  • Published Online First 25 May 2007

  • Competing interests: None.