Europace Advance Access originally published online on October 30, 2008
Europace 2008 10(12):1458-1459; doi:10.1093/europace/eun295
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LETTERS TO THE EDITOR
Homocysteine and heavy metal interactions in atrial fibrillation and ablation treatments: reply
Department of Cardiology,
Nagoya University Graduate School of Medicine,
65 Tsurumai, Showa,
Nagoya 466-8550, Japan
Department of Cardiology,
Nagoya University Graduate School of Medicine,
Nagoya, Japan
Department of Cardiovascular Research,
Research Institute of Environmental Medicine,
Nagoya University, Nagoya, Japan
Department of Cardiology,
Nagoya University Graduate School of Medicine,
Nagoya, Japan
Department of Cardiology,
Nagoya University Graduate School of Medicine,
Nagoya, Japan
Tel: +81 52 744 2147; fax: +81 52 744 2138. E-mail address: mshimano{at}med.nagoya-u.ac.jp
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We appreciate the comments from Ravasini and colleagues, who proposed that heavy metals such as lead or mercury involved with homocysteine were associated with atrial fibrillation (AF). However, we respectfully disagree with their proposal that the methylmercury contamination by Minamata diseases caused sustained AF in our study.
Almost 60 years have passed over since the outbreak of Minamata diseases. The methylmercury as an industrial and trade waste was no more emitted in the surrounding ocean from the 1960s onward.1
There is no methylmercury contamination at any where in Japan after the Minamata disease. Thus, it is supposed to be no effect on our study population because the methylmercury was not stored in a significant quantity in the body of Japanese nowadays. In fact, homocysteine levels in patients with sustained AF in our study were quite similar to Italian subjects.2
For developing AF, there are many classical risk factors such as aging, cardiac disease, hypertension, diabetes mellitus, and thyroid disease. In addition, much other factors in the pathogenesis of AF have gained attention, including obesity, sleep apnoea, alcohol abuse and other intoxications, excessive sports practice, latent hypertension, genetic factors, and inflammation.3 Environmental stress also, described above, caused oxidative damage in the atrium.4,5 Thiol ratios were more oxidized and cysteine with thiol was reduced in AF status.6 Furthermore, homocysteine induces oxidative stress and is inversely related to the expression of peroxisome proliferators activated receptor (PPAR).7 We recently showed PPAR activator attenuated AF8 and observed 30% reduction in derivatives of reactive oxidative metabolisms. Thus, a potential link between homocysteine and other factors such as oxidative stress in AF management could be more important than the link between homocysteine and heavy metals.
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This work was supported by grant from the Japanese Ministry of Education, Culture, Sports, Science and Technology, the Nakashima Foundation and the Aichi D.R.G. Foundation to R. Shibata.
Conflict of interest: None declared.
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[1] Sakamoto M, Nakano A, Kinjo Y, Higashi H, Futatsuka M. Present mercury levels in red blood cells of nearby inhabitants about 30 years after the outbreak of Minamata disease. Ecotoxicol Environ Saf (1991) 22:58–66.[CrossRef][Web of Science][Medline]
[2] Marcucci R, Betti I, Cecchi E, Poli D, Giusti B, Fedi S, et al. Hyperhomocysteinemia and vitamin B6 deficiency: new risk markers for nonvalvular atrial fibrillation? Am Heart J (2004) 148:456–61.[CrossRef][Web of Science][Medline]
[3] Schoonderwoerd BA, Smit MD, Pen L, Van GI. New risk factors for atrial fibrillation: causes of ‘not-so-lone atrial fibrillation. Europace (2008) 10:668–73.
[4] Lozano HF, Conde CA, Florin T, Lamas GA. Treatment and prevention of atrial fibrillation with non-antiarrhythmic pharmacologic therapy. Heart Rhythm (2005) 2:1000–7.[CrossRef][Web of Science][Medline]
[5] Korantzopoulos P, Kolettis TM, Galaris D, Goudevenos JA. The role of oxidative stress in the pathogenesis and perpetuation of atrial fibrillation. Int. J. Cardiol. (2007) 115:135–43.[CrossRef][Web of Science][Medline]
[6] Neuman RB, Bloom HL, Shukrullah I, Darrow LA, Kleinbaum D, Jones DP, et al. Oxidative stress markers are associated with persistent atrial fibrillation. Clin Chem (2007) 53:1652–7.
[7] Tyagi SC, Rodriguez W, Patel AM, Roberts AM, Falcone JC, Passmore JC, et al. Hyperhomocysteinemic diabetic cardiomyopathy: oxidative stress, remodeling, and endothelial-myocyte uncoupling. J Cardiovasc Pharmacol Ther (2005) 10:1–10.
[8] Shimano M, Tsuji Y, Inden Y, Kitamura K, Uchikawa T, Harata S, et al. Pioglitazone, a peroxisome proliferator-activated receptor-gamma activator, attenuates atrial fibrosis and atrial fibrillation promotion in rabbits with congestive heart failure. Heart Rhythm (2008) 5:451–9.[CrossRef][Web of Science][Medline]
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