| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2013-08-27 |
| タイトル |
|
|
タイトル |
Arrhythmogenic Effects of Arsenic Trioxide in Patients With Acute Promyelocytic Leukemia and an Electrophysiological Study in Isolated Guinea Pig Papillary Muscles |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題 |
Action potential |
| キーワード |
|
|
主題 |
Arsenic |
| キーワード |
|
|
主題 |
QT interval |
| キーワード |
|
|
主題 |
Triggered activity |
| キーワード |
|
|
主題 |
Ventricular arrhythmias |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| その他のタイトル |
|
|
その他のタイトル |
急性前骨髄性白血病患者における三酸化ヒ素の催不整脈作用と単離モルモット乳頭筋標本における電気生理学的研究 |
| 著者 |
Yamazaki, Keisuke
Terada, Hajime
Satoh, Hiroshi
Naito, Kensuke
Takeshita, Akihiro
Uehara, Akihiko
Katoh, Hideki
Ohnishi, Kazunori
Hayashi, Hideharu
|
| 書誌情報 |
en : Circulation Journal
巻 70,
号 11,
p. 1407-1414,
発行日 2006-10-20
|
| 出版者 |
|
|
出版者 |
THE JAPANESE CIRCULATION SOCIETY |
|
言語 |
en |
| 権利 |
|
|
権利情報 |
Copyright 2006 THE JAPANESE CIRCULATION SOCIETY |
| 権利 |
|
|
権利情報 |
本文データは学協会の許諾に基づきCiNiiから複製したものである |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Background Arsenic trioxide (As2O3) is a new promising regimen for patients with a relapse of acute promyelocytic leukemia (APL), but causes life-threatening arrhythmias. This study aimed to investigate the incidence and mechanism of arrythmogenesis caused by As2O3. Methods and Results Standard 12-lead ECGs were monitored throughout As2O3 therapy in 20 APL patients. As2O3 (0.15 mg/kg) significantly prolonged the corrected QT interval (QTc: 445±7 to 517±17 ms, means±SE, p<0.01), and also increased the QTc dispersion and transmural dispersion of repolarization. Non-sustained ventricular tachycardias and torsades de pointes occurred in 4 and 1 patients, respectively. The action potentials and isometric contraction were measured in guinea pig papillary muscles during As2O3 perfusion (350μmol/L). The action potential duration was prolonged (APD90: 150±11 to 195±12 ms at 60 min, p<0.01, n=5) and perfusion of As2O3 in a low K+ solution with a low stimulation rate augmented the prolongation of APD, and provoked early after-depolarizations and triggered activities. The prolonged exposure to As2O3 induced muscle contracture, after-contractions, triggered activities and electromechanical alternans. Tetrodotoxin or butylated hydroxytoluene partially prevented the As2O3-induced prolongation of APD. Conclusions The prolonged QTc and spatial heterogeneity are responsible for the As2O3-induced ventricular tachyarrhythmias. In addition to prolongation of the APD, cellular Ca2+ overload and lipid peroxidation might contribute to the electrophysiological abnormalities caused by As2O3. |
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
13469843 |
| EISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
13474820 |
| NII論文ID |
|
|
関連タイプ |
isIdenticalTo |
|
|
識別子タイプ |
NAID |
|
|
関連識別子 |
110004858628 |
| 出版社DOI |
|
|
関連タイプ |
isIdenticalTo |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.1253/circj.70.1407 |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
CircJ-70-1407.pdf (726.2 kB)
