ディゴキシンは,心拍不全によって誘発された心房の電気的改造からの回復を遅らせます
R G Tieleman1, Y Blaauw, I C Van Gelder
1Department of Cardiology, Thoraxcenter, University of Groningen, Netherlands.
Circulation
|October 27, 1999
まとめ
ディゴキシンは,心拍数が高まる時に心房の電気的改造を悪化させ,回復を遅らせ,心房動 (AF) のリスクと期間を増加させます. この山羊の研究は,ディゴキシンがAF管理に悪影響を及ぼす可能性があることを示唆しています.
科学分野:
- 心臓病学 心臓病学
- 電気生理学 電気生理学
- 薬理学 薬理学とは
背景:
- 心房細動 (AF) は電気の再構築を引き起こし,抗不律性治療の成功率を低下させます.
- この改造は,心拍の急増によるカルシウム過負荷と関連しています.
- AFのペースコントロールに使用されるディゴキシンは,細胞内カルシウムを増加させ,潜在的に改造を悪化させる可能性があります.
研究 の 目的:
- ディゴキシンが心拍動脈によって誘発される前庭の電気的改造を悪化させるかどうかを調査する.
- 心房効果性耐火期 (AERP) とAF誘導性に対するディゴキシンの効果を評価する.
主な方法:
- 意識のあるヤギは,24時間間にわたって急激な心房/心房ペース (300/150bpm) を受けました.
- 動物はディゴキシンまたは塩水による治療を受けた.
- アトリアル有効耐火期 (AERP) は,さまざまなサイクル長 (430,300,200 ms) で測定されました.
主要な成果:
- ディゴキシンは,ペースアップ中に電気再構築率をわずかに増加させた.
- ディゴキシンは,ペース停止後のAERP回復を著しく遅らせた (P<0.007).
- ディゴキシン治療は,AFの誘導性および持続期間が増加し,AERPが短くなった.
結論:
- ディゴキシンは,ヤギの心拍動脈に起因する心房の電気的改造を悪化させる.
- ディゴキシン (Digoxin) は,急速なペースアップの後,電気的特性の回復を遅らせます.
- これらの効果は,心房細動の誘導性と持続時間を増加させます.
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