左心室壁の表心部活性化がQT間隔を延長し,再極化のトランスムラ分散:双心室ペースへの影響
Jeffrey M Fish1, José M Di Diego, Vladislav Nesterenko
1Masonic Medical Research Laboratory, Utica, NY 13501-1787, USA.
Circulation
|April 14, 2004
まとめ
左心室のエピカルディアルペースはQT間隔を延長し,再偏極化の分散を増加させ,危険な不律性のための基板を生み出します. この細胞の研究は,上心部活性化逆転の背後にある不律性メカニズムを説明しています.
科学分野:
- 心臓病学 心臓病学
- 電気生理学 電気生理学
- 心律不整症とは,心律不整症のことです.
背景:
- 左心室 (LV) の表心ペースは,QT間隔を延長し,トーサード・ド・ポインテス不律症のリスクを増やすことが知られている.
- 逆のLV活性化方向によるQT延長と arritmogenesisの基礎となる細胞メカニズムについては,さらなる調査が必要です.
研究 の 目的:
- LV活性化の方向が逆転したときに,QT延長と arritmogenesisの細胞基礎を調査する.
- エピカルディアル対エンドカルディアルペースのトランスムラレポラライゼーションと伝導に対する影響を明らかにする.
主な方法:
- 犬用LVケイジ製剤からのトランスムラ電心図 (ECG) とトランスムラアクションポテンシャルの同時記録.
- 測定は,大動脈の perfused 条件下で,表心,M,および内心細胞から採取されました.
- 実験は,遅延整流器のカリウム電流阻害剤 (例えば,E-4031,シサプリド) を迅速に活性化させるか否かで行われました.
主要な成果:
- ペースを内心臓から表心臓に移行すると,QT間隔と反極化のトランムラル分散 (TDR) が著しく増加します.
- M細胞と表心細胞の伝導時間は,表心ペースで増加した.
- TDR増幅はさらにカリウム電流阻害剤によって強化され,これらの条件下で表心臓ペースでTorsade de pointes不律が誘発可能であった.
結論:
- 双心筋ペースで観察されるように,逆のLVアクティベーションは,表皮細胞とM細胞の差異的リポラライゼーションにより,QTとTDRを著しく増加させます.
- 増加したTDRは,長時間のQT間隔の文脈でTorsade de pointes不律を誘導する電気生理学的基板を作成します.
関連する概念動画
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