心臓のトロポニン値上昇,心血管疾患,および下arachnoid出血後の結果
Andrew M Naidech1, Kurt T Kreiter, Nazli Janjua
1Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Circulation
|November 4, 2005
まとめ
サバラクノイド出血 (SAH) の後の心臓トロポニンI (cTI) の上昇は一般的であり,神経原性心筋損傷に関連しています. 高いCTIレベルは,心肺疾患のリスクの増加と,退院時のより悪い結果と相関しています.
科学分野:
- 心臓病学 心臓病学
- 神経学 神経学とは
- クリティカルケア・メディシン
背景:
- 心臓トロポニンI (cTI) の放出は,下頭下出血 (SAH) の後に頻繁に行われ,神経原性心筋損傷を示唆する.
- これらのcTI上昇の予後的意義はよく定義されていません.
研究 の 目的:
- サバラクノイド出血後の心臓のトロポニンI値上昇の臨床的影響と予後的意義を調査する.
主な方法:
- シリアルCTI測定は,心臓損傷の臨床的またはECGの徴候を有する253人のSAH患者に実施されました.
- 病院でのイベントと3ヶ月のアウトカム (修正されたランキンスケール) を前向きに記録しました.
- ピークのcTIレベルは,さまざまな臨床およびエコーカルディオグラフィックパラメータに関連して分析されました.
主要な成果:
- cTI上昇の入院予測要因には,臨床グレードが低い,心室内出血,意識喪失が含まれていました.
- ピークのCTIレベルは,左心室機能不全,肺腫,低血圧,遅延性脳不全のリスクの増加と関連していました.
- 増加したCTIは,入院中の死亡または重度の障害を予測した (調整されたOR,1.4 per quintile; P=0.02).
結論:
- SAH後の心臓トロポニンIの上昇は,心肺合併症のより高いリスクと関連しています.
- また,CTIの上昇は,遅延性脳缺血および退院時の機能的アウトカムが悪化することとも関連しています.
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