アンジオテンシン変換酵素の阻害は,リウマチ性関節炎における血管機能を改善します
Andreas J Flammer1, Isabella Sudano, Frank Hermann
1Cardiovascular Centre, Cardiology, University Hospital, Rämistrasse 100, 8091 Zurich, Switzerland.
Circulation
|April 23, 2008
まとめ
ラミプリルは,フローメディエートされた膨張を強めることで,リウマチ性関節炎患者の内皮機能を有意に改善しました. このアニオテンシン変換酵素阻害剤は,炎症マーカーを減少させ,新しい心血管疾患予防戦略を示唆しました.
科学分野:
- 心血管医学は,心臓血管医学である.
- レウマトロジーの病理学
- 薬理学 薬理学とは
背景:
- リウマチ性関節炎 (RA) 患者は,心血管疾患のリスクが高くなります.
- 動脈硬化症とRAの間の類似性は,共通の治療目標を示唆しています.
- アンジオテンシン変換酵素 (ACE) 阻害剤は,動脈硬化性血管疾患において有益であることが示されています.
研究 の 目的:
- RA患者の内皮機能に対するラミプリルの影響を評価する.
- RAにおける炎症および酸化ストレスマーカーに対するラミプリルの効果を評価する.
- ラミプリルがRAにおける心血管疾患のリスクを軽減できるかどうかを判断する.
主な方法:
- 11人のRA患者を含むランダム化,ダブルブラインド,クロスオーバー研究.
- ラミプリル (2.5-10 mg) またはプラセボを標準の抗炎症療法に加えて8週間投与する.
- 内皮機能の評価 (流動媒介拡張),炎症マーカー,酸化ストレス,および疾患活動.
主要な成果:
- ラミプリルは,内皮機能を有意に改善した (フローメディエーションによる膨張は2.85%から4.00%に増加し,P=0.017).
- ラミプリル (P=0.03) を服用すると,ダイアストリック血圧はわずかに低下した (P=0.03).
- 腫瘍死滅因子-αは,フローメディエーションによる膨張と逆相関する (r=-0.408,P=0.02);CD40濃度が低下した (P=0.049).
結論:
- ラミプリル (10 mg/日8週間) は,RA患者の内皮機能を著しく改善しました.
- ラミプリルによるACE阻害は,RAにおける心血管疾患の予防のための新しい戦略を提供することができる.
- RAにおける心血管疾患のリスクを減らすためにACE阻害剤に関するさらなる研究が必要である.
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