安定した冠動脈疾患を有する患者のスタチン療法による循環内皮原生細胞の増加
M Vasa1, S Fichtlscherer, K Adler
1Division of Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Theodor-Stern-Kai 7, Frankfurt, Germany.
Circulation
|June 20, 2001
まとめ
アトルバスタチン治療は,循環中の内皮原生細胞 (EPC) を著しく増加させ,冠動脈疾患 (CAD) の患者でその機能を強化します. これは,スタチンが組織修復を促進することによって,CAD患者の臨床結果を改善する方法を説明するかもしれません.
科学分野:
- 心血管研究 循環器科の研究
- 再生医学は,再生医療である.
背景:
- 治療的な新血管化は,不血性組織を救うための鍵です.
- 内皮原生細胞 (EPCs) は,不血症領域における新血管化を促進する.
- スタチンは,脂質を下げること以外に,新血管化を強化する可能性があります.
研究 の 目的:
- 安定した冠動脈疾患 (CAD) の患者の循環中のEPCに対するアトルバスタチンの効果を調査する.
- スタチン治療後のEPCの機能能力を評価する.
主な方法:
- 15人の安定したCAD患者を対象に4週間にわたって毎日アトルバスタチン40mgを投与した前向きな研究.
- 毎週隔離し,外周血液EPCを数える.
- 血液形成原始細胞 (CD34,CD133,CD34/キナーゼ挿入ドメイン受容体) とEPCの移動能力の分析.
主要な成果:
- アトルバスタチンは1週間で循環中のEPCを約1.5倍増加させ,4週間で3倍に達しました.
- CD34/キナーゼ挿入ドメイン受容体陽性細胞の有意な増加が4週間後に観察されました.
- アトルバスタチンは,EPCの機能的移住能力を高めました.
結論:
- スタチンの治療は,循環中のEPCを増加させ,安定したCAD患者の機能的活動を改善します.
- スタチンによるこのEPC刺激は,CAD管理において観察された臨床的利点に寄与する可能性があります.
- CADにおけるスタチン作用の新たなメカニズムを特定した.
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