アトルバスタチンによりPCI後のMI率が低下する

NAPLES II：高用量アトルバスタチンは多面的効果によりPCI後の非Q波心筋梗塞発現率を低下させる
NAPLES II: High dose atorvastatin reduces non Q-wave myocardial infarction following PCI through pleiotropic effects
経皮的冠動脈インターベンション（PCI）後24時間以内に80mgのアトルバスタチンを投与することによりPCI後の非Q波心筋梗塞（MI）発現率が低下するとの研究結果が2009年第58回American College of Cardiology学会i2サミットで発表された。過去に施行されたNovel Approaches for Preventing or Limiting Events ：NAPLES（イベントを抑制および減少させる新たなアプローチ）Iトライアルの結果、PCIの7日以上前にアトルバスタチン40mgを投与することにより周術期の非Q波MI発現率が低下することが示された。NAPLES IIではインターベンションの24時間以内に高用量のアトルバスタチン投与もまた予防効果があるか否かを調査することが目的であった。このトライアルでは、選択的PCIを予定されているスタチンを内服していない患者668人をアトルバスタチン80mg投与群（338人）またはアトルバスタチン非投与群（330人）に無作為に割り付けた。周術期のMI発現率はアトルバスタチン群で9.5%でありコントロール群で15.8%であった（P=0.014；オッズ比0.56）。トロポニンの正常上限値の3倍以上の上昇発現率はアトルバスタチン群で26.6%でありコントロール群で39.1%であった（P<0.001；オッズ比0.56）。筆者らは、今回の結果からスタチンが周術期の心筋壊死を予防するという概念が支持されると述べている。
Full Text

Giving 80 mg of atorvastatin within 24 hours of a percutaneous coronary intervention (PCI) reduces the incidence of non Q-wave myocardial infarction (MI) after PCI, according to research presented during the i2 Summit at the American College of Cardiology's 58th annual scientific session.

An earlier trial, Novel Approaches for Preventing or Limiting Events (NAPLES) I, showed that 40 mg of atorvastatin administered at least seven days before PCI reduced the rate of periprocedural non Q-wave MI. NAPLES II sought to determine whether a high loading dose of atorvastatin given in the 24 hours before an intervention would also be protective.

"One of the complications after stent implantation is the rise in troponin and CK-MB, which may occur in up to 30 percent of patients, even though their procedure has been completely successful. This rise is associated with worse outcomes after PCI. There are many data to support that statins administered one week before stenting can prevent CK-MB and troponin increase," said Carlo Briguori, M.D., PhD of Clinica Mediterranea, Naples, Italy. "We wanted to learn if giving a high dose of atorvastatin right before stenting would have a similar protective effect."

NAPLES II randomly assigned 668 patients scheduled for elective PCI who were not on statin therapy to atorvastatin 80 mg (n = 338) or no atorvastatin (n = 330). The primary endpoint was the incidence of periprocedural MI as assessed by analysis of creatine kinase myocardial enzyme (CK-MB) and cardiac troponin I before and at intervals of six and 12 hours after the intervention.

Periprocedural MI was defined as a CK-MB elevation greater than three times the upper limit of normal (ULN) alone or associated with chest pain or ST segment or T-wave abnormalities.

The incidence of periprocedural MI was 9.5 percent in the atorvastatin group and 15.8 percent in the control group (P = 0.014; odds ratio, 0.56). The incidence of troponin elevation greater than three times ULN was 26.6 percent in the atorvastatin group and 39.1 percent in the control group (P < 0.001; odds ratio, 0.56).

"These findings support the concept that statins prevent periprocedural necrosis," Dr. Brigouri said.

"The fact that atorvastatin was effective when we started it at a very high dose 24 hours before PCI suggests that the major mechanism by which statins are effective is through their pleiotropic effects - interference with the inflammatory and thrombotic pathways that may be involved in the CK-MB increase following stenting."