Impact of platelet reactivity on late lumen loss after primary percutaneous coronary intervention with second-generation drug-eluting stents in acute coronary syndrome

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  • Igawa Wataru
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Isomura Naoei
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Saito Jumpei
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Shimazu Suguru
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Kimura Taro
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Oyama Yuji
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Ono Morio
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Kido Takehiko
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Ebara Seitaro
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Okabe Toshitaka
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Yamamoto Myong Hwa
    Department of Cardiology, Showa University Northern Yokohama Hospital
  • Ochiai Masahiko
    Department of Cardiology, Showa University Northern Yokohama Hospital

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  • 急性冠症候群において第二世代の薬剤溶出性ステントを留置後の血小板機能と晩期内腔損失との関連

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Abstract

It is necessary to use enough antiplatelet treatment for treating acute coronary syndrome. There are few studies that consider the connection between platelet function and late lumen loss （LLL）. This study aimed to investigate the relationship between major adverse cardiac and cerebrovascular events （MACCE） and LLL. Platelet reactivity units （PRU） 2-4 weeks after percutaneous coronary intervention were evaluated using a VerifyNow system （PCI）. Twelve months following PCI, a follow-up coronary angiography was conducted. PRU patients＜221 were classified into low platelet reactivity （LPR） and high platelet reactivity （HPR） groups. The study enrolled 138 patients who received PCI and implantation of everolimus-eluting stents （EES） or biolimus-eluting stents （BES）; 83 and 51 patients were in the LPR and HPR groups, respectively. There was no considerable difference in MACCE between LPR and HPR groups （1% vs. 5%, P＝0.15）. LLL was substantially higher in the HPR group compared to the LPR in quantitative coronary angiography （QCA） （0.04 ± 0.37 vs. 0.19±0.38, P＝0.02）. In addition, in BES, but not in EES, LLL was considerably higher in the HPR group compared to the LPR group （0.03±0.57 vs. 0.30±0.72, P＝0.004）. When the risk of LLL ≧0.5mm was evaluated, HPR was found to be a risk factor in both univariate and multivariate analyses （Odds ratio 3.34, 95% CI：1.21-9.16, P＝0.01） （Odds ratio 4.42, 95% CI：1.48-13.22, P＝0.007）. One year after PCI, HPR and MACCE were unrelated. In the HPR group, LLL rose, and HPR was the sole risk factor for LLL ≧0.5mm. It was indicated that HPR is a risk factor for clinical results.

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