Volume 26, Issue 3 pp. 153-157
Clinical Investigation
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Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarction

Teruo Inoue M.D.

Corresponding Author

Teruo Inoue M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

Department of Cardiology Koshigaya Hospital Dokkyo University School of Medicine 2-1-50 Minamikoshigaya, Koshigaya-City Saitama 343-8555, JapanSearch for more papers by this author
Isao Yaguchi M.D.

Isao Yaguchi M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Keiichi Mizoguchi M.D.

Keiichi Mizoguchi M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Toshihiko Uchida M.D.

Toshihiko Uchida M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Kan Takayanagi M.D.

Kan Takayanagi M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Terumi Hayashi M.D.

Terumi Hayashi M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Shigenori Morooka M.D.

Shigenori Morooka M.D.

Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

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Yutaka Eguchi M.D.

Yutaka Eguchi M.D.

Intensive Care Unit, Shiga University of Medical Science, Shiga, Japan

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First published: 05 December 2006
Citations: 2

Abstract

Background: Although acceleration of plasma plasminogen activator inhibitor-1 (PAI-1) level after emergent coronary angioplasty in acute myocardial infarction (AMI) has been documented, its pathophysiologic role is still unknown.

Hypothesis: This study was designed to elucidate the role of PAI-1 in the development of restenosis after primary coronary stenting in AMI.

Methods: We selected for this study 66 patients with AMI, who underwent primary coronary stenting for infarct-related coronary artery lesions in an emergent situation. In all patients, plasma PAI-1 level was measured at admission, and at 3 h, 24 h, 48 h, and 1 month after coronary stenting.

Results: At admission, the PAI-1 level was equivalent in 24 patients who experienced restenosis and in 42 patients without restenosis (28 ± 4 vs. 29 ± 4 ng/ml). In patients with restenosis, the levels did not change during the course after coronary stenting. In patients without restenosis, however, the level significantly increased at 3 h (48 ± 9 ng/ml, p < 0.001), 24 h (42 ± 9, p < 0.01), and 48 h (38 ± 7, p < 0.05) after coronary stenting, and was restored to the level equivalent to that at admission (27 ± 2 ng/ml) 1 month after coronary stenting. The PAI-1 level at 3 h after coronary stenting in patients without restenosis was significantly higher (p < 0.05) than the level (33 ± 6 ng/ml) in patients with restenosis. Multiple logistic regression analysis indicated that the PAI-1 level 3 h after coronary stenting was an independent predictor of restenosis (Wald x2 = 3.826, p = 0.019, odds ratio 0.921, 95% confidence interval 0.866-0.961).

Conclusion: Accelerated PAI-1 after coronary stenting in patients with AMI may protect against the development of late restenosis.

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