Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis

Sakata, Kazuki; Miura, Fumiharu; Sano, Hiroshi; Shinobe, Michitaka; Shirotani, Manabu; Yoshida, Hiroshi; Mori, Noriko; Hoshino, Tsuneo; Takada, Akikazu

doi:10.1016/s0002-8703(96)90043-5

Cited by 43 publications

(23 citation statements)

References 27 publications

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“…Our data also suggest a mechanism that could account for a causal relationship between elevated PAI-1 expression and arterial disease. [1][2][3][4][5][6][7] In addition, this study and its predecessors 10,11 create an integrated picture of the role of PAI-1 in the formation of arterial lesions. Local PAI-1 expression significantly limits cell migration early after arterial injury, but this affects neointima formation only transiently.…”

Section: Discussionmentioning

confidence: 99%

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Plasminogen Activator Inhibitor Type 1 Increases Neointima Formation in Balloon-Injured Rat Carotid Arteries

2001

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Background-Elevated plasma levels of plasminogen activator inhibitor type 1 (PAI-1) are associated with myocardial infarction, atherosclerosis, and restenosis. PAI-1 is increased in atherosclerotic arteries and failed vein grafts. No experimental data, however, support a causal relationship between elevated PAI-1 expression and vascular lesions. Paradoxically, data generated in PAI-1 knockout mice suggest that PAI-1 might decrease lesion formation after arterial injury and that PAI-1 gene transfer might prevent restenosis. Methods and Results-Using the rat carotid balloon injury model and a PAI-1-expressing adenoviral vector, we tested whether elevated arterial PAI-1 expression would alter neointima formation. Compared with control-transduced arteries, neointima formation in PAI-1-transduced arteries was initially retarded. By 14 days, however, the intimas of PAI-1-transduced arteries were significantly larger than intimas of control-transduced arteries (1.6Ϯ0.1ϫ10 5 versus 1.2Ϯ0.1ϫ10 5 m 2 , nϭ18 to 19, PϽ0.03). PAI-1 expression in individual arteries correlated with increased cell proliferation at 4 and 8 days after injury (Rϭ0.6, PϽ0.02 and PϽ0.006). PAI-1 expression also correlated with fibrin(ogen) accumulation (Rϭ0.77, PϽ0.001), and fibrin(ogen) accumulation correlated strongly with proliferation (Rϭ0.86, PϽ0.00001). Conclusions-Increased expression of PAI-1 in the artery wall promotes neointima growth after balloon injury. Therefore, despite encouraging data generated in other animal models, PAI-1 is not a promising agent for gene therapy to prevent restenosis. Moreover, our data associate elevated PAI-1 expression with fibrin(ogen) accumulation and increased cell proliferation. These data suggest a mechanism to explain the association between elevated PAI-1 expression and the progression of arterial disease.

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Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4] PAI-1 is elevated in atherosclerotic human arteries and failed vein grafts. [5][6][7] In animal models, arterial wall PAI-1 expression is upregulated after injury and is elevated during neointima formation.…”

mentioning

confidence: 98%

Plasminogen Activator Inhibitor Type 1 Increases Neointima Formation in Balloon-Injured Rat Carotid Arteries

2001

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“…Post procedural plasma PAI-1 has also been implicated in the risk of restenosis after percutaneous coronary angioplasty. Most of the studies have described a deleterious effect of high plasma PAI-1 levels which may predict restenosis [80][81][82][83][84]. The same effect was obtained in a group of 251 consecutive patients who underwent femoro-popliteal percutaneous transluminal angioplasty [85].…”

Section: Pai-1mentioning

confidence: 79%

Adipose Tissue and Atherothrombosis

Alessi

Lijnen

Bastelica

et al. 2003

Pathophysiol Haemos Thromb

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“…[8][9][10] On the other hand, several investigators showed that increased levels of PAI-1 post angioplasty were associated with restenosis. [11][12][13] However, Shah and Amin 14 demonstrated a significant negative correlation between the preangioplasty PAI-1 level and later development of restenosis. Strauss et al 15 also demonstrated that plasma PAI-1 levels were lower in the restenosis group than in the nonrestenosis group at both preangioplasty and postangioplasty time points.…”

Section: Discussionmentioning

confidence: 96%

Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarction

Inoue¹,

Yaguchi²,

Mizoguchi³

et al. 2003

Clinical Cardiology

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SummaryBackground: 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

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Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis

Cited by 43 publications

References 27 publications

Plasminogen Activator Inhibitor Type 1 Increases Neointima Formation in Balloon-Injured Rat Carotid Arteries

Plasminogen Activator Inhibitor Type 1 Increases Neointima Formation in Balloon-Injured Rat Carotid Arteries

Adipose Tissue and Atherothrombosis

Accelerated plasminogen activator inhibitor may prevent late restenosis after coronary stenting in acute myocardial infarction

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