Effect of Cilostazol in Preventing Restenosis After Percutaneous Transluminal Coronary Angioplasty

Take, Shunsuke; Matsutani, Masahide; Ueda, Hiroyasu; Hamaguchi, Hidehito; Konishi, Hirokazu; Baba, Yuji; Kawaratani, Hitoshi; Suguira, Tetsuro; Iwasaka, Toshiji; Inada, Mitsuo

doi:10.1016/s0002-9149(97)00052-0

Cited by 61 publications

(34 citation statements)

References 13 publications

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“…In earlier controlled studies of cilostazol with placebo groups, restenosis rates of 17% and 17.9% after balloon angioplasty were reported with cilostazol as compared to 40% and 39.5% in the controls. 6,9) The rates in the present study are thus in line with the literature in demonstrating an advantage with antiplatelet drugs, further suggesting that both ticlopidine and cilostazol are effective for reducing restenosis after PTCA.…”

Section: Discussionsupporting

confidence: 90%

“…21) However, no follow-up angiographic data are available. The efficacy of cilostazol for prevention of restenosis after balloon angioplasty 6,7,9) and stent implantation 8) has been repeatedly demonstrated in controlled studies. Cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)-butoxy]-3,4-dihydro-2-(1H)-quinolinone) interferes with platelet function by increasing the cellular concentration of cyclic adenosine monophosphate (cAMP), this effect being mediated by inhibition of the cyclic nucleotide phosphodiesterase responsible for converting cAMP to 5'-adenosine monophosphate.…”

Section: Discussionmentioning

confidence: 97%

“…[3][4][5] Antiplatelet agents hinder platelets from aggregating and one example, cilostazol, has already been shown to prevent restenosis after PTCA in controlled studies. [6][7][8][9] Ticlopidine is another promising antiplatelet agent, which has similar pharmacological properties. A prospective and randomized comparison of ticlopidine and cilostazol for this purpose was therefore conducted in the present study.…”

mentioning

confidence: 99%

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Comparison of Ticlopidine and Cilostazol for the Prevention of Restenosis after Percutaneous Transluminal Coronary Angioplasty.

et al. 2001

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SUMMARYPrevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA) continues to be a significant problem. Recent controlled studies have demonstrated that cilostazol suppresses restenosis after PTCA. The effects of ticlopidine, another antiplatelet agent, were compared in terms of outcomes of patients randomized for treatment with the two drugs after PTCA. A total of 35 patients (47 lesions) were assigned prospectively and randomly to ticlopidine (17 patients, 24 lesions) and cilostazol (18 patients, 23 lesions) groups. Minimal luminal diameter (MLD) and percentage of stenosis to reference diameter were estimated before PTCA, just after the procedure and after 4 months follow-up. All patients underwent 4 months angiographic follow-up, at the end of which MLD was 2.03 ± 0.71 mm in the ticlopidine group and 2.05 ± 0.68 mm in the cilostazol group (p = 0.95), and the percentage of stenosis to reference diameter was 31.4 ± 16.7% and 30.0 ± 17.0%, respectively (p = 0.78). The restenosis rate was 12.5% in the ticlopidine group and 17.4% in the cilostazol group (p = 0.69), relatively low as compared to the 20% to 30% reported in previous studies. Adverse drug reactions during the followup period were observed in two of the ticlopidine group and none of the cilostazol group. We conclude that both ticlopidine and cilostazol are effective for the prevention of restenosis after PTCA, however the former may be associated with slight side effects. (Jpn Heart J 2001; 42: 43-54) Key words: Antiplatelet therapy, Follow-up studies, Quantitative coronary arteriography RESTENOSIS after percutaneous transluminal coronary angioplasty (PTCA) is still a major limitation to long-term successful therapy. Coronary stent implantation is associated with a significant reduction in the angiographic restenosis rate compared with conventional simple balloon angioplasty, with decreases to 20% to 30% reported by the BENESTENT 1) and STRESS 2) trials, but the search for

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

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Comparison of Ticlopidine and Cilostazol for the Prevention of Restenosis after Percutaneous Transluminal Coronary Angioplasty.

et al. 2001

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“…In one of the first studies to evaluate the effect of cilostazol on restenosis, Take et al (19) randomly assigned 68 patients to cilostazol immediately after percutaneous transluminal coronary angioplasty (PTCA) versus ASA or ticlopidine (Table 1). Follow-up coronary angiography four to six months after PTCA revealed that restenosis was significantly lower (17%) in the cilostazol group than in the noncilostazol group (40%) (P<0.05).…”

Section: Inhibition Of Restenosis After Coronary Stent Implantationmentioning

confidence: 99%

The vascular effects of cilostazol

Weintraub

2006

Canadian Journal of Cardiology

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“…[13][14][15] Several lines of evidence indicate that cilostazol additionally inhibits the proliferation of VSMCs, reduces neointimal formation in balloon-injured rat carotid arteries, 16 -18 and inhibits restenosis after percutaneous transluminal coronary angioplasty. 19,20 One mechanism by which cilostazol may inhibit VSMC proliferation is via an increase in intracellular cAMP, because cAMP inhibits the proliferation of VSMCs by induction of p53-mediated and p21-mediated apoptosis. 21 However, Nadri et al demonstrated that increased cAMP leads to inhibition of phosphorylation of pRB, which regulates the activity of the E2F family, and consequently leads to arrest of cells at G1 in human lymphocytes.…”

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Cilostazol Inhibits Vascular Smooth Muscle Cell Growth by Downregulation of the Transcription Factor E2F

et al. 2005

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Abstract-Neointimal formation, the leading cause of restenosis, is caused by proliferation of vascular smooth muscle cells (VSMCs). Patients with diabetes mellitus have higher restenosis rates after coronary angioplasty than nondiabetic patients. Cilostazol, a selective type 3 phosphodiesterase inhibitor, is currently used to treat patients with diabetic vascular complications. Cilostazol is a potent antiplatelet agent that inhibits VSMC proliferation. In the present study, we examine whether the antiproliferative effect of cilostazol on VSMCs is mediated by inhibition of an important cell cycle transcription factor, E2F. Cilostazol inhibited the proliferation of human VSMCs in response to high glucose in vitro and virtually abolished neointimal formation in rats subjected to carotid artery injury in vivo. Moreover, the compound suppressed high-glucose-induced E2F-DNA binding activity, and the expression of E2F1, E2F2, cyclin A, and PCNA proteins. These data suggest that the beneficial effects of cilostazol on high-glucose-stimulated proliferation of VSMCs are mediated by the downregulation of E2F activity and expression of its downstream target genes, including E2F1, E2F2, cyclin A, and PCNA. The transcription factor, E2F, has been implicated in the periodic regulation of cellular genes required for transition through G1 and entry into the S phase, including dihydrofolate reductase, c-myc, DNA polymerase, cdc2, and proliferating cell nuclear antigen (PCNA). 5-7 E2F activity is regulated by interactions with RB family members. As cells progress toward S phase, RB family proteins are phosphorylated by G1 cyclin-complexes, resulting in the release of transcriptionally active E2F, which then leads to the activation of genes required for cell cycle progression. 8 -10 We recently showed that high glucose activates the DNA-binding activity of E2F, and decoy oligodeoxynucleotides against E2F inhibit the proliferation of VSMCs. 11 These data suggest that downregulation of E2F could constitute a therapeutic target to prevent restenosis after angioplasty in patients with diabetes.Cilostazol increases intracellular cAMP concentrations by selectively blocking phosphodiesterase type III. The clinical implications and pharmacokinetics with respect to the effects and safety of this drug have been well-established, especially in peripheral vascular disease. 12 Cilostazol is a potent antiplatelet agent currently used in clinical practice to treat patients with diabetic vascular complications. [13][14][15] Several lines of evidence indicate that cilostazol additionally inhibits the proliferation of VSMCs, reduces neointimal formation in balloon-injured rat carotid arteries, 16 -18 and inhibits restenosis after percutaneous transluminal coronary angioplasty. 19,20 One mechanism by which cilostazol may inhibit VSMC proliferation is via an increase in intracellular cAMP, because cAMP inhibits the proliferation of VSMCs by induction of p53-mediated and p21-mediated apoptosis. 21 However, Nadri et al demonstrated that increased cAMP...

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Effect of Cilostazol in Preventing Restenosis After Percutaneous Transluminal Coronary Angioplasty

Cited by 61 publications

References 13 publications

Comparison of Ticlopidine and Cilostazol for the Prevention of Restenosis after Percutaneous Transluminal Coronary Angioplasty.

Comparison of Ticlopidine and Cilostazol for the Prevention of Restenosis after Percutaneous Transluminal Coronary Angioplasty.

The vascular effects of cilostazol

Cilostazol Inhibits Vascular Smooth Muscle Cell Growth by Downregulation of the Transcription Factor E2F

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