Cilostazol, clopidogrel or ticlopidine to prevent sub-acute stent thrombosis: A meta-analysis of randomized trials

Schleinitz, Mark D.; Olkin, Ingram; Heidenreich, Paul A.

doi:10.1016/j.ahj.2004.03.066

Cited by 40 publications

(21 citation statements)

References 44 publications

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“…Cilostazol (Petal), a PDE3 inhibitor, is approved for treatment of symptoms of intermittent claudication associated with peripheral arterial occlusive disease (180,181). Other potential applications of this medication include prevention of stroke, attenuation of restenosis of blood vessels following angioplasty (172,203,330,334), treatment of vasospastic angina pectoris (404), promotion of cerebral vascular dilatation (34), and slowing progression of atherosclerosis in diabetics (250). There are some indications that milrinone may be useful in treatment of patients with NPH particularly when used in conjunction with iNO (62, 241).…”

Section: Expanded Uses For Approved Pde3 Inhibitorsmentioning

confidence: 99%

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Francis

Blount

Corbin

2011

Physiological Reviews

560

546

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The superfamily of cyclic nucleotide (cN) phosphodiesterases (PDEs) is comprised of 11 families of enzymes. PDEs break down cAMP and/or cGMP and are major determinants of cellular cN levels and, consequently, the actions of cN-signaling pathways. PDEs exhibit a range of catalytic efficiencies for breakdown of cAMP and/or cGMP and are regulated by myriad processes including phosphorylation, cN binding to allosteric GAF domains, changes in expression levels, interaction with regulatory or anchoring proteins, and reversible translocation among subcellular compartments. Selective PDE inhibitors are currently in clinical use for treatment of erectile dysfunction, pulmonary hypertension, intermittent claudication, and chronic pulmonary obstructive disease; many new inhibitors are being developed for treatment of these and other maladies. Recently reported x-ray crystallographic structures have defined features that provide for specificity for cAMP or cGMP in PDE catalytic sites or their GAF domains, as well as mechanisms involved in catalysis, oligomerization, autoinhibition, and interactions with inhibitors. In addition, major advances have been made in understanding the physiological impact and the biochemical basis for selective localization and/or recruitment of specific PDE isoenzymes to particular subcellular compartments. The many recent advances in understanding PDE structures, functions, and physiological actions are discussed in this review.

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Section: Expanded Uses For Approved Pde3 Inhibitorsmentioning

confidence: 99%

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Francis

Blount

Corbin

2011

Physiological Reviews

560

546

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“…[3][4][5][6] It also reduces the risk of stroke by approximately 40%, 7 and prevents recurrence of cerebral infarction. 8 Furthermore, cilostazol has been recommended in the international guideline, TASCII, 9,10 as a first-line therapy for peripheral arterial disease because it improves the symptoms.…”

mentioning

confidence: 99%

Evaluation of the Antiplatelet Effects of Cilostazol, a Phosphodiesterase 3 Inhibitor, by VASP Phosphorylation and Platelet Aggregation

Yamamoto

Takahashi

Watanabe

et al. 2008

Circ J

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Background Cilostazol, a phosphodiesterase 3 inhibitor, is an antiplatelet drug that is widely used for preventing cardiovascular events, although, to date, there are few methods for evaluating its effects. Methods and Results Blood samples were taken at baseline and at 3 and 12 h in 10 healthy male subjects after 100 mg cilostazol intake. Each sample was examined by Western blot for phosphorylation levels of vasodilatorstimulated phosphoprotein (VASP), an abundant cAMP-dependent kinase substrate in platelets, and by the optical aggregometer for ADP-and collagen-induced aggregation, before and after 8 nmol/L prostaglandin E1 (PGE1) treatment. Cilostazol intake did not affect VASP phosphorylation levels or the maximal aggregation rates without PGE1 treatment. However, cilostazol intake apparently enhanced PGE1-induced VASP phosphorylation and PGE1-mediated reduction of ADP-and collagen-induced maximal aggregation rates. Levels of VASP phosphorylated at Ser157 were correlated and the maximal aggregation rates induced by ADP were inversely correlated with cilostazol concentrations in the plasma. Conclusion The antiplatelet effects of cilostazol intake could be evaluated by measuring VASP phosphorylation levels and maximal aggregation rates in platelets by ex vivo treatment with a low concentration of PGE1. (Circ J 2008; 72: 1844 -1851

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“…19) In patients undergoing PCI, combined antiplatelet therapy with cilostazol and aspirin was as effective as ticlopidine and aspirin or clopidogrel and aspirin for preventing acute complications after stent implantation. 22) Furthermore, a double-blind, randomized non-inferiority trial showed that cilostazol seems to be non-inferior, and might be superior, to aspirin for prevention of secondary stroke in Japanese people. 24) In our study, the incidence of any stroke within 30 days after CAS was not significantly different between the cilostazol and thienopyridine groups.…”

Section: Discussionmentioning

confidence: 99%

“…4) However, the optimal regimen of antiplatelet therapy for CAS remains to be established. Some reports that cilostazol can prevent subacute thrombosis 22) and has the potential to reduce in-stent restenosis (ISR) after PCI 7,29) led us to hypothesize that it may also be useful in patients treated by CAS.…”

Section: Introductionmentioning

confidence: 99%

Cilostazol Reduces Periprocedural Hemodynamic Depression in Carotid Artery Stenting

Tsutsumi

Aikawa

Nii

et al. 2013

Neurol. Med. Chir.(Tokyo)

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The clinical effects of two different types of antiplatelet drugs, cilostazol and thienopyridine drugs, were compared in patients treated by carotid artery stenting (CAS). Two hundred patients scheduled for CAS were randomized to either cilostazol or a thienopyridine drug (ticlopidine or clopidogrel). The study was conducted in open-label design. Aspirin was also given to all patients. All episodes of periprocedural hemodynamic instability (bradycardia, hypotension) were recorded together with all instances of stroke, cardiac morbidity, and death within 30 days of the procedure. Angiographic followup studies were conducted about 6 months after CAS. Finally, 197 patients were enrolled in this study; 97 were treated with cilostazol (cilostazol group) and 100 with a thienopyridine drug (thienopyridine group). In the 30-day follow-up period, the incidence of stroke, cardiac adverse effects, and death was not significantly different between the 2 groups (cilostazol group 7.2%, thienopyridine group 11.0%; p ＝ 0.85). The incidence of intra-and postprocedural bradycardia was significantly lower in the cilostazol group (cilostazol group 18.6% and 2.1%, thienopyridine group 40.0% and 18.0%, respectively; p º 0.01). Although the incidence of intraprocedural hypotension did not significantly differ between the 2 groups, postprocedural hypotension was significantly lower in the cilostazol group (16.5% vs. 34.0%, p º 0.01). In-stent restenosis on follow-up angiograms was lower in the cilostazol group but not significantly (0% vs. 4.4%, p ＝ 0.12). This small open-label study shows that cilostazol may reduce periprocedural bradycardia and hypotension compared with thienopyridine drugs in patients treated by CAS.

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Cilostazol, clopidogrel or ticlopidine to prevent sub-acute stent thrombosis: A meta-analysis of randomized trials

Cited by 40 publications

References 44 publications

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Mammalian Cyclic Nucleotide Phosphodiesterases: Molecular Mechanisms and Physiological Functions

Evaluation of the Antiplatelet Effects of Cilostazol, a Phosphodiesterase 3 Inhibitor, by VASP Phosphorylation and Platelet Aggregation

Cilostazol Reduces Periprocedural Hemodynamic Depression in Carotid Artery Stenting

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