Pharmacoeconomic Analysis of Cilostazol for the Secondary Prevention of Cerebral Infarction

Inoue, Tadao; Kobayashi, Makoto; Uetsuka, Yoshio; Uchiyama, Shinichiro

doi:10.1253/circj.70.453

Cited by 20 publications

(15 citation statements)

References 13 publications

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“…Most recently, Huang (2007) reported that both cilostazol and aspirin prevented ischemic stroke recurrence in patients with ischemic disease, but severe cerebral hemorrhage was higher in aspirin‐treated as compared to cilostazol‐patients. Another recent report showed that cilostazol is cost‐effective in prevention of the recurrence of cerebral infarction (Inoue et al 2006). Cilostazol also effectively arrested the progression of asymptomatic infarction areas when assessed by MRI in Japanese subjects with type II diabetes mellitus without symptomatic coronary vascular events (Shinoda‐Tagawa et al 2002).…”

Section: Recent Clinical Trials In Strokementioning

confidence: 99%

Protective Effects of Cilostazol against Transient Focal Cerebral ischemia and Chronic Cerebral Hypoperfusion Injury

Lee

Park

Shin

et al. 2008

CNS Neuroscience & Therapeutics

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Cilostazol increases intracellular cyclic adenosine monophosphate (cyclic AMP) levels by inhibiting type III phosphodiesterase. It was approved by the Food and Drug Administration for the treatment of intermittent claudication. Its principal actions include inhibition of platelet aggregation, antithrombotic action in cerebral ischemia, and vasodilation, mediated by increased cyclic AMP levels. In a multicenter, randomized, placebo-controlled, double-blind clinical trial, cilostazol has been shown to protect patients from recurrent cerebral infarction. It has been recently suggested that cilastozol could be useful in the treatment of transient focal cerebral ischemic injury. Beneficial effects of cilostazol in cerebral ischemic infarction and edema formation has been confirmed in rats by the magnetic resonance imaging (MRI). The preventive effect was ascribed to cAMP-dependent protein kinase (PKA)-coupled maxi-K channel activation with additional antioxidant and poly(adenosine diphosphate [ADP]-ribose) polymerase inhibitory actions. Most recently, cilostazol has been shown to prevent vacuolation and rarefaction in the white matter of the rats subjected to chronic cerebral hypoperfusion in association with suppression of astrocyte and microglial activation. Taken together, recent experimental studies with cilostazol showed promising results in cerebral ischemia and chronic cerebral hypoperfusion.

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Section: Recent Clinical Trials In Strokementioning

confidence: 99%

Protective Effects of Cilostazol against Transient Focal Cerebral ischemia and Chronic Cerebral Hypoperfusion Injury

Lee

Park

Shin

et al. 2008

CNS Neuroscience & Therapeutics

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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. 11 Some agonists, including prostacyclin, a well established antiplatelet agent, 12 and adenosine 13 increase cAMP via G scoupled receptors.…”

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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“…63 Prevention of silent cerebral infarction was reported in a study of 89 patients, placebo-controlled, and with a 3.6-year follow-up (p < 0.001). Mochizuki et al, using single photon emission computed tomography (SPECT), 64 demonstrated increased cerebral blood flow in a non-controlled study with a 3-month follow-up.…”

Section: Actions Of Cilostazol In Central Nervous System Blood Flowmentioning

confidence: 93%

Contribuição na prevenção da isquemia cerebral pelo cilostazol, um inibidor da fosfodiesterase III: revisão de literatura

2008

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This literature review aims at presenting the main possibilities for the clinical application of cilostazol in the central nervous system. Cilostazol, a selective phosphodiesterase type III inhibitor, increases adenosine 3',5'-cyclic monophosphate levels on platelets, endothelial and smooth muscle cells, having vasodilatory, antiplatelet and antithrombotic properties. Currently, it is the first-choice drug for intermittent claudication, due to peripheral occlusive vascular disease. In addition, there is evidence showing that cilostazol is efficacious in cerebral atherosclerotic process, resulting in increase of blood flow and volume and preventing infarctions, especially lacunar and recurrent, since it reduces cellular death due to apoptosis and oxidative stress in white and gray substances.Keywords: Phosphodiesterase inhibitors, cerebral infarction, cerebral blood flow, cilostazol. RESUMOEsta revis•o bibliogr‚fica objetiva expor estas pesquisas sobre as a€ƒes do cilostazol no sistema nervoso central. O cilostazol " uma droga que demonstrou exercer inibi€•o seletiva e potente da fosfodiesterase tipo III, ocasionando o aumento de adenosina c…clica -3',5'-monofosfato nas plaquetas, nas c"lulas endoteliais e nas c"lulas musculares lisas, sendo classificado como vasodilatador, antiagregante plaquet‚rio e antitromb ‡tico. ˆ o f‚rmaco de primeira escolha na claudica€•o intermitente devido ‰ doen€a arterial obstrutiva perif"rica. Al"m disso, h‚ evidŠncias de que o cilostazol " eficaz no processo ateroscler ‡tico cerebral, promovendo aumento do fluxo e volume sang‹…neos e prevenindo infartos, especialmente lacunares e recorrentes, por diminuir a morte celular devido ‰ apoptose e ao estresse oxidativo nas substOEncias branca e parda.Palavras-chave: Inibidores de fosfodiesterase, infarto cerebral, fluxo sang‹…neo cerebral, cilostazol.

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Pharmacoeconomic Analysis of Cilostazol for the Secondary Prevention of Cerebral Infarction

Cited by 20 publications

References 13 publications

Protective Effects of Cilostazol against Transient Focal Cerebral ischemia and Chronic Cerebral Hypoperfusion Injury

Protective Effects of Cilostazol against Transient Focal Cerebral ischemia and Chronic Cerebral Hypoperfusion Injury

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

Contribuição na prevenção da isquemia cerebral pelo cilostazol, um inibidor da fosfodiesterase III: revisão de literatura

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