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Supervised Exercise, Stent Revascularization, or Medical Therapy for Claudication Due to Aortoiliac Peripheral Artery Disease: The Clever Study
Published in Juan Carlos Jimenez, Samuel Eric Wilson, 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Juan Carlos Jimenez, Samuel Eric Wilson
Intervention OMC was established by the 2005 ACC/AHA Guidelines for the management of patients with peripheral artery disease to promote best practices for risk factor management, use of antiplatelet therapy and use of claudication pharmacotherapy.7 All participants received cilostazol 100 mg by mouth twice daily. In addition, OMC included advice about home exercise and diet in the form of standardized verbal instruction and printed material. Cardiovascular risk factor data were collected and feedback was provided to the sites by a central risk factor committee. Risk factors were managed directly by the local study site.
Hematologic Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: It should be used with caution because the pregnancy experience in humans is limited, and the reproduction studies in animals have shown the risk of teratogenicity associated with the use of Cilostazol.
Management of peripheral arterial disease in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Cilostazol inhibits phosphodiesterase type 3, increasing intracellular concentration of cyclic adenosine monophosphate. Cilostazol suppresses platelet aggregation and also acts as a direct arterial vasodilator. Cilostazol has been documented in numerous trials to improve exercise capacity in patients with intermittent claudication (141,148–151), and in a dose of 100 mg twice daily, was shown to be superior to both placebo and pentoxifylline (150).
Cilostazol Attenuates Retinal Oxidative Stress and Inflammation in a Streptozotocin-Induced Diabetic Animal Model
Published in Current Eye Research, 2019
Po-Ting Yeh, Yu-Hsun Huang, Shu-Wen Chang, Lu-Chun Wang, Chung-May Yang, Wei-Shiung Yang, Chung-Wu Lin, Chang-Hao Yang
Cilostazol, 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxyl]-3,4-dihydro-2-(1H)-quinolinone, is a phosphodiesterase 3 (PDE3) inhibitor which has been shown to increase intracellular cyclic adenosine monophosphate (cAMP) levels and then decrease intracellular Ca2+ levels in platelets, resulting in inhibition of platelet aggregation and vasodilation leading to a reduction in arterial pressure.17,18 Cilostazol is used to treat intermittent claudication in diabetic patients and peripheral vascular occlusive diseases because of its anti-platelet, vasodilatory, anti-proliferative and anti-atherosclerotic effects.19–21 Recent studies have shown that the potent anti-inflammatory and anti-oxidative effects of cilostazol might occur through several pathways: (a) cilostazol represses vascular cell adhesion molecule-1 (VCAM-1) gene transcription via inhibiting NF-κB binding to its recognition sequence; (b) cilostazol inhibits high glucose-mediated endothelial-neutrophil adhesion; (c) cilostazol may dose-dependently inhibit tumor necrosis factor alpha-induced NF-κB activation and pro-inflammatory gene expressions in human endothelial cells of the umbilical vein; (d) PDE3 plays a role in mediating the effect of cAMP/protein kinase A (PKA) in the inhibition of NF-κB-dependent gene expression; (e) cilostazol inhibits the cytokine-induced expression of various pro-inflammatory and adhesion molecule genes by suppressing NF-κB activity via AMP-activated protein kinase (AMPK) activation.19,22–25
Cilostazol for treatment of cerebral infarction
Published in Expert Opinion on Pharmacotherapy, 2018
Kensuke Noma, Yukihito Higashi
Cilostazol, an antiplatelet agent, is a selective PDE3A inhibitor that can inhibit the degradation of cyclic adenosine monophosphate (cAMP), resulting in an increase in the active form of protein kinase A (PKA). Therefore, cilostazol has both an inhibitory effect on platelet aggregation and a vasodilatory effect by relaxation of vascular smooth muscle cells (VSMCs) via PKA-mediated inhibition of myosin light-chain kinase [12,13]. Also, cAMP has been reported to not only upregulate p53 and p21, anti-oncogenes, subsequently inducing apoptosis in VSMCs, but also upregulate hepatocyte growth hormone (HGF), resulting in re-endothelialization and improvement of endothelial function [14,15]. In addition, cilostazol has been revealed to inhibit inflammation [16], platelet activity [17], inflammation-mediated vascular damage [18], and cerebral hypoperfusion-mediated neuronal damage [19,20]. In the US and Europe, cilostazol has been licensed for treatment of patients with intermittent claudication to improve their walking distance in the absence of tissue necrosis or rest pain. On the other hand, mainly in Asia, cilostazol is licensed for treatment of patients with peripheral artery disease (PAD) to improve their ulceration and ischemic symptoms and also for treatment of patients with cerebral thrombosis to prevent secondary ischemic events [11].
Preparation and optimization of glyceryl behenate-based highly porous pellets containing cilostazol
Published in Pharmaceutical Development and Technology, 2018
Kyu-Mok Hwang, Woojin Byun, Cheol-Hee Cho, Eun-Seok Park
Cilostazol is a quinolinone derivative that acts as a vasodilator and platelet aggregation inhibitor17. The mechanism of action of cilostazol is based on its phosphodiesterase-III-selective blocking activity18. Clinically, cilostazol is used for the treatment of intermittent claudication19 and secondary prevention of cerebral infarction20. The development of a sustained release dosage form for cilostazol is beneficial for improving patient compliance and reducing adverse events such as headache21. However, absorption of cilostazol is significantly reduced in sites other than upper small intestine22. Therefore, designing a gastroretentive (GR) dosage form of cilostazol will improve the delivery of cilostazol to the upper part of the gastrointestinal tract and ensure constant plasma concentrations over time.