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Safety of Tirofiban for Patients with Acute Ischemic Stroke in Routine Clinical Practice
EXPERIMENTAL AND THERAPEUTIC MEDICINE 10: 169-174, 2015 Safety of tirofiban for patients with acute ischemic stroke in routine clinical practice YUAN-QUN ZHU1, YAN-JUN ZHANG2, HAI-LIN RUAN3, QING LIU2, QIN ZHAN2 and QIONG LI2 1Department of Neurology, Liuzhou Worker's Hospital, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005; 2Department of Geriatrics, People's Hospital of Zhengzhou, Zhengzhou, Henan 450003; 3Department of Emergency, Liuzhou Worker's Hospital, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, P.R. China Received April 11, 2014; Accepted December 8, 2014 DOI: 10.3892/etm.2015.2495 Abstract. The aim of the present study was to investigate the Introduction safety of tirofiban alone and in combination with various treat- ments in acute ischemic stroke (AIS). A total of 120 patients Acute ischemic stroke (AIS) is a common cause of morbidity with AIS were included in the study, and these patients were and mortality worldwide. Thrombolysis with recombinant divided into three treatment groups: Group A (tirofiban alone, tissue plasminogen activator (rtPA) is the only proven beneficial n=68), group B (tirofiban plus thrombolytic therapy, n=26), therapy in AIS, and this is received by <2% of patients (1). The and group C (tirofiban as a ‘bridging therapy’, n=26). Risk inaccessibility of this treatment to the majority of patients is due factors, stroke severity, initial imaging, treatment regimens, to a number of factors: A lack of adequate transport facilities complications and long‑term outcomes were analyzed. In and infrastructure, including facilities for thrombolysis in most total, eight patients (6.7%) [six patients (23.1%) in group B centers; the high cost of tPA; and a lack of awareness among and two patients (7.7%) in group C] had hemorrhage during the public and doctors (2). -
Cangrelor Ameliorates CLP-Induced Pulmonary Injury in Sepsis By
Luo et al. Eur J Med Res (2021) 26:70 https://doi.org/10.1186/s40001-021-00536-4 European Journal of Medical Research RESEARCH Open Access Cangrelor ameliorates CLP-induced pulmonary injury in sepsis by inhibiting GPR17 Qiancheng Luo1†, Rui Liu2†, Kaili Qu3, Guorong Liu1, Min Hang1, Guo Chen1, Lei Xu1, Qinqin Jin1 , Dongfeng Guo1* and Qi Kang1* Abstract Background: Sepsis is a common complication of severe wound injury and infection, with a very high mortality rate. The P2Y12 receptor inhibitor, cangrelor, is an antagonist anti-platelet drug. Methods: In our study, we investigated the protective mechanisms of cangrelor in CLP-induced pulmonary injury in sepsis, using C57BL/6 mouse models. Results: TdT-mediated dUTP Nick-End Labeling (TUNEL) and Masson staining showed that apoptosis and fbrosis in lungs were alleviated by cangrelor treatment. Cangrelor signifcantly promoted surface expression of CD40L on platelets and inhibited CLP-induced neutrophils in Bronchoalveolar lavage fuid (BALF) (p < 0.001). We also found that cangrelor decreased the infammatory response in the CLP mouse model and inhibited the expression of infamma- tory cytokines, IL-1β (p < 0.01), IL-6 (p < 0.05), and TNF-α (p < 0.001). Western blotting and RT-PCR showed that cangre- lor inhibited the increased levels of G-protein-coupled receptor 17 (GPR17) induced by CLP (p < 0.001). Conclusion: Our study indicated that cangrelor repressed the levels of GPR17, followed by a decrease in the infam- matory response and a rise of neutrophils in BALF, potentially reversing CLP-mediated pulmonary injury during sepsis. Keywords: Sepsis, Infammation, Cangrelor, Platelet, GPR17 Background Te lung is one of the initial target organ of the systemic Sepsis is a serious disease and will lead a high mortal- infammatory response caused by sepsis, leading to alve- ity rate of approximately 22% in all over the world [1]. -
Summary of the Product Characteristics
Tirofiban hydrochloride Hikma Pharma GmbH SUMMARY OF PRODUCT CHARACTERISTICS 1 NAME OF THE MEDICINAL PRODUCT <TIROFIBAN>® *50 micrograms/mL Solution for infusion <TIROFIBAN>® *250 micrograms/mL Concentrate for solution for infusion 2 QUALITATIVE AND QUANTITATIVE COMPOSITION <TIROFIBAN> Solution: 1 ml of solution for infusion contains 56 micrograms of tirofiban hydrochloride monohydrate which is equivalent to 50 micrograms Tirofiban. This medicinal product contains 31 mmol (or 715 mg) sodium per bag (250 ml). To be taken into consideration by patients on a controlled sodium diet. <TIROFIBAN> Concentrate: 1 ml of concentrate for solution for infusion contains 281 micrograms of tirofiban hydrochloride monohydrate which is equivalent to 250 micrograms Tirofiban. 50 ml of concentrate for solution for infusion contains 14,05 mg of tirofiban hydrochloride monohydrate which is equivalent to 12,5 mg Tirofiban. This medicinal product contains less than 1 mmol sodium (23 mg) per vial (50 ml), i.e. essentially ‘sodium- free’. For the full list of excipients, see section 6.1. 3 PHARMACEUTICAL FORM <TIROFIBAN> Solution: Solution for Infusion (250 ml bag) A clear, colourless solution. <TIROFIBAN> Concentrate: Concentrate for solution for infusion. A clear, colourless concentrated solution. * in the following document the abbreviated terms detailed below are used. • <TIROFIBAN> means <TIROFIBAN> Solution for Infusion or <TIROFIBAN> Concentrate for Solution for Infusion. • <TIROFIBAN> Solution will be used when referring to <TIROFIBAN> Solution for Infusion -
Kengrexal, INN-Cangrelor Tetrasodium
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 1. NAME OF THE MEDICINAL PRODUCT Kengrexal 50 mg powder for concentrate for solution for injection/infusion 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each vial contains cangrelor tetrasodium corresponding to 50 mg cangrelor. After reconstitution 1 mL of concentrate contains 10 mg cangrelor. After dilution 1 mL of solution contains 200 micrograms cangrelor. Excipient with known effect Each vial contains 52.2 mg sorbitol. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Powder for concentrate for solution for injection/infusion. White to off-white lyophilised powder. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Kengrexal, co-administered with acetylsalicylic acid (ASA), is indicated for the reduction of thrombotic cardiovascular events in adult patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) who have not received an oral P2Y12 inhibitor prior to the PCI procedure and in whom oral therapy with P2Y12 inhibitors is not feasible or desirable. 4.2 Posology and method of administration Kengrexal should be administered by a physician experienced in either acute coronary care or in coronary intervention procedures and is intended for specialised use in an acute and hospital setting. Posology The recommended dose of Kengrexal for patients undergoing PCI is a 30 micrograms/kg intravenous bolus followed immediately by 4 micrograms/kg/min intravenous infusion. The bolus and infusion should be initiated prior to the procedure and continued for at least two hours or for the duration of the procedure, whichever is longer. At the discretion of the physician, the infusion may be continued for a total duration of four hours, see section 5.1. -
Eptifibatide Is Noninferior to Abciximab: Implications for Clinical Practice
RESEARCH HIGHLIGHTS ANTIPLATELET THERAPY Eptifibatide is noninferior to abciximab: implications for clinical practice he glycoprotein IIb/IIIa (GPIIb/ randomized, open, parallel-group January 2004 and December 2007, IIIa) inhibitors eptifibatide and comparison of eptifibatide and abciximab and eptifibatide was used in 2,355 Tabciximab have comparable efficacy in 427 patients presenting within 12 h such procedures over this time frame. and safety in patients with ST-segment of STEMI onset and who underwent During the 1-year follow-up period, elevation myocardial infarction (STEMI) primary PCI. Enrolled patients were from no significant difference was reported undergoing primary percutaneous 22 centers in France and Germany. The for the incidence of death (8.0% and coronary intervention (PCI). These two study drugs were administered in 7.6%), myocardial infarction (9.0% and findings, from a randomized trial and a combination with background therapy 8.4%), or bleeding (2.7% and 3.2%) registry study, are reported in two papers comprising clopidogrel, aspirin, and between abciximab and eptifibatide, published in the Journal of the American heparin or enoxaparin. This study used respectively. Multivariable analysis College of Cardiology (JACC). the surrogate primary end point of showed that eptifibatide was noninferior Platelet aggregation and thrombus complete electrocardiographic ST-segment to abciximab for the prevention of death formation can be inhibited by blocking resolution (STR) 60 min after completion or myocardial infarction (odds ratio 0.94, the GPIIb/IIIa receptor on the platelet of PCI. 95% CI 0.82–1.09). membrane, thereby preventing the binding In the intention-to-treat analysis, These findings “fuel an already much of fibrinogen. -
P2 Receptors in Cardiovascular Regulation and Disease
Purinergic Signalling (2008) 4:1–20 DOI 10.1007/s11302-007-9078-7 REVIEW P2 receptors in cardiovascular regulation and disease David Erlinge & Geoffrey Burnstock Received: 3 May 2007 /Accepted: 22 August 2007 /Published online: 21 September 2007 # Springer Science + Business Media B.V. 2007 Abstract The role of ATP as an extracellular signalling Introduction molecule is now well established and evidence is accumulating that ATP and other nucleotides (ADP, UTP and UDP) play Ever since the first proposition of cell surface receptors for important roles in cardiovascular physiology and pathophysi- nucleotides [1, 2], it has become increasingly clear that, in ology, acting via P2X (ion channel) and P2Y (G protein- addition to functioning as an intracellular energy source, the coupled) receptors. In this article we consider the dual role of purines and pyrimidines ATP, adenosine diphosphate ATP in regulation of vascular tone, released as a cotransmitter (ADP), uridine triphosphate (UTP) and uridine diphosphate from sympathetic nerves or released in the vascular lumen in (UDP) can serve as important extracellular signalling response to changes in blood flow and hypoxia. Further, molecules [3, 4] acting on 13 P2X homo- and heteromul- purinergic long-term trophic and inflammatory signalling is timer ionotropic and 8 P2Y metabotropic receptor subtypes described in cell proliferation, differentiation, migration and [5, 6] (Table 1). To terminate signalling, ectonucleotidases death in angiogenesis, vascular remodelling, restenosis and are present in the circulation and on cell surfaces, rapidly atherosclerosis. The effects on haemostasis and cardiac degrading extracellular ATP into ADP, AMP and adenosine regulation is reviewed. The involvement of ATP in vascular [7, 8]. -
The Role of Low-Molecular-Weight Heparin in the Management of Acute Coronary Syndromes Marc Cohen, MD, FACC Newark, New Jersey
CORE Metadata, citation and similar papers at core.ac.uk Provided by ElsevierJournal - ofPublisher the American Connector College of Cardiology Vol. 41, No. 4 Suppl S © 2003 by the American College of Cardiology Foundation ISSN 0735-1097/03/$30.00 Published by Elsevier Science Inc. doi:10.1016/S0735-1097(02)02901-7 The Role of Low-Molecular-Weight Heparin in the Management of Acute Coronary Syndromes Marc Cohen, MD, FACC Newark, New Jersey A substantial number of clinical studies have consistently demonstrated that low-molecular- weight heparin (LMWH) compounds are effective and safe alternative anticoagulants to unfractionated heparins (UFHs). They have been found to improve clinical outcomes in acute coronary syndromes and to provide a more predictable therapeutic response, longer and more stable anticoagulation, and a lower incidence of UFH-induced thrombocytopenia. Of the several LMWH agents that have been studied in large clinical trials, including enoxaparin, dalteparin, and nadroparin, not all have shown better efficacy than UFH. Enoxaparin is the only LMWH compound to have demonstrated sustained clinical and economic benefits in comparison with UFH in the management of unstable angina/ non–ST-segment elevation myocardial infarction (NSTEMI). Also, LMWH appears to be a reliable and effective antithrombotic treatment as adjunctive therapy in patients undergoing percutaneous coronary intervention. Clinical trials with enoxaparin indicate that LMWH is effective and safe in this indication, with or without the addition of a glycoprotein IIb/IIIa inhibitor. The efficacy demonstrated by enoxaparin in improving clinical outcomes in unstable angina/NSTEMI patients has led to investigations of its role in the management of ST-segment elevation myocardial infarction. -
Deliverable 5.A Interim Report on the Study Results APPENDIX 2
Deliverable 5.a Interim report on the study results APPENDIX 2: Algorithms used to identify study variables for service contract EMA/2011/38/CN ‐ PIOGLITAZONE November 28th 2012 D5.a Interim report on the study results (Appendix 2) for Service Contract EMA/2011/38/CN PIOGLITAZONE Author(s): Vera Ehrenstein (AUH‐AS) APPENDIX 2. ALGORITHMS USED TO IDENTIFY STUDY VARIABLES Algorithms for AU Database DISEASE/CONDITION ICD-8 CODE (1977-1993) ICD-10 CODE (1994-) Diabetes type 2 250.00; 250.06; 250.07; 250.09 E11.0; E11.1; E11.9 Cancer of bladder 188 C67 Haematuria N/A R31 Haematuria, unspecified B18, K70.0–K70.3, K70.9, K71, K73, Mild hepatic impairment 571, 573.01, 573.04 K74, K76.0 Moderate to severe hepatic 070.00, 070.02, 070.04, 070.06, B15.0, B16.0, B16.2, B19.0, K70.4, impairment 070.08, 573.00, 456.00–456.09 K72, K76.6, I85 Acute myocardial infarction 410 I21-I23 Acute coronary syndrome 410, 413 I20-I24 Ischemic heart disease 410-414 I20-I25 427.09, 427.10, 427.11, 427.19, Congestive heart failure I50, I11.0, I13.0,I13.2 428.99, 782.49; Acute renal failure N/A N17 Diabetic coma N/A E10.0, E11.0, E12.0,E13.0, E14.0 Diabetic acidosis N/A E10.1, E11.1, E12.1,E13.1, E14.1 F10.1-F10.9, G31.2, G62.1, G72.1, Alcoholism 291, 303, 577.10, 571.09, 571.10 I42.6, K29.2, K86.0, Z72.1 Obesity 277.99 E65-E66 D5.a Interim report on the study results (Appendix 2) for Service Contract EMA/2011/38/CN PIOGLITAZONE Author(s): Vera Ehrenstein (AUH‐AS) Algorithms for defining acute events in Denmark, ICD-10 code Event ICD-10 code I21.x, I23.x http://apps.who.int/classifications/icd10/browse/2010/en#/I21 -
Nerve Blocks for Surgery on the Shoulder, Arm Or Hand
Nerve blocks for surgery on the shoulder, arm or hand Information for patients and families First Edition 2015 www.rcoa.ac.uk/patientinfo Nerve blocks for surgery on the shoulder, arm or hand This leaflet is for anyone who is thinking about having a nerve block for an operation on the shoulder, arm or hand. It will be of particular interest to people who would prefer not to have a general anaesthetic. The leaflet has been written with the help of patients who have had a nerve block for their operation. Throughout this leaflet we have used the above symbol to highlight key facts. Brachial plexus block? The brachial plexus is the group of nerves that lies between your neck and your armpit. It contains all the nerves that supply movement and feeling to your arm – from your shoulder to your fingertips. A brachial plexus block is an injection of local anaesthetic around the brachial plexus. It ‘blocks’ information travelling along these nerves. It is a type of nerve block. Your arm becomes numb and immobile. You can then have your operation without feeling anything. The block can also provide excellent pain relief for between three and 24 hours, depending on what kind of local anaesthetic is used. A brachial plexus block rarely affects the rest of the body so it is particularly advantageous for patients who have medical conditions which put them at a higher risk for a general anaesthetic. A brachial plexus block may be combined with a general anaesthetic or with sedation. This means you have the advantage of the pain relief provided by a brachial plexus block, but you are also unconscious or sedated during the operation. -
FDA Approves ZONTIVITY™ (Vorapaxar), First-In-Class PAR-1
NEWS RELEASE FDA Approves ZONTIVITY™ (vorapaxar), First-in-Class PAR-1 Antagonist, for the Reduction of Thrombotic Cardiovascular Events in Patients with a History of Heart Attack or with Peripheral Arterial Disease 5/12/2014 ZONTIVITY Added to Standard of Care Demonstrated Long-Term Benet Through Three Years Merck (NYSE:MRK), known as MSD outside the United States and Canada, today announced that the U.S. Food and Drug Administration (FDA) has approved ZONTIVITY™ (vorapaxar) for the reduction of thrombotic cardiovascular events in patients with a history of heart attack (myocardial infarction) or in patients with narrowing of leg arteries, called peripheral arterial disease (PAD). For patients with a history of heart attack or with PAD who had no history of stroke or transient ischemic attack (TIA), ZONTIVITY added to standard of care produced a signicant 17 percent relative risk reduction over the three years of the study for the combined events of cardiovascular (CV) death, myocardial infarction (MI), stroke, and urgent coronary revascularization (UCR) [event rate 10.1 percent vs. 11.8 percent for placebo]. For the key secondary composite ecacy endpoint of CV death, MI and stroke alone, ZONTIVITY produced a signicant 20 percent relative risk reduction in these patients [7.9 percent vs. 9.5 percent for placebo]. These results were driven by an 18 percent relative risk reduction in MI [5.4 percent vs. 6.4 percent for placebo] and a 33 percent relative risk reduction in rst stroke [1.2 percent vs. 1.6 percent for placebo]. The prescribing information for ZONTIVITY includes a boxed warning regarding bleeding risk. -
Zontivity (Vorapaxar)
HIGHLIGHTS OF PRESCRIBING INFORMATION antiplatelet drugs or with ZONTIVITY as the only antiplatelet These highlights do not include all the information needed to use agent. (2.2) ZONTIVITY safely and effectively. See full prescribing information for ZONTIVITY. --------------------- DOSAGE FORMS AND STRENGTHS --------------------- Tablets: 2.08 mg vorapaxar. (3) ZONTIVITY™ (vorapaxar) Tablets 2.08 mg*, for oral use *Equivalent to 2.5 mg vorapaxar sulfate ------------------------------- CONTRAINDICATIONS ------------------------------- Initial U.S. Approval: 2014 History of stroke, TIA, or ICH. (4.1) Active pathologic bleeding. (4.2) WARNING: BLEEDING RISK See full prescribing information for complete boxed warning. ----------------------- WARNINGS AND PRECAUTIONS ----------------------- • Do not use ZONTIVITY in patients with a history of stroke, Like other antiplatelet agents, ZONTIVITY increases the risk of transient ischemic attack (TIA), or intracranial hemorrhage (ICH); bleeding. (5.1) or active pathological bleeding. (4.1, 4.2) Avoid use with strong CYP3A inhibitors or inducers. (5.2) • Antiplatelet agents, including ZONTIVITY, increase the risk of bleeding, including ICH and fatal bleeding. (5.1) ------------------------------ ADVERSE REACTIONS ------------------------------ Bleeding, including life-threatening and fatal bleeding, is the most ----------------------------INDICATIONS AND USAGE ---------------------------- commonly reported adverse reaction. (6.1) ZONTIVITY is a protease-activated receptor-1 (PAR-1) antagonist indicated for the reduction of thrombotic cardiovascular events in To report SUSPECTED ADVERSE REACTIONS, contact Merck patients with a history of myocardial infarction (MI) or with peripheral Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., at 1-877 arterial disease (PAD). ZONTIVITY has been shown to reduce the rate 888-4231 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. of a combined endpoint of cardiovascular death, MI, stroke, and urgent coronary revascularization. -
I Used to Smoke Menthol Cigarettes. There Was Something About The
In response to the scent of the soap I used to smoke menthol cigarettes. There was something about the Alice Hattrick combination of smoke, produced by fire, and menthol, a chemical in every kind of mint that tricks your brain into thinking it’s tasting something cold, that was so appealing. Alcohol is still the active ingredient in mouthwash but it is nearly always flavoured mint. Listerine was developed by the doctors who founded Johnson & Johnson after Jospeh Lister became the first person to conduct a surgical procedure in sterilised conditions. In the 16th century, a number of herbs were used to clean the mouth and teeth, mint but also sage and rosemary in vinegar, alongside practical solutions like wine, which replaced urine (containing ammonia) as a popular disinfectant. In the 20th century, mint became the predominant flavour of mouthwash and toothpaste because it was widely available and made the mouth cool, counteracting the fiery sensation of astringent products. When menthol binds with a particular receptor in our brains – TRPM8 – it has the same effect as exposing it to cool temperatures. It’s the menthol that makes it feel like it’s working. There aren’t many perfumes that smell predominantly of mint, but they do exist. Aqua Allegoria Herba Fresca by Guerlain (1999) smells uber clean, like actual hygiene: mint gum, and then lemon and grass as the mint fades like a… mint? Apparently, Jean-Paul Guerlain wanted to evoke the memory of playing barefoot in the grass as a child, crushing mint leaves underfoot, which is probably why this smells like the kind of green you imagine, but have never actually experienced.