Antiplatelet drugs/heparin/ondansetron

2021 ◽  
Vol 1872 (1) ◽  
pp. 61-61
Keyword(s):  
Antiplatelet Drugs

PPI, Antiplatelet Drugs in Combo Deemed Safe

2009 ◽  
Vol 39 (16) ◽  
pp. 8
Author(s):  
ROBERT FINN
Keyword(s):  
Antiplatelet Drugs

The Effect of Antiplatelet Drugs on Plasma Betathromboglobulin in Coronary Artery Disease

1979 ◽  
Author(s):  
P Han ◽  
A Turpie ◽  
E Genton ◽  
M Gent
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Crossover Trial ◽  
Specific Protein ◽  
Antiplatelet Drugs ◽  
Significant Difference ◽  
Pre Treatment ◽  
Artery Disease ◽  
Therapeutic Doses ◽  
Granule Release

Platelets play a role in the development and complications of coronary artery disease (CAD) and a number of abnormalities of platelet function which can be corrected by antiplatelet drugs have been described. Betathromboglobulin (BTG), a platelet-specific protein which is released from α-granules during platelet activation is significantly elevated in patients with angiographically demonstrated CAD (51.0 ± 31.0 ng/ml., n = 50) compared to normal (28.0 ± 8.0 ng/ml., n = 70) p < 0.001. The effect of sulphinpyrazone (800 mg.) or aspirin (1200 mg.)/dipyridamole (200 mg.) on plasma BTG in CAD was studied in a blind prospective crossover trial in 25 patients. Mean BTG concentration pre-treatment was 52.3 ng/ml. and after 1 month’s treatment with placebo, sulphinpyrazone or aspirin/dipyridamole mean plasma BTG concentrations were 53.5, 49.6 and 56.7 ng/ml. respectively. Analysis of variance showed no significant difference between the means (p > 0.1) . This study confirms increased plasma BTG concentrations in patients with CAD and indicates that therapeutic doses of these antiplatelet drugs do not significantly effect the BTG level and thus appear not to prevent α-granule release in CAD.

Antiplatelet Therapy in Acute Coronary Syndromes

2010 ◽  
Vol 6 (1) ◽  
pp. 58
Author(s):  
Sasha Koul ◽  
David Erlinge ◽  
◽  
Keyword(s):  
Platelet Function ◽  
Acute Coronary Syndromes ◽  
New Drugs ◽  
Antiplatelet Drugs ◽  
Bleeding Complications ◽  
Great Promise ◽  
Mortality Data ◽  
Poor Responders ◽  
Coronary Syndromes

Drugs inhibiting platelet function play a major role in the treatment of acute coronary syndromes (ACS). The first drug used, which is still considered the cornerstone of therapy today, is aspirin. Although very impressive in acutely decreasing rates of myocardial infarction as well as death, long-term data are scarce, despite our current recommendation for lifelong aspirin. The thienopyridines, most notably clopidogrel, are the next line of antiplatelet drugs. Well-documented data support the usage of clopidogrel for non-STEMI-ACS (NSTE-ACS). Although positive mortality data exist regarding clopidogrel and STEMI patients in a medically treated population, including thrombolysis, no larger amounts of randomised data exist in a primary PCI setting. Poor responders to aspirin and/or clopidogrel are a clinical problem, with these individuals constituting a higherrisk group for recurrent ischaemic events. Whereas very little can be done regarding aspirin resistance, clopidogrel resistance might be diminished by increasing the dosage or changing to more potent and newer-generation antiplatelet drugs. The role of glycoprotein IIb/IIIa inhibitors has diminished drastically and instead paved the way for thrombin antagonists (bivalirudin), which have fewer bleeding complications with resulting better long-term mortality. Novel adenosine diphosphate (ADP)-receptor blockers such as prasugrel and ticagrelor have shown increased efficacy over clopidogrel and hold great promise for the future. However, not all patients may benefit from these new drugs and economic constraints may also limit their use. Platelet function tests could possibly help in identifying risk groups in need of stronger platelet inhibition.

Interaction between Traditional Chinese Medicine and Anticoagulant/Antiplatelet Drugs

2019 ◽  
Vol 20 (9) ◽  
pp. 701-713 ◽  
Author(s):  
Jiajia Li ◽  
Qing Liang ◽  
GuangChun Sun
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Drug Interactions ◽  
Adverse Reactions ◽  
Bleeding Risk ◽  
Antiplatelet Drugs ◽  
Pharmacokinetic Studies ◽  
Drug Databases ◽  
Concurrent Use ◽  
Anticoagulant Drugs

Background: Traditional Chinese medicine (TCM) has been used for medical purposes since the ancient time and has gradually gained recognition worldwide. Nowadays, patients with thrombus presiding to anticoagulant/ antiplatelet drugs prefer taking TCM. However, an increasing number of studies on herb–drug interactions have been shown. Nevertheless, findings are frequently conflicting and vague. In this review, we discuss the herb–drug interactions between TCM and anticoagulant/antiplatelet drugs to provide guidance on concomitant ingestion with anticoagulant/antiplatelet drugs. Methods: We undertook a structured search of medicine and drug databases for peer-reviewed literature using focused review questions. Results: Danshen, Ginkgo, Ginger, H. Perforatum, SMY and Puerarin injection had directional regulation effects on the efficacy of anticoagulant drugs by altering the CYPs, pharmacokinetic indexs and hemorheological parameters. H. Perforatum inhibited the efficacy of Clopidogrel by enhancing the CYP3A4 activity and Ginkgo increased the efficacy of Ticlopidine. Additionally, Renshen, the formulae except SMY and injections except Puerarin injection could increase or decrease the efficacy of anticoagulant/antiplatelet drugs via regulating the CYPs, platelet aggregation, hemorheological parameters and others. Conclusion: Some cases have reported that TCMs may increase the bleeding risk or has no effect on coagulation when anticoagulant/antiplatelet drugs are concurrently used. However, pharmacokinetic studies have presented either consistent or slightly varying results. So it is difficult to ascertain whether the concurrent use of TCM may increase or reduce the pharmacologic effects of anticoagulant/antiplatelet drugs with adverse reactions. Therefore, herb–drug interactions of TCM and anticoagulant/antiplatelet drugs should be further explored and defined.

AB1118 OPEN MUSCLE BIOPSY AS A SAFE AND USEFUL MEANS OF DIAGNOSING VASCULITIS: A SINGLE-CENTER EXPERIENCE OF 210 BIOPSY CASES

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1848.1-1848
Author(s):  
T. Mori ◽  
N. Yokogawa ◽  
K. Shimada
Keyword(s):  
Adverse Events ◽  
Muscle Biopsy ◽  
Safety Profile ◽  
Granulomatosis With Polyangiitis ◽  
Wound Dehiscence ◽  
Antiplatelet Drugs ◽  
Surgical Removal ◽  
Diagnostic Utility ◽  
Open Muscle ◽  
Muscle Biopsies

Background:We previously reported the utility of open muscle biopsies in diagnosing vasculitis [1]. The number of open muscle biopsies performed at our department has increased to over 200. The purpose of the present study was to evaluate the diagnostic utility of vasculitis and the safety of the open muscle biopsies.Objectives:To clarify the diagnostic utility of vasculitis and the safety profile of the open muscle biopsy.Methods:We retrospectively examined all cases of open muscle biopsy performed between May 2012 and June 2018 in our department. The biopsy results, the presence or absence of adverse events, and blood test data at the time of the biopsy were extracted from the patients’ electronic medical records.Results:Between May 2012 and June 2018, 210 open muscle biopsies were performed, 120 of which were done for vasculitis diagnosis. Diagnostic histopathological findings were obtained in 42 of the 120 cases (35%). The definitive diagnosis in these cases was microscopic polyangiitis (30 cases), eosinophilic granulomatosis with polyangiitis (seven cases), granulomatosis with polyangiitis (one case), polyarteritis nodosa (three cases), and other vasculitis (one case). In 57 cases with myeloperoxidase-anti-neutrophil cytoplasmic antibody (MPO-ANCA) ≥ 10 U/ml, 31 cases (54.3%) showed histopathology of vasculitis. In six cases with protainase-3-ANCA (PR3-ANCA) ≥ 10 U/ml, histopathology of vasculitis was found in one case (16.7%).In all 210 open muscle biopsy cases, complications included minor wound dehiscence (11 cases) and small subcutaneous hematoma (six cases), which were able to be managed by local treatment. Albumin was significantly lower in the patients with wound dehiscence (mean 3.2 vs 2.7, p = 0.049)Serious complications included anaphylaxis due to local anesthesia (one case), compartment syndrome due to hematoma (one case), hematoma requiring surgical removal (one case), and arterial hemorrhage requiring surgical intervention (one case). The patients in the latter three hemorrhagic cases were receiving antiplatelet drugs.Conclusion:An open muscle biopsy is useful for diagnosing vasculitis, especially for MPO-ANCA-positive anca-associated vasculitis. Its safety profile is acceptable. Serious adverse events are rare, but the procedure should be performed carefully when patients are receiving antiplatelet drugs.References:[1]Nunokawa T. et al. The use of muscle biopsy in the diagnosis of systemic vasculitis affecting small to medium-sized vessels: A prospective evaluation in Japan. Scand. J. Rheumatol. 2016;45:210–214Disclosure of Interests:None declared

Antiplatelet Drugs for Neurointerventions: Part 2 Clinical Applications

2021 ◽  
Author(s):  
Samuel Pearce ◽  
Julian T. Maingard ◽  
Hong Kuan Kok ◽  
Christen D. Barras ◽  
Jeremy H. Russell ◽  
...  
Keyword(s):  
Clinical Applications ◽  
Antiplatelet Drugs

scholarly journals Vascular Endothelial Repair and the Influence of Circulating Antiplatelet Drugs in a Carotid Coil Model

2021 ◽  
Vol 13 ◽  
pp. 117957352110117
Author(s):  
Norihito Fukawa ◽  
Takahiro Ueda ◽  
Tomofumi Ogoshi ◽  
Yasuhide Kitazawa ◽  
Jun Takahashi
Keyword(s):  
Endothelial Cells ◽  
Carotid Artery ◽  
Vascular Endothelial Cells ◽  
Repair Process ◽  
Diabetic Rats ◽  
Antiplatelet Drugs ◽  
Endovascular Coiling ◽  
Vascular Endothelial ◽  
Embolization Coil ◽  
Endothelial Repair

Background: Clinicians may choose to administer antiplatelet medications to patients with cerebral aneurysms following endovascular coiling to prevent thrombus formation and vascular occlusion, if they fear a thrombus will form on the platinum wire where it diverges into the vessel from the aneurysm sac. However, the mechanism by which vascular endothelial cells repair a vessel in the living body in the event of a coil deviation and the effects of antiplatelet drugs on these cells have not been fully elucidated. We aimed to investigate the association between endothelial progenitor cells (EPCs) and endothelium formation at the surface of the platinum coils deployed in the carotid artery of rats, and to determine the effects of different antiplatelet drugs on this process. Subjects and Methods: We established an experimental model using normal and diabetic rats at 12 months of age. The diabetic rats were assigned to 4 different diet groups, distinguished by whether they were fed plain rat feed, or the same feed supplemented by 1 of 3 antiplatelet drugs (cilostazol, aspirin, or clopidogrel: all 0.1%) for 2 weeks, and the carotid artery was perforated by an embolization coil (“carotid coil model”). We monitored the process by which vascular endothelial cells formed the new endothelium on the surface of the coil by sampling and evaluating the region at 1, 2, and 4 weeks after placement. This repair process was also compared among 3 groups treated with different antiplatelet drugs (i.e. aspirin, clopidogrel, and cilostazol). One-way analysis of variance tests were performed to evaluate the differences in vascular thickness between groups, and P < .05 was considered statistically significant. Results: The diabetic rats showed delayed neoendothelialization and marked intimal hyperplasia. Cilostazol and clopidogrel effectively counteracted this delayed endothelial repair process. Flk1 immunostaining revealed greater expression in the diabetic rats administered cilostazol, second only to normal rats, suggesting that this agent acted to recruit EPCs. Conclusion: Neoendothelialization is delayed when vascular endothelial cells fail to function normally, which consequently leads to the formation of hyperplastic tissue. Cilostazol may remedy this dysfunction by recruiting EPCs to the site of injury.

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