antiplatelet drugs
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Author(s):  
Pornwasa Wongpanya ◽  
Jaruwan Siritapetawee ◽  
Thipusa Wongpinij ◽  
Pat Photongkam

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Zongliang Yu ◽  
Xiaoya Li ◽  
Xiaonan Zhang ◽  
Dan Li ◽  
Yimeng Gu ◽  
...  

Ischemic heart disease is a significant risk factor that threatens human health, and antiplatelet drugs are routinely used to treat cases in clinical settings. Chinese medicine for promoting blood circulation and removing blood stasis (PBCRBSCM) can often be combined with antiplatelet drugs to treat ischemic heart disease. PBCRBSCM can inhibit platelet adhesion, activation, and aggregation; moreover, PBCRBSCM in combination with antiplatelet drugs exerts antiplatelet effects. The mechanism is related to several factors, including the inhibition of platelet activation and aggregation, improvement of the hemodynamic status and coagulation function, and correction of metabolism and inflammation. PBCRBSCM can also regulate the absorption and metabolism of conventional antiplatelet drugs and protect the gastric mucosal epithelial cells against damage induced by conventional antiplatelet drugs. Randomized controlled trials have confirmed that PBCRBSCM preparations and the active ingredients in these preparations can reduce resistance to aspirin and clopidogrel so that the combination of these drugs can exert their antiplatelet effects. In the perioperative treatment of patients with stable angina pectoris, unstable angina pectoris, and acute coronary syndrome undergoing percutaneous coronary intervention therapy, preparations of the active ingredients of PBCRBSCM combined with antiplatelet drugs and other conventional Western medicine treatments have been proven effective. The efficacy and safety of such combinations have also been extensively verified. Considerable progress has been made to understand the antiplatelet mechanism of PBCRBSCM. However, most clinical studies had problems, such as limited sample size and inappropriate research design, which has limited the translational use of PBCRBSCM in antiplatelet therapy. A large-scale, multicenter, randomized controlled study with cardiovascular events as the endpoint is still to be conducted to provide evidence for the combined application of PBCRBSCM and antiplatelet drugs in the prevention and treatment of ischemic heart disease.


2021 ◽  
Vol 17 ◽  
Author(s):  
Marcel Hrubša ◽  
Khondekar Nurjamal ◽  
Alejandro Carazo ◽  
Nayana Nayek ◽  
Jana Karlíčková ◽  
...  

Background: Antiplatelet drugs represent the keystone in the treatment and prevention of diseases of ischemic origin, including coronary artery disease. The current palette of drugs represents efficient modalities in most cases, but their effect can be limited in certain situations or associated with specific side effects. In this study, representatives of compounds selected from series having scaffolds with known or potential antiplatelet activity were tested. These compounds were previously synthetized by us, but their biological effects have not yet been reported. Objective: The aim of this study was to examine the antiplatelet and anticoagulation properties of selected compounds and determine their mechanism of action. Methods: Antiplatelet activity of compounds and their mechanisms of action were evaluated using human blood by impedance aggregometry and various aggregation inducers and inhibitors and compared to appropriate standards. Cytotoxicity was tested using breast adenocarcinoma cell cultures and potential anticoagulation activity was also determined. Results: In total, four of 34 compounds tested were equally or more active than the standard antiplatelet drug acetylsalicylic acid (ASA). In contrast to ASA, all 4 active compounds decreased platelet aggregation triggered not only by collagen, but also partly by ADP. The major mechanism of action is based on antagonism at thromboxane receptors. In higher concentrations, inhibition of thromboxane synthase was also noted. In contrast to ASA, the tested compounds did not block cyclooxygenase-1. Conclusion: The most active compound, 2-amino-4-(1H-indol-3-yl)-6-nitro-4H-chromene-3-carbonitrile (2-N), which is 4-5x times more potent than ASA, is a promising compound for the development of novel antiplatelet drugs.


2021 ◽  
Author(s):  
Jie Chen ◽  
Hui Wang ◽  
Jie Yuan ◽  
Bing Xiao ◽  
Bo Lu ◽  
...  

Abstract Background Cerebral stroke is common and associated with high rates of mortality, disability, and recurrence while the chance of complete recovery is low. It adversely affects human physical and mental health and represents the leading cause of death in China. Aspirin is the cornerstone of secondary prevention of cerebral stroke. However, recurrence of stroke cannot be completely prevented by regular oral administration of aspirin due to aspirin resistance, which is an independent risk factor for stroke recurrence. In this instance, several strategies have been taken, including dose incrementation, frequency increaseof drug administration, combination with other antiplatelet drugs, or replacing it with new antiplatelet drugs. However, these measures have led to several other undesirable outcomes, including gastrointestinal tract stimulation, increased risk of bleeding, higher cost, and poor patient compliance to treatment.let aggregation, but its efficacy and mechanism in the secondary prevention Numerous studies have confirmed that Panax notoginseng has the effect of anti-plateof cerebral stroke among patients with aspirin resistance have not been ascertained. Method/Design: This is a two-center, triple-blinded, randomized, controlled, and optimal efficiency trial. A total of 120 patients aged 45–65 years old with semi-resistance to antiplatelet drugs treated in the secondary prevention clinics for cerebral stroke in the Shaanxi Traditional Chinese Medicine Hospital and Xi'an Hospital of Traditional Chinese Medicine from October 2020 to June 2022 will be recruited. Patients are randomly divided into the experimental group and control group at the ratio of 1:1, with 60 cases in each group. The blood pressure, blood glucose, and blood lipid are controlled within the normal range as the basic standards of treatment. The experimental group is given aspirin enteric coated tablets 100 mg/day + Panax Notoginseng Powder (3 g/day, oral administrationafter dissolved), while the control group is given aspirin enteric coated tablets 100 mg/day + placebo (Panax Notoginseng Powder 0.03 g + malt powder/day, oral administration after dissolved). Measurements on the platelet aggregation rate, thromboxane A2 (TXA2), prostacyclin (PGI2), adenosine diphosphate (ADP), and changes of the coagulation index of the two groups are performed on the day-14 and day-30. The efficacy, mechanism, and safety of Panax notoginseng in the treatment of patients with aspirin resistance will be evaluated. The data are analyzed and the mean and confidence interval (CI) of 95% level are calculated by the SPSS 21.0 software. The intention-to-treat (ITT) analysis is used to account for the missing data or dropouts. Descriptive analyses are performed on the baseline population data. Repeated ANOVA (general linear model) is used to compare the differences ofkey indicators (platelet aggregation rate, thromboxane A2, prostacyclin, ADP) between the two groups.For the secondary indicators (coagulation function), two independent samples t-test and Wilcoxon rank-sum test are used. P < 0.05 is considered a statistically significant difference between the two groups. Conclusion This study aims is to explore the efficacy and mechanism of Panax notoginseng in the secondary prevention for stroke patients with aspirin resistance. The results will provide evidence-based practice for traditional Chinese medicine, and also shed light on how it may influence the secondary prevention of cerebral stroke. Trial registration: The trial has been registered with the Chinese Clinical Trial Registry (http://www.chictr.org.cn/index.aspx,) on 24th October 2020, with the registration number ChiCTR2000037833.


2021 ◽  
Vol 22 (20) ◽  
pp. 11199
Author(s):  
Bibian M. E. Tullemans ◽  
Alicia Veninga ◽  
Delia I. Fernandez ◽  
Maureen J. B. Aarts ◽  
Johannes A. Eble ◽  
...  

Current antiplatelet drugs for the treatment of arterial thrombosis often coincide with increased bleeding risk. Several tyrosine kinase inhibitors (TKIs) for cancer treatment inhibit platelet function, with minor reported bleeding symptoms. The aim of this study was to compare the antiplatelet properties of eight TKIs to explore their possible repurposing as antiplatelet drugs. Samples of whole blood, platelet-rich plasma (PRP), or isolated platelets from healthy donors were treated with TKI or the vehicle. Measurements of platelet aggregation, activation, intracellular calcium mobilization, and whole-blood thrombus formation under flow were performed. Dasatinib and sunitinib dose-dependently reduced collagen-induced aggregation in PRP and washed platelets; pazopanib, cabozantinib, and vatalanib inhibited this response in washed platelets only; and fostamatinib, axitinib, and lapatinib showed no/limited effects. Fostamatinib reduced thrombus formation by approximately 50% on collagen and other substrates. Pazopanib, sunitinib, dasatinib, axitinib, and vatalanib mildly reduced thrombus formation on collagen by 10–50%. Intracellular calcium responses in isolated platelets were inhibited by dasatinib (>90%), fostamatinib (57%), sunitinib (77%), and pazopanib (82%). Upon glycoprotein-VI receptor stimulation, fostamatinib, cabozantinib, and vatalanib decreased highly activated platelet populations by approximately 15%, while increasing resting populations by 39%. In conclusion, the TKIs with the highest affinities for platelet-expressed molecular targets most strongly inhibited platelet functions. Dasatinib, fostamatinib, sunitinib, and pazopanib interfered in early collagen receptor-induced molecular-signaling compared with cabozantinib and vatalanib. Fostamatinib, sunitinib, pazopanib, and vatalanib may be promising for future evaluation as antiplatelet drugs.


2021 ◽  
Author(s):  
kuwabara masashi ◽  
Shigeyuki Sakamoto ◽  
Takahito Okazaki ◽  
Takafumi Mitsuhara ◽  
Koji Shimonaga ◽  
...  

Abstract PurposeTo investigate temporal changes in imaging findings of conservatively treated unruptured vertebral basilar artery dissection and its contributing factors.MethodsFifty-three patients who underwent conservative treatment for 64 cases of vertebral basilar artery dissection diagnosed between January 2006 and March 2019 and follow-up of at least 12 months after onset were retrospectively investigated. Statistical analyses of age, sex, medical history, pattern of onset, lesion site, imaging findings and changes over time, regular medication, and outcomes were performed. ResultsChanges in the vascular morphology of the lesion site during the follow-up period were observed in only 23 (43%) patients (median time until change: 19 days). Univariate analysis of factors contributing to morphological changes at the dissection site showed that changes were significantly more likely in younger patients (p = 0.011). Patients taking antiplatelet drugs had a significantly greater rate of deterioration at the dissection site (p = 0.028) than others. On multivariate analysis, age was an independent factor contributing to changes at the dissection site, and taking antiplatelet drugs, particularly clopidogrel, was an independent factor contributing to deterioration. No patient developed intracranial hemorrhage, cerebral infarction, or worsening of neurological symptoms during follow-up.ConclusionsMorphological changes at the dissection site are more likely in younger patients with unruptured vertebral basilar artery dissection and those taking antiplatelet drugs. However, chances of intracranial hemorrhage, cerebral infarction, or worsening of neurological symptoms during conservative therapy are low. Therefore, unruptured vertebral basilar artery dissection may be considered a benign condition.


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