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Las enfermedades cardiovasculares representan la primera causa de muerte en el mundo. El manejo de los síndromes coronarios ha avanzado formidablemente en los últimos 50 años, reduciendo el riesgo isquémico, a expensas del consiguiente aumento del riesgo hemorrágico. La Sociedad Europea de Cardiología publicó en el año 2020 la guía sobre el manejo de síndrome coronario agudo sin elevación del segmento ST, donde se destacan cambios en los algoritmos de estratificación de riesgo y la terapia antiplaquetaria y anticoagulante como dos de los aspectos principales. En el presente editorial se resumen las principales novedades publicadas en este documento.
Cardiovascular disease is the leading cause of death worldwide. The management of coronary syndromes has advanced dramatically in the last 50 years, reducing ischemic risk, but observing an increase in bleeding risk. The European Society of Cardiology published in 2020 the guideline on the management of acute coronary syndrome without ST-segment elevation, where changes in risk stratification algorithms and antiplatelet and anticoagulant therapy are highlighted as two of the main aspects. This editorial summarizes the main developments published in this document.
A doença cardiovascular é a principal causa de morte em todo o mundo. O manejo das síndromes coronarianas avançou dramaticamente nos últimos 50 anos, reduzindo o risco isquêmico, mas observando um aumento no risco de sangramento. A Sociedade Europeia de Cardiologia publicou em 2020 a diretriz sobre o manejo da síndrome coronariana aguda sem supradesnivelamento do segmento ST, onde as alterações nos algoritmos de estratificação de risco e na terapia antiplaquetária e anticoagulante são destacadas como dois dos principais aspectos. Este editorial resume os principais desenvolvimentos publicados neste documento.
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Humans , Practice Guidelines as Topic , Non-ST Elevated Myocardial Infarction/diagnosis , Non-ST Elevated Myocardial Infarction/therapy , EuropeABSTRACT
Objective: The purpose of this study was to investigate the effects of CYP2C19 gene mutations on clopidogrel antiplatelet activity in the patients with coronary heart disease treated by percutaneous coronary intervention. Methods: Patients with coronary heart disease, who hospitalized in the Second Affiliated Hospital of Nanchang University from March 2011 to June 2019, and healthy individuals with matching genetic background, gender, and age as controls were included in this study. Basic clinical data were analyzed and blood samples of all research subjects were obtained for extraction of DNA, and Sanger first-generation sequencing method was used to detect CYP2C19 gene mutation from full exon and exon and intron junction. CYP2C19 gene variations in patients with coronary heart disease were compared with the 1000 Genomes Browse database and the sequencing results of healthy controls to determine whether the gene variation was a genetic mutation or a genetic polymorphism. After that, PolyPhen-2 prediction software was used to analyze the harmfulness of gene mutations to predict the effect of mutations on protein function. The same dose of CYP2C19 wild-type plasmid and the CYP2C19 gene mutant plasmids were transfected into human normal liver cells HL-7702. After transfection of 24 h, the expression of CYP2C19 protease in each group was detected. The liver S9 protein was incubated with clopidogrel, acted on platelets to detect the platelet aggregation rate and the activity of human vasodilator-activated phosphoprotein (VASP). Results: A total of 1 493 patients with coronary heart disease (59.36%) were enrolled, the average age was (64.5±10.4) years old, of which 1 129 were male (75.62%). Meanwhile, 1 022 healthy physical examination volunteers (40.64%) were enrolled, and the average age was (64.1±11.0) years old, of which 778 were male (76.13%). A total of 5 gene mutations of CYP2C19 gene were identified in 12 patients (0.80%), namely, 4 known mutations T130K (1 case), M136K (6 cases), N277K (3 cases), V472I (1 case) and one new mutation G27V (1 case), no corresponding gene mutation was found in healthy controls. It was found that T130K and M136K were probably damaging, G27V was possibly damaging, and N277K and V472I were benign mutations. In vitro, we demonstrated that the platelet aggregation rate of the M136K gene mutation group was 24.83% lower than that of the wild type (59.58% vs. 34.75%; P<0.05), and the phosphorylated VASP level was 23.0% higher than that of the wild type (1.0 vs. 1.23; P<0.05). However, the platelet aggregation rate and phosphorylated VASP level were similar between of G27V, T130K, N277K, V472I gene mutation groups and wild type group (P>0.05). Conclusions: In this study, 5 gene mutations are defined in patients with coronary heart disease, namely G27V, T130K, M136K, N277K, V472I. In vitro functional studies show that CYP2C19 gene mutation M136K, as a gain-of-function gene mutation, can enhance the activation of CYP2C19 enzyme on clopidogrel, thereby inhibiting the platelet aggregation rate.
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Bulbine natalensis Baker is a native succulent herb that belongs to the family Asphodelaceae, and is regarded asprecious, highly valued, and extensively used throughout the continent for medicinal purposes and in treating maleimpotency due to the aphrodisiac and invigorating effect. This study reviews the status of B. natalensis ethnobotanicaluses, biological and chemical properties. This review was conducted from April 2019 to February 2020 by applyingthe mixed-method review approach, and in the framework of a complete description of B. natalensis species, dataon morphology, distribution, and economic importance were discussed. Pharmacological screening reported thatB. natalensis possesses anti-inflammatory and broad-spectrum antimicrobial properties. The bulbous plant vapourcontains substances such as tannins, anthraquinones, cardiac glycosides, saponins, and alkaloids. Scientific evaluationsfrom various researchers have substantiated the use of B. natalensis in the enhancement of male sexual disorders, cureof wounds, rashes, itches, ringworm, diabetes, rheumatism, cracked lips and herpes, diarrhea, and paroxysms amongother diseases.
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To search for potent anti-ischemic stroke agents, a series of tetramethylpyrazine (TMP)/resveratrol (RES) hybrids 6a-t were designed and synthesized. These hybrids inhibited adenosine diphosphate (ADP)- or arachidonic acid (AA)-induced platelet aggregation, among them, 6d, 6g-i, 6o and 6q were more active than TMP. The most active compound 6h exhibited more potent anti-platelet aggregation activity than TMP, RES, as well as positive control ticlopidine (Ticlid) and aspirin (ASP). Furthermore, 6h exerted strong antioxidative activity in a dose-dependent manner in rat pheochromocytoma PC12 cells which were treated with hydrogen peroxide (HO) or hydroxyl radical (·OH). Importantly, 6h significantly protected primary neuronal cells suffered from oxygen-glucose deprivation/reoxygenation (OGD/R) injury, comparable to an anti-ischemic drug edaravone (Eda). Together, our findings suggest that 6h may be a promising candidate warranting further investigation for the intervention of ischemic stroke.
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Butylphthalide and ferulic acid exhibit excellent therapeutic effects in ischemic stroke. In this research, twelve 3-n-butylphthalide derivatives were designed by molecular hybridization strategy. The target compounds were obtained by nucleophilic substitution, reduction reaction, esterification reaction and elimination reaction, and the structure was confirmed by 1H NMR, 13C NMR and ESI-MS. All compounds were evaluated for neuroprotective activity against OGD/R-induced neurotoxicity in rat cortical neurons by MTT assay. The compounds with the best neuroprotective activity were biologically evaluated for their ability to inhibit platelet aggregation induced by arachidonic acid (AA) and adenosine diphosphate (ADP) via the Bron method．The results indicate that 7b exhibited potent neurocyte protective activity as well as prominent anti-platelet aggregation activity. Compound 7b has potential to be developed as a drug for ischemic stroke.
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Higenamine (HG) is an active cardiotonic component isolated from Aconite. Chinese and foreign scholars have done a lot of research on the metabolism and pharmacological effects of HG, which confirmed that it has cardiovascular pharmacological effects of cardiactonic action and vasodilation for the treatment of heart failure and bradycardia, anti-oxidative and anti-apoptotic effects which can be used to protect the heart and reduce heart ischemia and reperfusion injury. In addition, HG inhibits the expression of iNOS mRNA by inhibiting the activity of the transcription factor NF-κB, inhibits the lipopolysaccharide (LPS)-induced NO product, and inhibits platelet aggregation and thrombus formation, thereby improving the experimental septic shock in animals. This article reviews the recent progress in cardiovasular pharmacology of HG, which will contribute to the further development and clinical application of it in the future.
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The objective of this work was to develop a bioassay to quantify the antiplatelet aggregation activity of hirudo for quality evaluation and control. Antithrombin activity of hirudo extracted by high temperature decoction was determined by thrombin titration. Antiplatelet aggregation activity of hirudo was determined through pharmacodynamic experiments in vitro and in vivo using a bioassay we developed for quantifying inhibition of platelet aggregation. Methodological investigation was carried out and the titers of 12 batches of hirudo samples were determined. During the experiment, the disposal of animals is in accordance with the ethical standards of animal experiments. The results showed that the antithrombin activity of hirudo decocted at high temperature decreased significantly and almost lost its activity. Hirudo inhibited platelet aggregation and results in vivo and in vitro were consistent. These assays were employed to test 12 batches of hirudo. The results demonstrated that the biopotency of 12 batches was 113.49, 96.13, 121.22, 127.33, 83.48, 108.72, 131.41, 127.95, 76.90, 126.27, 132.89 and 573.53 U·mg-1. The method was reliable and reproducible and can be used to assess the quality of hirudo.
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The thrombus is a deposit that is formed on the surface of the endovascular or at the site of repair,and known as the main complication of cardiovascular disease and the cause of death. At the same time,thrombus is mainly treated by the following three ways: anticoagulation,anti-platelet aggregation and thrombolysis. In this study,the chemical constituents of seven traditional Chinese medicines in the Xixian Tongshuan Preparation were collected to construct a component database. Subsequently,the pharmacophore were used to screen out the component database,and molecular docking was used to screen out the results of pharmacophore for explaining the material basis and mechanism that Xixian Tongshuan Preparation exerts anti-thrombotic activity by inhibiting platelet aggregation. First of all,P2 Y12,GPⅡb/Ⅲa and PAR1 were selected as study vectors,the optimal models of inhibitors were obtained respectively through verification and evaluation of the pharmacophore models. Afterwards,the component database was screened out by the optimal pharmacophore models of PAR1,P2 Y12 and GP Ⅱ b/Ⅲ a,and the molecular docking method was used to further refine the screening results. The screening results indicated that the anti-platelet aggregation effect of Xixian Tongshuan Preparation was correlated with the inhibition of P2 Y12,PAR1 and GPⅡb/Ⅲa expressions with saffower yellower,hirudin and candidin and notoginseng triterpenes,folinic acid,respectively. The material basis and mechanism of anti-platelet aggregation of Xixian Tongshuan Preparation provided a theoretical basis for the clinical use of the preparation and the lead compounds for the development of anti-platelet aggregation drugs.
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Humans , Databases, Pharmaceutical , Drugs, Chinese Herbal , Pharmacology , Molecular Docking Simulation , Platelet Aggregation , Platelet Aggregation Inhibitors , Pharmacology , ThrombosisABSTRACT
Nine alkaloids and two phenolic glycosides were isolated from EtOH extract of the whole plants of Corydalis hendersonii by various chromatographic techniques including silica gel, ODS, Sephadex LH-20, and semi-preparative HPLC. Their structures were identified as groenlandicine (1), berberine (2), protopine (3), cryptopine (4), N-trans-feruloyloctopamine(5), 3-(4-hydroxy-3-methoxyphenyl)-N-[2-(4-hydroxyphenyl)-2-methoxyethyl] acrylamide (6), N-cis-p-coumaroyloctopamine (7), N-trans-p-coumaroylnoradrenline (8),N-cis-feruloyloctopamine (9), apocynin (10), and glucoacetosyringone (11) by the spectroscopic data analysis and comparison with those in the literature. Among them, compounds 10 and 11 were isolated from this genus for the first time, and 1, 2, and 5-9 were isolated from the species for the first time. All isolates were tested for their protection for in vitro PC12 cell line and antiplatelet aggregation activity. The results showed that compounds 5 and 7 displayed protective effects at a concentration of 10 μmol·L⁻¹, and compound 2 showed antiplatelet aggregation activity induced by THR, ADP, and AA, and compound 3 exhibted inhibitory effect induced by THR.
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Twenty phenylpropenamide analogs with structural novelty were designed and synthesized upon pharmacophore-combination strategy. The structures of target compounds were elucidated by IR, 1H NMR, 13C NMR and MS, and all the target compounds were biologically evaluated for the inhibitory activities of platelet aggregation induced by adenosine diphoshate (ADP) and (AA) arachidonic acid via Bron method. As a result, compounds 6b, 9b, 9d and 9h demonstrated potent inhibitory activity against platelet aggregation induced by AA. Meanwhile, compounds 6b, 6d, 6j, 9b and 9g exhibited significant suppression of platelet aggregation induced by ADP.
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To explore the active substance of antiplatelet aggregation of Polygoni Multiflori Radix by using chemical fingerprints and antiplatelet aggregation bioactivity test for spectrum-effect correlation analysis. The Polygoni Multiflori Radix was tested by antiplatelet aggregation in vitro, and the results showed that 50% aqueous ethanol extract of Polygoni Multiflori Radix had more potent antiplatelet aggregation effect than 10% or 90% aqueous ethanol extract, and ultrasonic extraction was superior to refluxing extraction in the aspect of antiplatelet aggregation. The antiplatelet aggregation bioactivity of the different Polygoni Multiflori Radix extracts was evaluated and the results showed that the inhibition rate was 32.03%-74.56%. Spectrum-effect correlation analysis indicated that trans-stilbene glucoside, cis-stilbene glucoside and catechinic acid had higher correlation coefficient and they were 0.963 (P<0.01), 0.902 (P<0.01) and 0.656 (P<0.05) respectively; furthermore, all of the above three compounds demonstrated significant antiplatelet aggregation bioactivities. Considering their content difference in Polygoni Multiflori Radix, we calculated the relative active contributions, and the results suggested that trans-stilbene glucoside was the main active substance of Polygoni Multiflori Radix in the aspect of antiplatelet aggregation in vitro.
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Objective To observe the inhibition of piperlongumine in vitro on platelet aggregation and blood coagulation tests for children,to provide the experimental basis for clinical medication.Methods Venous blood samples from 30 children were randomly devided into 5 groups,and was centrifuge to separate platelet-rich plasma (PRP).After storing in 37 ℃ thermostat water bath for 5 minutes,the PRP which have been added DMSO as blank group,and added Aspirin (10 μmol/L)as control group,and added PL (20 μmol/L),PL(100 μmol/L),PL(200 μmol/L) as different concentrations of PL groups respectively,were induced by the addition of adenosine diphosphate (10 μmol/L),collagen(2.5 μg/mL) and the arachidonic acid(500 μg/mL).Then the platelet aggregation rate of the PRP from 5 groups could be measured by turbidimetry.Blood plasma isolated from venous blood was divided into 5 groups.In the PL groups,blood plasma were mixed up with PRP concentrations of which were 5,10,20 μmol/L.In the bland group,blood plasma were mixed up with DMSO (1％).In the control group,blood plasma were mixed up with heparin sodium(35 U/mL).After storing in 37 ℃ thermostat water bath for 5 minutes,fibrinogen(FIB),prothrombin time(PT),thrombin time(TT) and activated partial thromboplastin time of different groups were detected.Results Compared to the control group,the groups which were add PL with different concentrations (20,100,200 μmol/L) showed significant inhibition on platelet aggregation induced by AA and collagen(P<0.05).PL with concentrations of 100 μmol/L and 200 μmol/L showed significant inhibition on platelet aggregation induced by ADP(P<0.05).The PT,APTT,TT of blood plasma from children had been significantly prolonged by the intervention of PL 10 μmol/L and PL 20 μmol/L(P<0.05),however,no significant change of FIB was observed.Conclusion There are inhibitory effects of PL on platelet aggregation of blood plasma from children and anticoagulant activity in this study.
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OBJECTIVE:To compare the preventive effects and safety of aspirin and clopodogrel respectively used for vascular restenosis after coronary intimal striping with coronary artery bypass grafting. METHODS:110 patients with coronary atherosclerot-ic heart disease were divided into aspirin group (55 cases) and clopodogrel group (55 cases). All patients intravenously mi-cro-pumped Nitroglycerin injection 10 mg+5% Glucose injection totally 20 mL for maintaining 48-72 h after coronary intimal strip-ing with coronary artery bypass grafting,intravenously pumped Dopamine hydrochloride injection 1-5 μg/kg if necessary. Unplug the endotracheal tube after surgery,patients received Cefuroxime sodium for injection 1.5 g adding into Sterile water for injection 50 mL,intravenous injection,3 times a day,for 2-3 d. Meanwhile,patients were orally given Rosuvastatin calcium tablet 10 mg 30 min after daily dinner,8-week was a course,for 3 courses. Based on it,aspirin group received Aspirin enteric-coated tablet with initial dose of 300 mg,once a day,orally taking 100 mg from the second day,once a day,for 6 months;clopodogrel group received Clopidogrel hydrogen sulfate tablet with initial dose of 300 mg,once a day,orally taking 75 mg from the second day, once a day,for 6 months. Graft patency rate,and platelet aggregation rate,platelet aggregation compliance rate,fibrinogen(Fg), D-dimer (D-D),platelet count (PLT),tissue-type plasminogen activator (t-PA) before and after treatment,and the incidence of adverse reactions in 2 groups were observed. RESULTS:There were no significant differences in the graft patency rate and inci-dence of adverse reactions in 2 groups (P>0.05). Before treatment,there were no significant differences in platelet aggregation rate,platelet aggregation compliance rate,Fg,D-D,PLT and t-PA in 2 groups (P>0.05). After treatment,platelet aggregation rate,Fg and D-D level in 2 groups were significantly lower than before,platelet aggregation compliance rate,PLT and t-PA level were significantly higher than before,with statistical significance(P0.05). CONCLUSIONS:Based on conventional treatment,both aspirin and clopidogrel used for coronary intimal strip-ing with coronary artery bypass grafting can inhibit platelet aggregation,reduce thrombosis,maintain vascular patency and prevent vascular restenosis,with good safety.
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Objective To evaluate the anti-platelet aggregation effect of ergosterol in vitro and explore the preliminary mechanism. Methods The anti-platelet aggregation activity of ergosterol was assessed in vitro on rabbit platelet aggregation. Different inducers, ADP ( 4 μmol?L-1 ) , collagen ( 4 μg?mL-1 ) , arachidonic acid ( AA, 1 mmol?L-1 ) and thrombin (0.5 U?mL-1), and blockers (ozagrel, dipyridamole, clopidogrel and aspirin) were applied to observe the potential targets of ergosterol, platelet aggregation induced by ADP (0, 1, 2, 4, 6μmol?L-1) or fibrinogen (0, 1, 2, 4, 6, 10 mg?mL-1). Results Ergosterol exhibited an obvious anti-platelet aggregation effect in vitro with IC50 values on different inducers ( ADP, collagen, AA and thrombin) of (19.3±0.8), (23.4±1.2), (26.7±0.7), (32.9±1.5) μmol?L-1, respectively. Conclusion Ergosterol can significantly inhibit aggregation and activation of platelet. It provides experimental basis for full exploration of ergosterol and development of novel anti-platelet aggregation drugs.
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Objective To evaluate the anti-platelet aggregation effect of ergosterol in vitro and explore the preliminary mechanism. Methods The anti-platelet aggregation activity of ergosterol was assessed in vitro on rabbit platelet aggregation. Different inducers, ADP ( 4 μmol?L-1 ) , collagen ( 4 μg?mL-1 ) , arachidonic acid ( AA, 1 mmol?L-1 ) and thrombin (0.5 U?mL-1), and blockers (ozagrel, dipyridamole, clopidogrel and aspirin) were applied to observe the potential targets of ergosterol, platelet aggregation induced by ADP (0, 1, 2, 4, 6μmol?L-1) or fibrinogen (0, 1, 2, 4, 6, 10 mg?mL-1). Results Ergosterol exhibited an obvious anti-platelet aggregation effect in vitro with IC50 values on different inducers ( ADP, collagen, AA and thrombin) of (19.3±0.8), (23.4±1.2), (26.7±0.7), (32.9±1.5) μmol?L-1, respectively. Conclusion Ergosterol can significantly inhibit aggregation and activation of platelet. It provides experimental basis for full exploration of ergosterol and development of novel anti-platelet aggregation drugs.
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Six novel ligustrazine chalcone aromatic oxygen alkyl acids compounds and two pyridine chalcone aromatic oxygen alkyl acids ester compounds were synthesized according to the traditional Chinese medicine theory removing blood stasis. The structures of target compounds were identified by IR, NMR and ESI-MS. The inhibitory activities of platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid (AA) were measured by the liver microsomal incubation method in vitro. Hypolipidemic activities of compounds were tested in vivo for better inhibitory activities of platelet aggregation. Preliminary pharmacological results showed that compounds 7c, 8a and 11a had potent inhibitory activity against platelet aggregation induced by AA, compounds 7c, 7d, 8a and 11b showed significant inhibitory activity against platelet aggregation induced by ADP. Compounds 7c and 8a exhibited good hypolipidemic activities in high-fat-diet (HFD) induced hyperlipidemia C57/BL6 mice and worthy for further investigation.
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Objective To analysis of clinical symptoms and influencing factors of anti-platelet aggregation drugs in patients with upper gastrointestinal bleeding.Methods Using the research methods of retrospective analysis, collected 110 cases of gastrointestinal bleeding patients from June 2012 to June 2015 into the first affiliated hospital of xiamen university,and divided into two groups,the control group,79 patients were treated without antiplatelet aggregation drugs,the experimental group,31 patients were treated with single antiplatelet aggregation drug.observed the degree of gastrointestinal bleeding,the mode of bleeding, and the characteristics of endoscopic findings between two groups,according to the age,INR, and the type of drug taken, the clinical symptoms and influencing factors of the patients were analyzed further.Results The rate of gastrointestinal bleeding was significantly higher in the experimental group than in the control group(P3 had a significantly higher rate of gastrointestinal bleeding than patients with INR<3.Conclusion Anti-platelet aggregation drugs can significantly increase the chance of serious bleeding in the digestive tract,the patient's age, INR value and the type of medication can affect the incidence of gastrointestinal bleeding;long-term use of these drugs lead the most serious impact on the duodenum, can lead to the site intestinal mucosa damage,with the increasing age of patients,adverse reactions of the digestive tract increased.
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This study was aimed to search anti-platelet aggregation effectors from Gardenia jasminoides extract with the employment of platelet affinity extraction method coupled with HPLC, in order to provide pharmacological experi-mental evidences of the selected effectors to verify its feasibility. Under physiological conditions, washed rat platelets were added into G. jasminoides extract and then a mixture was gained. Consequently, some components from G. jas-minoides extract were combined to the platelets in the mixture while some were not owing to their special chemical structures and properties. Firstly, the uncombined components were washed off from the mixture. Secondly, the com-bined components in the leftover was washed down and collected, respectively, right after destroying the occupied platelets' structures. Thirdly, different collected eluents were analyzed, respectively, by HPLC established in the pre-vious work to search the effectors. Fourthly, pharmacological experiments were implemented for confirmation. The re-sults showed that dominant effective components from G. jasminoides extract acting on anti-platelet aggregation were identified as geniposide. Further evident was provided as well by pharmacological experiment that geniposide exhibit-ed significant inhibitory effect on anti-platelet aggregation in rats induced by ADP, rat tail collagen and thrombin(P< 0.01). It was concluded that the platelet affinity extraction-HPLC method proposed in this paper can be utilized to analyze the correlation of effectors from G. jasminoides extract and its pharmacological effects. Moreover, there are some correlations between screened chemical substances and their pharmacological effects.
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Objective: To find the new type of structures with protease activated receptor 1 (PAR-1) inhibition from plant ingredients. Methods: Thirty ingredients were docked into PAR-1, and then, docking score, occupied space, hydrogen bonding, and other indicators were used for virtual screening. In vitro platelet aggregation experiments in guinea pig were performed to screen the activities of all ingredients. Results: Virtual screening suggested that T30 and T21 had the prospects to inhibit PAR-1. Experiment screening showed that T21, T5, T28, and T29 have the real inhibitory effects on PAR-1. Combination analyses of virtual and experimental screening suggested the following results. Residue 258 and area III had the key effects. Hydrogen matching was required at area II. Area IV and V regions mainly need hydrophobic match. The hydrogen bonding played an important role in improving the activity. Conclusion: According to the binding mode of control drug, T21 is found. To examine the binding mode of T5, T28, and T29, their experimental activities suggest a novel action mode which provides a new direction to find the PAR-1 antagonist.
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@#The latest literatures showed that the anti-platelet aggregation drugs had a good application in cardiovascular disease, however still with hemorrhage side effects and some new drugs' mechanism was unknown. So further investigations on the mechanism of anti-platelet aggregation are necessary to discover a new type of anti-platelet drugs, such as antagonists of the EP3 receptor.