AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation Science
Platelet Aggregation InhibitorsPlatelet AggregationCrotalid VenomsSalivary Proteins and PeptidesDisintegrinsSalivary GlandsBlood PlateletsAmino Acid SequenceMolecular Sequence DataCongo RedPlatelet AdhesivenessPlatelet CountAmyloid beta-PeptidesPlatelet Membrane GlycoproteinsAdenosine DiphosphatePeptide FragmentsPlatelet Function TestsPlatelet Glycoprotein GPIIb-IIIa ComplexBleeding TimeThrombinCell AggregationPeptidesFibrinogenThromboxane A2Platelet ActivationPlatelet Factor 4Platelet Activating FactorPlatelet Glycoprotein GPIb-IX ComplexAspirinCollagenThrombosisReceptors, Purinergic P2Y12Thromboxane B2Platelet TransfusionRistocetinApyrasevon Willebrand FactorP-SelectinSerotoninBlood CoagulationEpoprostenolThromboxanesBlood Platelet DisordersThrombocytopeniaAntigens, Human Platelet15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidErythrocyte AggregationHemostasisProstaglandin Endoperoxides, SyntheticEpinephrineTiclopidineThrombastheniaPlatelet Factor 3Platelet Membrane Glycoprotein IIbMegakaryocytesImmunoglobulin Fab FragmentsReceptors, ThromboxaneArachidonic AcidDose-Response Relationship, DrugRabbitsReceptors, ThrombinArachidonic AcidsCalciumAntibodies, MonoclonalBlood Coagulation FactorsReceptors, Thromboxane A2, Prostaglandin H2HemorheologyReceptors, Purinergic P2Y1KineticsBlood Coagulation TestsPurinergic P2Y Receptor AntagonistsOligopeptidesDual Specificity Phosphatase 2Protein BindingThromboxane-A SynthasePlatelet-Rich PlasmaCarotid Artery ThrombosisHydrazines
Platelet Aggregation Inhibitors: Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Crotalid Venoms: Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.Salivary Proteins and Peptides: Proteins and peptides found in SALIVA and the SALIVARY GLANDS. Some salivary proteins such as ALPHA-AMYLASES are enzymes, but their composition varies in different individuals.Disintegrins: A family of polypeptides purified from snake venoms, which contain the arginine-glycine-aspartic acid (RGD) sequence. The RGD tripeptide binds to integrin receptors and thus competitively inhibits normal integrin-ligand interactions. Disintegrins thus block adhesive functions and act as platelet aggregation inhibitors.Salivary Glands: Glands that secrete SALIVA in the MOUTH. There are three pairs of salivary glands (PAROTID GLAND; SUBLINGUAL GLAND; SUBMANDIBULAR GLAND).Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Congo Red: An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.Platelet Adhesiveness: The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.Platelet Count: The number of PLATELETS per unit volume in a sample of venous BLOOD.Amyloid beta-Peptides: Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.Platelet Membrane Glycoproteins: Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Platelet Function Tests: Laboratory examination used to monitor and evaluate platelet function in a patient's blood.Platelet Glycoprotein GPIIb-IIIa Complex: Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.Thrombin: An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.Cell Aggregation: The phenomenon by which dissociated cells intermixed in vitro tend to group themselves with cells of their own type.Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.Thromboxane A2: An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).Platelet Activation: A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.Platelet Factor 4: A CXC chemokine that is found in the alpha granules of PLATELETS. The protein has a molecular size of 7800 kDa and can occur as a monomer, a dimer or a tetramer depending upon its concentration in solution. Platelet factor 4 has a high affinity for HEPARIN and is often found complexed with GLYCOPROTEINS such as PROTEIN C.Platelet Activating Factor: A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.Platelet Glycoprotein GPIb-IX Complex: Platelet membrane glycoprotein complex essential for normal platelet adhesion and clot formation at sites of vascular injury. It is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX. Glycoprotein Ib functions as a receptor for von Willebrand factor and for thrombin. Congenital deficiency of the GPIb-IX complex results in Bernard-Soulier syndrome. The platelet glycoprotein GPV associates with GPIb-IX and is also absent in Bernard-Soulier syndrome.Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Receptors, Purinergic P2Y12: A subclass of purinergic P2Y receptors that have a preference for ADP binding and are coupled to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI. The P2Y12 purinergic receptors are found in PLATELETS where they play an important role regulating PLATELET ACTIVATION.Thromboxane B2: A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).Platelet Transfusion: The transfer of blood platelets from a donor to a recipient or reinfusion to the donor.Ristocetin: An antibiotic mixture of two components, A and B, obtained from Nocardia lurida (or the same substance produced by any other means). It is no longer used clinically because of its toxicity. It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro.Apyrase: A calcium-activated enzyme that catalyzes the hydrolysis of ATP to yield AMP and orthophosphate. It can also act on ADP and other nucleoside triphosphates and diphosphates. EC 3.6.1.5.von Willebrand Factor: A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.P-Selectin: Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Epoprostenol: A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.Blood Platelet Disorders: Disorders caused by abnormalities in platelet count or function.Thrombocytopenia: A subnormal level of BLOOD PLATELETS.Antigens, Human Platelet: Human alloantigens expressed only on platelets, specifically on platelet membrane glycoproteins. These platelet-specific antigens are immunogenic and can result in pathological reactions to transfusion therapy.15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid: A stable prostaglandin endoperoxide analog which serves as a thromboxane mimetic. Its actions include mimicking the hydro-osmotic effect of VASOPRESSIN and activation of TYPE C PHOSPHOLIPASES. (From J Pharmacol Exp Ther 1983;224(1): 108-117; Biochem J 1984;222(1):103-110)Erythrocyte Aggregation: The formation of clumps of RED BLOOD CELLS under low or non-flow conditions, resulting from the attraction forces between the red blood cells. The cells adhere to each other in rouleaux aggregates. Slight mechanical force, such as occurs in the circulation, is enough to disperse these aggregates. Stronger or weaker than normal aggregation may result from a variety of effects in the ERYTHROCYTE MEMBRANE or in BLOOD PLASMA. The degree of aggregation is affected by ERYTHROCYTE DEFORMABILITY, erythrocyte membrane sialylation, masking of negative surface charge by plasma proteins, etc. BLOOD VISCOSITY and the ERYTHROCYTE SEDIMENTATION RATE are affected by the amount of erythrocyte aggregation and are parameters used to measure the aggregation.Hemostasis: The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.Prostaglandin Endoperoxides, Synthetic: Synthetic compounds that are analogs of the naturally occurring prostaglandin endoperoxides and that mimic their pharmacologic and physiologic activities. They are usually more stable than the naturally occurring compounds.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.Thrombasthenia: A congenital bleeding disorder with prolonged bleeding time, absence of aggregation of platelets in response to most agents, especially ADP, and impaired or absent clot retraction. Platelet membranes are deficient in or have a defect in the glycoprotein IIb-IIIa complex (PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX).Platelet Factor 3: A phospholipid from the platelet membrane that contributes to the blood clotting cascade by forming a phospholipid-protein complex (THROMBOPLASTIN) which serves as a cofactor with FACTOR VIIA to activate FACTOR X in the extrinsic pathway of BLOOD COAGULATION.Platelet Membrane Glycoprotein IIb: Platelet membrane glycoprotein IIb is an integrin alpha subunit that heterodimerizes with INTEGRIN BETA3 to form PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX. It is synthesized as a single polypeptide chain which is then postranslationally cleaved and processed into two disulfide-linked subunits of approximately 18 and 110 kDa in size.Megakaryocytes: Very large BONE MARROW CELLS which release mature BLOOD PLATELETS.Immunoglobulin Fab Fragments: Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.Receptors, Thromboxane: Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Receptors, Thrombin: A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.Arachidonic AcidsCalcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Blood Coagulation Factors: Endogenous substances, usually proteins, that are involved in the blood coagulation process.Receptors, Thromboxane A2, Prostaglandin H2: A subclass of eicosanoid receptors that have specificity for THROMBOXANE A2 and PROSTAGLANDIN H2.Hemorheology: The deformation and flow behavior of BLOOD and its elements i.e., PLASMA; ERYTHROCYTES; WHITE BLOOD CELLS; and BLOOD PLATELETS.Receptors, Purinergic P2Y1: A subclass of purinergic P2Y receptors that have a preference for ATP and ADP. The activated P2Y1 receptor signals through the G-PROTEIN-coupled activation of PHOSPHOLIPASE C and mobilization of intracellular CALCIUM.Kinetics: The rate dynamics in chemical or physical systems.Blood Coagulation Tests: Laboratory tests for evaluating the individual's clotting mechanism.Purinergic P2Y Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2Y RECEPTORS. Included under this heading are antagonists for specific P2Y receptor subtypes.Oligopeptides: Peptides composed of between two and twelve amino acids.Dual Specificity Phosphatase 2: A dual specificity phosphatase subtype that plays a role in intracellular signal transduction by inactivating MITOGEN-ACTIVATED PROTEIN KINASES. It has specificity for EXTRACELLULAR SIGNAL-REGULATED MAP KINASES and is primarily localized to the CELL NUCLEUS.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Thromboxane-A Synthase: An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC 5.3.99.5.Platelet-Rich Plasma: A preparation consisting of PLATELETS concentrated in a limited volume of PLASMA. This is used in various surgical tissue regeneration procedures where the GROWTH FACTORS in the platelets enhance wound healing and regeneration.Carotid Artery Thrombosis: Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.Hydrazines

Interleukin-12 is synthesized by mesangial cells and stimulates platelet-activating factor synthesis, cytoskeletal reorganization, and cell shape change. (1/4442)

Preliminary studies indicate the involvement of interleukin (IL)-12 in experimental renal pathology. In the present study, we evaluated whether cultured glomerular mesangial cells are able to produce IL-12 and whether IL-12 may regulate some of their functions, including the cytoskeletal reorganization, the change in cell shape, and the production of platelet-activating factor (PAF). The results obtained indicate that pro-inflammatory stimuli, such as tumor necrosis factor-alpha and bacterial polysaccharides, induce the expression of IL-12 mRNA and the synthesis of the protein by cultured mesangial cells. Moreover, cultured mesangial cells were shown to bind IL-12 and to express the human low-affinity IL-12 beta1-chain receptor. When challenged with IL-12, mesangial cells produced PAF in a dose- and time-dependent manner and superoxide anions. No production of tumor necrosis factor-alpha and IL-8 was observed. Moreover, we demonstrate that IL-12 induced a delayed and sustained shape change of mesangial cells that reached its maximum between 90 and 120 minutes of incubation. The changes in cell shape occurred concomitantly with cytoskeletal rearrangements and may be consistent with cell contraction. As IL-12-dependent shape change of mesangial cells was concomitant with the synthesis of PAF, which is known to promote mesangial cell contraction, we investigated the role of PAF using two chemically different PAF receptor antagonists. Both antagonists inhibited almost completely the cell shape change induced by IL-12, whereas they were ineffective on angiotensin-II-induced cell shape change. In conclusion, our results suggest that mesangial cells can either produce IL-12 or be stimulated by this cytokine to synthesize PAF and to undergo shape changes compatible with cell contraction.  (+info)

The mechanism of the increasing action of TA-993, a new 1,5- benzothiazepine derivative, on limb blood flow in anesthetized dogs: selective suppression of sympathetic nerve activity. (2/4442)

TA-993, (-)-cis-3-acetoxy-5-(2-(dimethylamino)ethyl)-2, 3-di-hydro-8-methyl-2-(4-methylphenyl)-1,5-benzothiazepin-4(5H)one maleate, a new 1,5-benzothiazepine derivative with l-cis configuration, has a unique and selective increasing action on limb blood flow with little influence on arterial pressure besides an antiplatelet action. We studied the mechanism of increasing action of TA-993 on limb blood flow in anesthetized dogs. In a canine blood-perfused hindlimb preparation with a donor dog, TA-993 (100 microg/kg i.v.) did not increase femoral blood flow when administered to the donor dog, but did when administered to a recipient dog. TA-993 did not show the increasing action on femoral blood flow in the presence of hexamethonium or phentolamine, whereas it did in the presence of propranolol or atropine. TA-993 also showed a weak increasing effect on heart rate, which was inhibited by any one of these blockers. TA-993 (300 microg/kg i.v.) did not alter the phenylephrine (1-100 ng/kg i.a.)- or the talipexole (3-100 ng/kg i.a.)-induced increase in perfusion pressure in an autoperfused hindlimb. These results suggest that the increasing action of TA-993 on limb blood flow is mediated by the sympathetic nervous system but that the adrenergic receptors are not likely to be the central point of action of this new agent. There is a possibility that the mechanism of the increasing action on heart rate is different from that of its increasing action on limb blood flow.  (+info)

Labeling of the internal pool of GP IIb-IIIa in platelets by c7E3 Fab fragments (abciximab): flow and endocytic mechanisms contribute to the transport. (3/4442)

Abciximab is a new antiplatelet therapeutic in ischemic cardiovascular disease. The drug, chimeric Fab fragments of a murine monoclonal antibody (MoAb) (c7E3), blocks GP IIb-IIIa function. However, its capacity to reach all receptor pools in platelets is unknown. Electron microscopy and immunogold labeling were used to localize abciximab in platelets of patients receiving the drug for up to 24 hours. Studies on frozen-thin sections showed that c7E3 Fab, in addition to the surface pool, also labeled the surface-connected canalicular system (SCCS) and alpha-granules. Analysis of gold particle distribution showed that intraplatelet labeling was not accumulative and in equilibrium with the surface pool. After short-term incubations of platelets with c7E3 Fab in vitro, gold particles were often seen in lines within thin elements of the SCCS, some of which appeared in contact with alpha-granules. Little labeling was associated with Glanzmann's thrombasthenia platelets, confirming that the channels contained bound and not free c7E3 Fab. Endocytosis of abciximab in clathrin-containing vesicles was visualized by double staining and constitutes an alternative mechanism of transport. The remaining free pool of GP IIb-IIIa was evaluated with the MoAb AP-2; flow cytometry showed it to be about 9% on the surface of nonstimulated platelets but 33% on thrombin-activated platelets. The ability of drugs to block all pools of GP IIb-IIIa and then to be associated with secretion-dependent residual aggregation must be considered when evaluating their efficiency in a clinical context.  (+info)

Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (4/4442)

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (5/4442)

Exogenously hypercholesterolemic (ExHC) rats were fed on an atherogenic diet supplemented with 1% each of either ethyl ester docosahexaenoic acid [EE-DHA, 22:6(n-3)], ethyl ester eicosapentaenoic acid [EE-EPA, 20:5(n-3)] or safflower oil (SO) for 6 months. The rats fed on the diets containing EE-EPA or EE-DHA, compared with those fed on SO, had lower serum cholesterol and triacylglycerol levels, less aggregation of platelets and slower progress of intimal thickening in the ascending aorta. Relative to the SO-fed rats, both of the (n-3) fatty acid-fed rats had a significantly reduced proportion of arachidonic acid in the platelet and aortic phospholipids, and lower production of thromboxane A2 by platelets and of prostacyclin by the aorta. These results suggest that EPA and DHA are similarly involved in preventing atherosclerosis development by reducing hypercholesterolemia and modifying the platelet functions.  (+info)

Predominant inhibition of ganodermic acid S on the thromboxane A2-dependent pathway in human platelets response to collagen. (6/4442)

Ganodermic acid S (GAS), a membrane acting agent, exerts multiple effects on human platelet function (C.N. Wang et al. (1991) Biochem. J. 277, 189-197). The study reported how GAS affected the response of human gel-filtered platelets (GFP) to collagen. The agent inhibited cell aggregation by prolonging lag and shape change periods and decreasing the initial cell aggregation rate. However, the inhibitory efficiency was less than its inhibition on GFP response to U46619, a thromboxane (TX) A2 mimetic. In the agent-effect on biochemical events, GAS effectively inhibited Ca2+ mobilization, phosphorylation of myosin light chain, dense granule secretion and TXB2 generation. The inhibitions might originate from blocking Ca2+ mobilization of the TXA2-dependent pathway. GAS partially decreased the phosphorylation of most phosphotyrosine proteins from early activation to the integrin alphaIIbbeta3-regulated steps. The agent did not affect the phosphorylation of three proteins at the steps regulated by integrin alphaIIbbeta3. The results suggest that GAS inhibits the collagen response predominantly on the TXA2-dependent signaling, and the tyrosine kinase-dependent pathway in collagen response plays a major role in aggregation.  (+info)

PAF binding to a single receptor in corneal epithelium plasma membrane. (7/4442)

PURPOSE: To study the binding characteristics and the expression of platelet-activating factor receptors (PAF-R) in corneal epithelium to elucidate the site of action of PAF. METHODS: Binding of [3H]PAF was investigated in subcellular fractions of the epithelia of bovine corneas and in membranes from cultured rabbit corneal epithelial cells. Dose-response inhibition curves of [3H]PAF-specific binding were generated using increasing concentrations of several PAF-R antagonists. RNA from rabbit corneal epithelial cells was probed for PAF-R expression by reverse transcription-polymerase chain reaction (RT-PCR) with specifically designed degenerated primers. RESULTS: Scatchard analysis showed a high-affinity binding site in bovine and rabbit corneal epithelium. The dissociation constant (Kd) and the maximum binding sites (Bmax) in a bovine membrane preparation and similar rabbit fraction were 0.77+/-0.03 nM and 180+/-21 femtomoles/mg protein and 4.3 nM and 1.3 picomoles/mg protein, respectively. Specific PAF-binding sites were found in bovine preparations enriched in plasma membranes with a Kd = 69.6 pM and Bmax = 80 femtomoles/mg protein; no specific binding was found in nuclei or microsomal fractions. RT-PCR of rabbit corneal epithelium generated a single product of the predicted size (478 bp). The deduced amino acid sequence of the purified PCR product was 87% homologous to human PAF-R. The hetrazepines BN 50727 and BN 50730 and the PAF structural analogues CV 3988 and CV 6209 competitively inhibited [3H]PAF binding to corneal epithelium with similar potency. WEB 2086 BS was two orders of magnitude less active in antagonizing PAF binding. CONCLUSIONS: Corneal epithelium contains a single population of receptors localized in the plasma membrane. PAF antagonists exert their actions by blocking this PAF-R. The partial sequence deduced in rabbit corneal PAF-R show a higher homology to the human PAF-R.  (+info)

Conformational changes in the A3 domain of von Willebrand factor modulate the interaction of the A1 domain with platelet glycoprotein Ib. (8/4442)

Bitiscetin has recently been shown to induce von Willebrand factor (vWF)-dependent aggregation of fixed platelets (Hamako J, et al, Biochem Biophys Res Commun 226:273, 1996). We have purified bitiscetin from Bitis arietans venom and investigated the mechanism whereby it promotes a form of vWF that is reactive with platelets. In the presence of bitiscetin, vWF binds to platelets in a dose-dependent and saturable manner. The binding of vWF to platelets involves glycoprotein (GP) Ib because it was totally blocked by monoclonal antibody (MoAb) 6D1 directed towards the vWF-binding site of GPIb. The binding also involves the GPIb-binding site of vWF located on the A1 domain because it was inhibited by MoAb to vWF whose epitopes are within this domain and that block binding of vWF to platelets induced by ristocetin or botrocetin. However, in contrast to ristocetin or botrocetin, the binding site of bitiscetin does not reside within the A1 domain but within the A3 domain of vWF. Thus, among a series of vWF fragments, 125I-bitiscetin only binds to those that overlap the A3 domain, ie, SpIII (amino acid [aa] 1-1365), SpI (aa 911-1365), and rvWF-A3 domain (aa 920-1111). It does not bind to SpII corresponding to the C-terminal part of vWF subunit (aa 1366-2050) nor to the 39/34/kD dispase species (aa 480-718) or T116 (aa 449-728) overlapping the A1 domain. In addition, bitiscetin that does not bind to DeltaA3-rvWF (deleted between aa 910-1113) has no binding site ouside the A3 domain. The localization of the binding site of bitiscetin within the A3 domain was further supported by showing that MoAb to vWF, which are specific for this domain and block the interaction between vWF and collagen, are potent inhibitors of the binding of bitiscetin to vWF and consequently of the bitiscetin-induced binding of vWF to platelets. Thus, our data support the hypothesis that an interaction between the A1 and A3 domains exists that may play a role in the function of vWF by regulating the ability of the A1 domain to bind to platelet GPIb.  (+info)

Dual anti-platelet therapy for secondary stroke prevention: risks outweigh potential benefitsDual anti-platelet therapy for secondary stroke prevention: risks outweigh potential benefits
In SPS3 Trial dual anti-platelet therapy compared to aspirin alone exhibited no benefit and significant evidence of harm including risk of hemorrhage of 2.1% for dual anti-platelet therapy compared to 1.1% for aspirin alone and the dual anti-platelet therapy group also showed higher rates of mortality
Lack of clopidogrel pretreatment effect on the relative efficacy of bivalirudin with provisional glycoprotein IIb/IIIa blockade...Lack of clopidogrel pretreatment effect on the relative efficacy of bivalirudin with provisional glycoprotein IIb/IIIa blockade...
The REPLACE-2 trial validated bivalirudin plus provisional GP IIb/IIIa blockade as an alternative anticoagulant regimen to heparin plus planned GP IIb/IIIa blockade during urgent or elective PCI. This substudy of the REPLACE-2 trial focused on the role of clopidogrel pretreatment with both these treatment strategies. Although administration of clopidogrel before PCI was associated with a trend toward lower rates of periprocedural ischemic events for patients who received either bivalirudin or heparin plus GP IIb/IIIa blockade, bivalirudin with provisional GP IIb/IIIa blockade was noninferior to heparin plus planned GP IIb/IIIa blockade in all subgroups irrespective of pretreatment or the duration of pretreatment. Moreover, there was no evidence that clopidogrel pretreatment attenuated the reduction in bleeding complications by bivalirudin. Therefore, clopidogrel pretreatment appears to improve clinical outcomes without compromising safety, but is not required for bivalirudin to achieve efficacy ...
Letter by Lin et al Regarding Article, Triple Versus Dual Antiplatelet Therapy in Patients With Acute ST-Segment Elevation...Letter by Lin et al Regarding Article, "Triple Versus Dual Antiplatelet Therapy in Patients With Acute ST-Segment Elevation...
To the Editor:. We read with interest the work by Chen et al,1 which reported that triple antiplatelet therapy seems to be superior to dual antiplatelet therapy in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention with drug-eluting stents. Chen et al1 reported the mortality benefits of triple antiplatelet therapy obtained mainly within 30 days after STEMI, reflecting the importance of the addition of cilostazol to aspirin and clopidogrel before stenting. Meanwhile, the authors pointed out the limitation of the nonrandomized trial, that several baseline differences were present between the groups. In our opinion, the advantage of the short-term outcome of triple therapy should be emphasized in higher-risk patients with STEMI undergoing primary percutaneous coronary intervention regardless of whether cilostazol or abciximab was selected.. Because glycoprotein IIb/IIIa inhibitors (abciximab) as adjunctive pharmacological therapy ...
Abstract 15246: Duration of Dual Anti-platelet Therapy after Drug-Eluting Stent Implantation in Patients with Acute Myocardial...Abstract 15246: Duration of Dual Anti-platelet Therapy after Drug-Eluting Stent Implantation in Patients with Acute Myocardial...
Background: The potential benefits and risks of the use of dual anti-platelet therapy (DAT) beyond 12 months in patients receiving drug-eluting stents (DES) with acute myocardial infarction (AMI) have not been clearly established.. Methods: We analyzed 795 patients who had undergone DES implantation with AMI and had been free of major adverse cardiac or cerebrovascular events at least for 12 months in prospective multi-center registry (Infarct Prognosis Study). The duration of DAT was categorized in group 1 (N=185): ≤ 12 months and group 2 (N=610): , 12 months. The incidence of cardiac death or recurrent MI was compared between 2 groups.. Results: The median duration of follow up was 28.4 months. The Kaplan Meier analysis indicated a benefit of group 2 compared with less than group 1. (2.5 % vs. 8.6 %, log rank test p , 0.001). Continuation of DAT beyond 12 months showed the significant reduction of cardiac death or recurrent MI in Cox proportional hazards analysis even after controlling of ...
Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES...Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES...
Participating Centers : 38 french high PCI volume (,700) centers Rationale: Clopidogrel / Prasugrel (75 mg/day), in combination with aspirin (75 mg/day), is currently the antiplatelet treatment of choice for prevention of stent thrombosis, and clinical trials have shown that, in high-risk patients, prolonged dual antiplatelet treatment is more effective than aspirin alone in preventing major cardiovascular events. However, despite the use of clopidogrel, a considerable number of patients continue to have cardiovascular events. Numerous in VITRO studies have shown that individual responsiveness to clopidogrel but also to aspirin is not uniform in all patients and is subject to inter- and intraindividual variability. The recent possibility of bedside monitoring of oral antiplatelet therapy offers the unique opportunity of tailoring antiplatelet therapy. However, the relevance of such strategy has never been evaluated in a randomized prospective adequately powered study having long term follow-up ...
One-month of dual anti-platelet therapy is safe and feasible after stent placementOne-month of dual anti-platelet therapy is safe and feasible after stent placement
A one-month treatment of dual anti-platelet therapy is safe and as effective as a longer duration of therapy at preventing cardiac events in patients one year after stent placement, according to late-breaking research presented today at the American Heart Associations Scientific Sessions 2020.
Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation a randomized, controlled trial<...Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation a randomized, controlled trial<...
TY - JOUR. T1 - Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation a randomized, controlled trial. AU - Lee, Cheol Whan. AU - Ahn, Jung Min. AU - Park, Duk Woo. AU - Kang, Soo Jin. AU - Lee, Seung Whan. AU - Kim, Young Hak. AU - Park, Seong Wook. AU - Han, Seungbong. AU - Lee, Sang Gon. AU - Seong, In Whan. AU - Rha, Seung Woon. AU - Jeong, Myung Ho. AU - Lim, Do Sun. AU - Yoon, Jung Han. AU - Hur, Seung Ho. AU - Choi, Yun Seok. AU - Yang, Joo Young. AU - Lee, Nae Hee. AU - Kim, Hyun Sook. AU - Lee, Bong Ki. AU - Kim, Kee Sik. AU - Lee, Seung Uk. AU - Chae, Jei Keon. AU - Cheong, Sang Sig. AU - Suh, Il Woo. AU - Park, Hun Sik. AU - Nah, Deuk Young. AU - Jeon, Doo Soo. AU - Seung, Ki Bae. AU - Lee, Keun. AU - Jang, Jae Sik. AU - Park, Seung Jung. PY - 2014/1/21. Y1 - 2014/1/21. N2 - Background-The risks and benefits of long-term dual antiplatelet therapy remain unclear. Methods and Results-This prospective, multicenter, open-label, randomized comparison trial was ...
Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and...Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and...
OBJECTIVE: To determine the effects of antiplatelet therapy among patients at high risk of occlusive vascular events. DESIGN: Collaborative meta-analyses (systematic overviews). INCLUSION CRITERIA: Randomised trials of an antiplatelet regimen versus control or of one antiplatelet regimen versus another in high risk patients (with acute or previous vascular disease or some other predisposing condition) from which results were available before September 1997. Trials had to use a method of randomisation that precluded prior knowledge of the next treatment to be allocated and comparisons had to be unconfounded-that is, have study groups that differed only in terms of antiplatelet regimen. STUDIES REVIEWED: 287 studies involving 135 000 patients in comparisons of antiplatelet therapy versus control and 77 000 in comparisons of different antiplatelet regimens. MAIN OUTCOME MEASURE: Serious vascular event: non-fatal myocardial infarction, non-fatal stroke, or vascular death. RESULTS: Overall, among these
Impact of platelet reactivity on 5-year clinical outcomes following percutaneous coronary intervention: a landmark analysis |...Impact of platelet reactivity on 5-year clinical outcomes following percutaneous coronary intervention: a landmark analysis |...
We investigated the impact of suboptimal platelet reactivity on clinical outcomes after percutaneous coronary intervention (PCI). We enrolled 500 patients with stable coronary artery disease...
Antiplatelet Medications | Types of antiplateletsAntiplatelet Medications | Types of antiplatelets
To help prevent this, physicians may prescribe antiplatelets in patients who are at high risk for developing a thrombus within their blood vessels. Antiplatelets are types of anticoagulants - medications used to help prevent the formation of blood clots when no injury has occurred. They work by reducing the platelets stickiness (viscosity). The most common antiplatelet in use today is the over-the-counter drug aspirin, which has been found to prevent platelet binding and clot formation. Today, many physicians place their heart patients on a small daily dose of aspirin (generally 81 milligrams) to prevent the formation of blood clots that may injure the heart. For patients who do not respond to aspirin as a preventive therapy, other antiplatelet medications are available. The most common are clopidogrel and ticlopidine ...
Perioperative management of patients with coronary stent in case of interventions other than cardiac surgery - Part I. -...Perioperative management of patients with coronary stent in case of interventions other than cardiac surgery - Part I. -...
[Percutaneous coronary intervention (PCI) is meant to optimalise cardiac status, that is, short-term and long-term outcomes. It is known from large Western databases that stent implantation is performed in 77-85% of coronary interventions, which means hundreds of thousands of new patients with stent every year. The great majority of these patients has to take platelet aggregation inhibitors, namely acetylsalicylic acid and thienopyridin, most often clopidrogel. It presents a major therapeutic dilemma when these patients require noncardiac surgery. First, surgery should be performed with the least possible blood loss, which would be optimal if the platelet aggregation inhibitor therapy - that is indispensable for a certain period because of the stent - was suspended. Second, stent thrombosis has to be avoided, which can only be achieved if platelet aggregation inhibitor therapy is continued. The aim of our paper is to summarise the current guidelines and the risk estimation on the basis of our current
We Need Further Studies for the Development of Optimized Antiplatelet Therapy Based on Ethnicity | JACC: Journal of the...We Need Further Studies for the Development of "Optimized Antiplatelet Therapy" Based on Ethnicity | JACC: Journal of the...
We read with interest the CILON-T (Influence of Cilostazol-based Triple Antiplatelet Therapy on Ischemic Complication After Drug-Eluting Stent Implantation) trial on the efficacy of cilostazol on ischemic complications after drug-eluting stent (DES) implantation (1), which suggested the potential link between platelet reactivity and ischemic events in Asians.. Asians exhibit poor response to clopidogrel, maybe due to the high prevalence of CYP2C19*2/*3 allele carriage (∼55% to 70%) (1). In the CILON-T study, ,50% of the patients receiving dual antiplatelet therapy had high platelet reactivity based on Western population (P2Y12 reaction units [PRU] ,235). However, similar to other Asian studies, the CILON-T study showed a low ischemic events rate (∼2% during 6 months). In the CILON-T study, patients under the certain PRU (,210) were absent from ischemic events (1). Meanwhile, the GRAVITAS trial demonstrated a different threshold (∼175 PRU), showing the complete immunity against 6-month ...
No Benefit to Prolonged Dual Antiplatelet Therapy After Drug-Eluting Stent Placement - POEMs - American...No Benefit to Prolonged Dual Antiplatelet Therapy After Drug-Eluting Stent Placement - POEMs - American...
Prolonging dual antiplatelet therapy with aspirin plus clopidogrel (Plavix) for more than one year after the placement of a drug-eluting stent confers no clinical benefit.
Development and Validation of a Prediction Rule for Benefit and Harm of Dual Antiplatelet Therapy Beyond 1 Year After...Development and Validation of a Prediction Rule for Benefit and Harm of Dual Antiplatelet Therapy Beyond 1 Year After...
IMPORTANCE: Dual antiplatelet therapy after percutaneous coronary intervention (PCI) reduces ischemia but increases bleeding.. OBJECTIVE: To develop a clinical decision tool to identify patients expected to derive benefit vs harm from continuing thienopyridine beyond 1 year after PCI.. DESIGN, SETTING, AND PARTICIPANTS: Among 11,648 randomized DAPT Study patients from 11 countries (August 2009-May 2014), a prediction rule was derived stratifying patients into groups to distinguish ischemic and bleeding risk 12 to 30 months after PCI. Validation was internal via bootstrap resampling and external among 8136 patients from 36 countries randomized in the PROTECT trial (June 2007-July 2014).. EXPOSURES: Twelve months of open-label thienopyridine plus aspirin, then randomized to 18 months of continued thienopyridine plus aspirin vs placebo plus aspirin.. MAIN OUTCOMES AND MEASURES: Ischemia (myocardial infarction or stent thrombosis) and bleeding (moderate or severe) 12 to 30 months after ...
Is There A LIfe for Drug Eluting Stent (DES) After Discontinuation of Clopidogrel - Full Text View - ClinicalTrials.govIs There A LIfe for Drug Eluting Stent (DES) After Discontinuation of Clopidogrel - Full Text View - ClinicalTrials.gov
The use of drug-eluting stents has resulted in a significant reduction in the restenosis rate and in the need for repeat angioplasty of the stented lesion. However, the occurrence of late stent thrombosis has resulted in an increase in the duration of dual antiplatelet treatment.. According to the guidelines of the ESC, the current recommended duration of dual antiplatelet treatment is 12 months.. A relationship has been demonstrated between the occurrence of late stent thrombosis and aspirin resistance.. Furthermore, dual anti-platelet treatment is associated with an increase in bleeding, the severity of which has been well documented. In addition, the patients involved, and especially those over 70, have significant co-morbidities often requiring extra-cardiac surgery which cannot easily be carried out in patients on dual antiplatelet treatment or clopidogrel.. The objective of this study is to determine whether, after a period of 6 months following Drug eluting stent (DES) implantation in ...
US Multicenter Experience With the Wingspan Stent System for the Treatment of Intracranial Atheromatous Disease: Periprocedural...US Multicenter Experience With the Wingspan Stent System for the Treatment of Intracranial Atheromatous Disease: Periprocedural...
To the Editor:. We read with great interest the recent article published by Fiorella et al who report a multicenter experience with the use of the Wingspan stent system (Boston Scientific) for the treatment of intracranial atherosclerosis.1 This collaborative effort should be applauded, but we would advocate for closer scrutiny to future registry designs in order to enhance our understanding of treatment modalities being used.. A total of 78 patients with 82 lesions were treated with a high technical success rate and a periprocedural complication rate (stroke or death) of 6.1%.1 We would like to bring attention to 3 issues that may help with further study in this area. The first is the patient selection for the registry. Nineteen of the 78 (24%) patients were not on antiplatelet therapy at the time of their stroke or transient ischemic attack. The natural history of patients who were not on antiplatelet therapy is not clear to date; thus, selection of such patients for angioplasty and stenting ...
Global Oral Antiplatelets Sales Industry Professional Survey, Growth, Size, Shares, Forecast, Analysis and Supply Demand to...Global Oral Antiplatelets Sales Industry Professional Survey, Growth, Size, Shares, Forecast, Analysis and Supply Demand to...
Get a Sample of Global Oral Antiplatelets Sales Market Report from- http://www.absolutereports.com/enquiry/request-sample/10374538. Whereas, on the basis of sales, data related to sales volume, sales price, cost, sales income, and profit margin etc. of Global Oral Antiplatelets Sales Market used in different fields, sold in different regions and by different companies is provided in this report.. Regions Covered in Global Oral Antiplatelets Sales Market Report:. • United States. • China. • Europe. • Japan. • Southeast Asia. • India. Have any Query Regarding this Report? Contact us at: http://www.absolutereports.com/enquiry/pre-order-enquiry/10374538. With a purpose of enlightening new entrants about the possibilities in this market, this Global Oral Antiplatelets Sales Market report investigates new project feasibility. A thorough SWOT analysis & investment analysis is provided in the report which forecasts imminent opportunities for the Global Oral Antiplatelets Sales market ...
The Worry About Clopidogrel Nonresponsiveness | JACC: Cardiovascular InterventionsThe Worry About Clopidogrel "Nonresponsiveness" | JACC: Cardiovascular Interventions
Arguably, antiplatelet agents are the most important therapy we administer to stented patients. Antiplatelet agents are given to prevent the most dreaded event that often has catastrophic consequences, coronary thrombosis. It is well established that platelet reactivity to adenosine diphosphate (ADP) mediated by the P2Y12 receptor plays a central role in the development of post-percutaneous coronary intervention (PCI) ischemic events, including stent thrombosis. The active metabolite of clopidogrel blocks this pivotal receptor (1,2). Platelet reactivity to ADP during clopidogrel therapy has been determined by turbidimetric aggregometry, VerifyNow (Accumetrics, San Diego, California) assay, Thrombelastography (TEG, Hemonetics, Braintree, Massachusetts), Multiplate Analyzer (Dynabyte Informationssysteme GmbH, Munich, Germany), and flow cytometry to measure phosphorylated vasodilator stimulated phosphoprotein (VASP Assay, Biocytex, Marseille, France). All of these methods have demonstrated ...
Current developments in dual antiplatelet therapy after stenting - Minerva Cardioangiologica 2014 June;62(3):261-76 - Minerva...Current developments in dual antiplatelet therapy after stenting - Minerva Cardioangiologica 2014 June;62(3):261-76 - Minerva...
Dual antiplatelet therapy (DAPT) with acetylsalicylic acid and an inhibitor of the adenosine diphosphate platelet receptor P2Y12 has been shown to reduce the risk of stent thrombosis (ST), myocardial infarction and cardiac death after percutaneous coronary intervention (PCI) with bare-metal stents (BMS) and drug-eluting stents (DES). However, while there is consensus on 1-month DAPT after BMS, the optimal duration and the risk-benefit ratio of DAPT duration after DES implantation remains controversial. Controversy surrounding this issue is demonstrated by differences in guideline recommendations for DAPT duration after PCI with DES. For example, while the ACC/AHA recommends a minimum of 12 months, ESC guidelines recommend at least 6 months of DAPT. Recent reports suggest that 6 months of DAPT after second-generation DES implantation might be safe compared with longer durations. Large randomized controlled trials powered to examine ST and bleeding events are currently ongoing and will shed novel ...
CO Clopidogrel - Uses, Side Effects, Interactions - Canada.comCO Clopidogrel - Uses, Side Effects, Interactions - Canada.com
CO Clopidogrel: Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by hardening of the arteries) and have already experienced at least one atherothrombotic event such as heart attack, stroke, or diagnosed peripheral arterial disease (problems with blood flow in the arteries). It is also used with ASA (acetylsalicylic acid) by people with acute coronary syndrome or atrial fibrillation (a fast, irregular heartbeat).
ACC/AHA Guideline Update on Duration of Dual Antiplatelet Therapy in CAD Patients - American College of CardiologyACC/AHA Guideline Update on Duration of Dual Antiplatelet Therapy in CAD Patients - American College of Cardiology
In patients with ACS (NSTE-ACS or STEMI) treated with coronary stent implantation who have tolerated DAPT without a bleeding complication and who are not at high bleeding risk (e.g., prior bleeding on DAPT, coagulopathy, oral anticoagulant use), continuation of DAPT (clopidogrel, prasugrel, or ticagrelor) for longer than 12 months may be reasonable (Class IIb). A new risk score (the "DAPT score"), derived from the Dual Antiplatelet Therapy study, may be useful for decisions about whether to continue (prolong or extend) DAPT in patients treated with coronary stent implantation ...
Wiley: Antiplatelet Therapy In Ischemic Heart Disease - Stephen D. WiviottWiley: Antiplatelet Therapy In Ischemic Heart Disease - Stephen D. Wiviott
Part I Concepts in Platelet Physiology, Function and Measurement. 1 Platelet physiology and the role of the platelet in ischemic heart disease.. Robert F. Storey .. 2 Laboratory assessment of platelet function and the effects of antiplatelet agents.. Alan D. Michelson, A.L. Frelinger .. Part II Pharmacology of Oral Antiplatelet Agents.. 3 Cyclooxygenase inhibitors.. Nina Chetty Raju, John W. Eikelboom .. 4 Aspirin response variability and resistance.. Wai-Hong Chen, Daniel I. Simon .. 5 P2Y12 inhibitors: Thienopyridines and direct oral inhibitors.. Jean-Philippe Collet, Boris Aleil, Christian Gachet, Gilles Montalescot .. 6 Thienopyridine response variability and resistance.. Udaya S. Tantry, Thomas A. Suarez, Paul A. Gurbel .. Part III Pharmacology of Intravenous Antiplatelet Agents.. 7 Pharmacology of intravenous glycoprotein IIb/IIIa antagonists.. James C. Blankenship, Peter B. Berger .. 8 Intravenous P2Y12 inhibitors.. Steven P. Dunn, Steven R. Steinhubl .. 9 Antiplatelet effects of thrombin ...
Altmetric - Prevalence and predictors of dual antiplatelet therapy prolongation beyond one year in patients with acute coronary...Altmetric - Prevalence and predictors of dual antiplatelet therapy prolongation beyond one year in patients with acute coronary...
There are limited real-world data on prevalence and predictors of dual antiplatelet therapy (DAPT) prolongation beyond one year after acute coronary syndrome (ACS). We have explored such issue in the START ANTIPLATELET Registry, which is a prospective, observational, multicenter, Italian registry performed in seven Italian cardiology institutions including patients admitted for ACS and followed up to one year. Out of a total population of 840 ACS patients, 596 patients had completed 12-month follow-up being on DAPT. Decision to prolong DAPT beyond one year was taken in 79 patients (13%), whereas in 517 patients DAPT was stopped. The strongest predictors of DAPT continuation were a new cardiovascular events after the index admission event (OR 3.3, 95% CI 1.4-7.7), no bleeding complications (OR 3.2, 95% CI 1.2-8.3) and no anemia during one-year follow-up (OR 2.6, 95% CI 1.1-5.9); other independent predictors were renal failure (OR 2.5, 95% CI 1.3-5.0) and peripheral artery disease (OR 1.8, 95% CI ...
Dual Antiplatelet Therapy | Clark Medical IllustrationDual Antiplatelet Therapy | Clark Medical Illustration
Journal cover image about duration of dual anti platelet therapy following angioplasty. Antiplatelet medicines work to keep platelets from sticking together and forming blood clots. There have been many recent studies debating whether shorter or longer courses of dual antiplatelet therapy are better for patients undergoing percutaneous coronary intervention.
Rivaroxaban plus aspirin, compared with aspirin alone, reduced cardiovascular events in patients with stable peripheral or...Rivaroxaban plus aspirin, compared with aspirin alone, reduced cardiovascular events in patients with stable peripheral or...
People with peripheral vascular disease are at high risk of vascular events and major adverse limb events. Use of antiplatelet therapy is effective at reducing this risk. Other antithrombotic strategies that have been tested, such as use of anticoagulation, dual antiplatelet therapy or novel antiplatelet agents, have not been found to be superior to single antiplatelet therapy. The new oral factor Xa inhibitors such as rivaroxaban have been shown to be at least as effective as vitamin K antagonists in preventing thromboembolic events in atrial fibrillation,1 and offer a potential alternative strategy, either in addition to, or instead of, a single antiplatelet agent. ...
Clinical Trials Registry | Internet Stroke CenterClinical Trials Registry | Internet Stroke Center
Clopidogrel has anti-platelet activity by irreversible inhibition of the P2Y12 platelet receptor. Clopidogrel must be converted into an active metabolite in order to show anti-platelet activity. Hepatic CYP2C19 enzyme is one of the key hepatic enzymes which convert clopidogrel into active metabolite and its genetic polymorphism is related to clopidogrel resistance. CYP2C19 poor or intermediate metabolizer groups show reduced anti-platelet activity of clopidogrel compared to extensive metabolizer group ...
Personalized antiplatelet treatment improves outcome... ( The findings were presented by Dr Jo...)Personalized antiplatelet treatment improves outcome... ( The findings were presented by Dr Jo...)
Health, ...The findings were presented by Dr Jolanta Siller-Matula from Medical U...Standard antiplatelet treatment in patients undergoing percutaneous co...But measurements of platelet aggregation in clopidogrel treated patien...Personalized antiplatelet treatment involves choosing a therapy base...,Personalized,antiplatelet,treatment,improves,outcome,after,PCI,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
Influence of oral antiplatelet therapy on hemorrhagic complications of pacemaker implantation | SpringerLinkInfluence of oral antiplatelet therapy on hemorrhagic complications of pacemaker implantation | SpringerLink
Objective We retrospectively assessed the incidence of hemorrhagic complications associated with pacemaker implantation in patients receiving one or more antiplatelet agents.
NIPPON follow-up: Shorter dual antiplatelet therapy stands the test of time (DAPT) | EurekAlert! Science NewsNIPPON follow-up: Shorter dual antiplatelet therapy stands the test of time (DAPT) | EurekAlert! Science News
Three year follow-up of patients who received dual antiplatelet therapy (DAPT) after placement of a drug-eluting stent (DES) shows that a short course of the therapy continues to be as beneficial as a longer course.
Sandoz Clopidogrel - Uses, Side Effects, Interactions - Drug Factsheets - C-HealthSandoz Clopidogrel - Uses, Side Effects, Interactions - Drug Factsheets - C-Health
Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by
Novel anticoagulants and antiplatelet agents; a guide for the urologist. - NextBio articleNovel anticoagulants and antiplatelet agents; a guide for the urologist. - NextBio article
Novel oral anti-coagulants (NOACs) are increasingly being used in clinical practice and are set to almost entirely replace the vitamin K antagonists, such as warfarin, in the near future. Similarly, new antiplatelet agents are now regularly used in place of older agents, such as aspirin and clopidogrel. In an ageing population, with an increasing burden of complex comorbidities, urologists will frequently encounter patients who will be using such agents. Some background knowledge, and an understanding, of these drugs and the issues that surround their usage, is essential. The present article will provide readers with an understanding of these new drugs, including their mechanisms of action, the up-to-date evidence justifying their recent introduction into clinical practice and the appropriate interval for stopping them before surgery. It will also consider the risks of perioperative bleeding for patients taking these drugs and the risks of venous thromboembolism in those in whom they are ...
Which medications in the drug class Antiplatelet agents are used in the treatment of Systemic Sclerosis?Which medications in the drug class Antiplatelet agents are used in the treatment of Systemic Sclerosis?
Antiplatelet agentsThese agents inhibit the cyclo-oxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.Aspirin (Bayer Buffered Aspirin, Bayer Aspirin, Anacin)... more
Thrombosis Therapy: Focus on Antiplatelet Agents | OMICS InternationalThrombosis Therapy: Focus on Antiplatelet Agents | OMICS International
Platelet adhesion, activation and aggregation to the injured vessel wall are crucially involved in the pathogenesis of thrombus formation. Agents in theory thwarting thes..
What is the difference between anti-platelet drug and anticoagulant? - Answered by top doctors on HealthTapWhat is the difference between anti-platelet drug and anticoagulant? - Answered by top doctors on HealthTap
Dr. Routh responded: Different Actions. Anticoagulants are medicines which keep the blood from clotting by action on factors in the blood which are needed to stop bleeding. Oral examples would include |a href="/topics/warfarin" track_data="{
Jamp-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.comJamp-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.com
Jamp-Clopidogrel: Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by hardening of the arteries) and have already experienced at least one atherothrombotic event such as heart attack, stroke, or have been diagnosed peripheral arterial disease (problems with blood flow in the arteries). It is also used with ASA (acetylsalicylic acid) by people with acute coronary syndrome or atrial fibrillation (a fast, irregular heartbeat) to reduce the risk of heart attack or stroke.
Riva-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.comRiva-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.com
Riva-Clopidogrel: Clopidogrel belongs to the class of medications called platelet aggregation inhibitors or antiplatelets. Clopidogrel is used to help prevent heart attacks, strokes, and other circulation problems in people who have atherosclerosis (narrowed blood vessels caused by hardening of the arteries) and have already experienced at least one atherothrombotic event such as heart attack, stroke, or have been diagnosed peripheral arterial disease (problems with blood flow in the arteries). It is also used with ASA (acetylsalicylic acid) by people with acute coronary syndrome or atrial fibrillation (a fast, irregular heartbeat) to reduce the risk of heart attack or stroke.
Similar papers for Genetic and platelet function testing of antiplatelet therapy for percutaneous coronary intervention: the...Similar papers for Genetic and platelet function testing of antiplatelet therapy for percutaneous coronary intervention: the...
The ARCTIC study randomized 2440 patients scheduled for stent implantation to a strategy of platelet function monitoring with drug adjustment in patients who had a poor response to antiplatelet therapy or to a conventional strategy without monitoring and drug adjustment. No significant improvement in clinical outcomes with platelet function monitoring was observed. The purpose of this study is to assess the relationships between CYP2C19 genotypes, clopidogrel pharmacodynamic response, and clinical outcome. In the ARCTIC-GENE study, 1394 patients were genotyped for loss- and gain-of-function CYP2C19 alleles. Randomization of treatment strategy was well balanced. Slow metabolizers identified as carriers of at least one loss-of-function allele CYP2C19*2 (n = 459) were more likely poor responders at randomization (41.6 vs. 31.6 %, p = 0.0112) and 14 days later (23.8 vs. 10.4 %, p | 0.0001) and more frequently on prasugrel (11.5 vs. 8.1 %, p = 0.039) as compared with rapid metabolizers (n = 935).
Platelet aggregation inhibitor | definition of Platelet aggregation inhibitor by Medical dictionaryPlatelet aggregation inhibitor | definition of Platelet aggregation inhibitor by Medical dictionary
Looking for online definition of Platelet aggregation inhibitor in the Medical Dictionary? Platelet aggregation inhibitor explanation free. What is Platelet aggregation inhibitor? Meaning of Platelet aggregation inhibitor medical term. What does Platelet aggregation inhibitor mean?
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Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban and abciximab, for the prevention of ischemic events...Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban and abciximab, for the prevention of ischemic events...
Comparison of two platelet glycoprotein IIb/IIIa inhibitors, tirofiban and abciximab, for the prevention of ischemic events with percutaneous coronary revascularization
Association between Peak Neutrophil Count, Clopidogrel Loading Dose, and Left Ventricular Systolic Function in Patients with...Association between Peak Neutrophil Count, Clopidogrel Loading Dose, and Left Ventricular Systolic Function in Patients with...
Inflammation plays an important role in plaque development and left ventricular remodeling during acute myocardial infarction (AMI). Clopidogrel may exhibit some anti-inflammatory properties and high loading dose of clopidogrel results in improved clinical outcomes in patients with AMI. 357 patients who received successful primary percutaneous coronary intervention from January 2008 to March 2011 in Peking University Third Hospital were included in this study. Different loading dose of clopidogrel (300 mg, 450 mg, or 600 mg) was given at the discretion of the clinician. Neutrophils reached their peak values on the first day after AMI. Higher levels of peak neutrophil and lower left ventricular ejection fraction (LVEF) were found in patients of low clopidogrel loading dose group (300 mg or 450 mg). After adjusting for the related confounders, a logistic regression model showed that low clopidogrel loading dose remained an independent predictor of low LVEF (LVEF ≤
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Personalized Approaches to Clopidogrel Therapy | StrokePersonalized Approaches to Clopidogrel Therapy | Stroke
PPIs are widely prescribed in conjunction with antiplatelet therapy. Current American Heart Association guidelines recommend that all patients on dual antiplatelet therapy be prescribed a PPI regardless of Helicobacter pylori status or gastrointestinal bleeding risk.20 PPIs are inhibitors of CYP2C19 in vitro, with omeprazole showing more potent inhibition than newer-generation PPIs such as pantoprazole.21 Based on this evidence, several studies have assessed RPA in patients coprescribed clopidogrel and a PPI. For omeprazole, there is a significant increase in RPA in patients prescribed both clopidogrel and a PPI compared with clopidogrel alone.22 The results for other PPIs, particularly pantoprazole, are less clear. One study showed that RPA in ACS patients on clopidogrel and pantoprazole was similar to that of patients on clopidogrel alone,23 suggesting a compound-specific effect.. Despite the evidence that at least some PPIs affect residual platelet function in patients taking clopidogrel, the ...
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Clopidogrel discontinuation and platelet reactivity following coronary by Darren Mylotte, Aaron Peace et al."Clopidogrel discontinuation and platelet reactivity following coronary" by Darren Mylotte, Aaron Peace et al.
Aims: Antiplatelet therapy with aspirin and clopidogrel are recommended for 1 year after drug-eluting stent (DES) implantation or myocardial infarction. However, the discontinuation of antiplatelet therapy has become an important issue as recent studies have suggested a clustering of ischaemic events within 90 days of clopidogrel withdrawal. The objective of this investigation was to explore the hypothesis that there is a transient rebound increase in platelet reactivity within three months of clopidogrel discontinuation. Methods and Results: In this prospective study, platelet function was assessed in patients taking aspirin and clopidogrel for at least 1 year following DES implantation. Platelet aggregation was measured using a modification of light transmission aggregometry in response to multiple concentrations of adenosine diphosphate (ADP), epinephrine, arachidonic acid, thrombin receptor activating peptide and, collagen. Clopidogrel was stopped and platelet function was reassessed 1 week, 1
Recommended Use of Aspirin and Other Antiplatelet Medications Among Adults - National Ambulatory Medical Care Survey and...Recommended Use of Aspirin and Other Antiplatelet Medications Among Adults - National Ambulatory Medical Care Survey and...
The findings provided in this report indicate that prevalence of prescribing aspirin or other antiplatelet medications at outpatient health-care visits is low for patients who have been recommended to receive these medications based on the presence of ischemic vascular disease or certain risk factors. Despite the low prevalence of aspirin prescribing identified in this analysis, other studies using the same data sources have demonstrated that aspirin and other antiplatelet medication prescribing among patients with ischemic vascular disease was only 32.8% in 2003 (16). Previous reports have estimated that for every 10% increase in the use of antiplatelet medication among eligible adults aged 18-79 years, an estimated 8,000 deaths per year would be prevented (21). A 2006 study that ranked clinical preventive services based on cost effectiveness and the clinically preventable burden of disease demonstrated that aspirin prevention counseling was one of three prevention services that received the ...
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Stenting and glycoprotein IIb/IIIa inhibition in patients with acute m by Gilles Montalescot, Frans Van de Werf et al."Stenting and glycoprotein IIb/IIIa inhibition in patients with acute m" by Gilles Montalescot, Frans Van de Werf et al.
Stenting and GP IIb/IIIa inhibition are promising adjunctive therapies in PCI. The Global Registry of Acute Coronary Events (GRACE) is a registry of unselected patients with acute coronary syndromes, allowing for the study of treatments in a real-world environment. Data from GRACE patients with AMI who underwent PCI were analyzed. After adjusting for demographics, baseline characteristics, and previous medications, treatment with GP IIb/IIIa inhibitors and a stent and treatment with a stent alone were significant predictors of survival at 6 months. Stents were used in 90.9% of patients. GP IIb/IIIa inhibitors were used in 59.7%; in most cases they were started after the beginning of the procedure. The in-hospital death rate (7.6%) was highest in patients undergoing urgent PCI. Mortality at 6 months following PCI was 14.4% among patients who received neither GP IIb/IIIa inhibitors nor a stent, compared to patients who received both GP IIb/IIIa inhibitors and a stent (7.3%), GP IIb/IIIa inhibitors alone
Meta-analysis finds benefit for dual antiplatelet therapy but limitations preclude changing standard mono antiplatelet therapy...Meta-analysis finds benefit for dual antiplatelet therapy but limitations preclude changing standard mono antiplatelet therapy...
Current guidelines recommend aspirin, aspirin plus clopidogrel or aspirin plus extended-release dipyridamole for treatment of acute ischaemic stroke (IS) or transient ischaemic attack (TIA) to prevent recurrent stroke, myocardial infarction and cardiovascular death.1 The Clopidogrel in High-risk patients with Acute Non-disabling Cerebrovascular Events (CHANCE) trial randomised 5170 Chinese patients within 24 h after the onset of IS or TIA to clopidogrel plus aspirin versus aspirin plus placebo for 90 days. Clopidogrel plus … ...
Short- Versus Long-Term Duration of Dual Antiplatelet Therapy After Coronary Stenting: A Randomized Multicentre Trial -...Short- Versus Long-Term Duration of Dual Antiplatelet Therapy After Coronary Stenting: A Randomized Multicentre Trial -...
This study found no significant benefit associated with clopidogrel continuation (use of clopidogrel plus aspirin) as compared with clopidogrel discontinuation (use of aspirin alone) after 6 months, in reducing the incidence of death from any cause, myocardial infarction, or cerebrovascular accident at 2 years. On the other hand, 2-year clopidogrel therapy resulted in a significant increase of actionable bleeding episodes, which included events requiring medical or surgical treatment, red blood cell transfusion, and life-threatening events. There seems to be little rationale for continuing dual antiplatelet therapy for more than a year after percutaneous coronary intervention, based on this and other available evidence.. ...
The case for routine genotyping in dual-antiplatelet therapy. - Semantic ScholarThe case for routine genotyping in dual-antiplatelet therapy. - Semantic Scholar
Over 1 million coronary stent procedures are performed annually in the U.S., with dual-antiplatelet therapy, which includes the use of both aspirin and clopidogrel, being a cornerstone in the management of these patients after coronary intervention. Now, recent data have surfaced demonstrating altered active metabolite levels of clopidogrel in patients harboring hepatic cytochrome gene variants. These variants, which have been validated through genome-wide association as the dominant explanation for the marked heterogeneity of clopidogrel response, are linked to a significant increase in the risk for bleeding, stent thrombosis, myocardial infarction, and death. With viable alternatives to clopidogrel now available, including higher clopidogrel maintenance and loading doses, prasugrel, and ticagrelor, clinicians can now effectively guide therapy in those with at-risk gene variants by simple genotyping. Such an individualized approach can potentially prevent tens of thousands of adverse cardiovascular
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Platelet aggregation inhibitors, also known as antiplatelet therapy (APT), are prescribed for the prevention of secondary cardiovascular events (CVE) after endovascular revascularization procedures.- Platelet aggregation inhibitors are not equally effective in all patients. The phenomenon of high residual platelet reactivity despite APT is called high on-treatment platelet reactivity (HTPR); ... read more it bears an increased risk of secondary CVE.- Platelet function tests (PFT) can be used to diagnose HTPR. There are various tests available; of those, light transmission aggregometry (LTA) is considered the gold standard. Some tests are only suitable for determining the effect of a certain category of APT.- Research into the usefulness of PFTs to optimise treatment with APT has not yet produced an unambiguous conclusion.- Currently there is not yet an indication for routine use of PFT in clinical practice. However, for the treatment of certain categories of patients with thromboembolic ...
Use of Contraindicated Antiplatelet Medications in the Setting of Percutaneous Coronary Intervention | Circulation:...Use of Contraindicated Antiplatelet Medications in the Setting of Percutaneous Coronary Intervention | Circulation:...
In this study of 64 294 patients undergoing PCI within the VA, the use of any contraindicated antiplatelet medications was associated with increased bleeding risk. Although the use of contraindicated medications was not significantly associated with risk-adjusted mortality, the point estimates suggested harm. Nearly 20% of patients undergoing PCI had a known contraindication to ≥1 antiplatelet medications, and ,1 in 20 of those patients received a contraindicated medication. In adjusted analyses, use of abciximab in patients with contraindications of thrombocytopenia or previous stroke likely increased the risk of major bleeding.. Although the overall rate of contraindicated mediation use among patients with PCI is low (1.1%), this study highlights the problem of medication errors in the United States. Importantly, these data illustrate that the use of contraindicated antiplatelet medications persist, despite high-profile reports and EMR built-in warnings.3 Medication errors are a major ...
Is Heparin an Acceptable Anticoagulant When Glycoprotein IIb/IIIa Inhibitors Are Not Used? | JACC: Cardiovascular InterventionsIs Heparin an Acceptable Anticoagulant When Glycoprotein IIb/IIIa Inhibitors Are Not Used? | JACC: Cardiovascular Interventions
The relationship between bleeding complications and increased mortality after percutaneous coronary intervention (PCI) has been well documented. Bivalirudin is superior to heparin and glycoprotein (GP) IIb/IIIa inhibitors, mainly due to the lower risk of bleeding but comparable rates of ischemic complications (1-3). Three trials presented at the 2014 American College of Cardiology Scientific Sessions raise questions regarding the superiority of bivalirudin in PCI (4-6).. In the HEAT-PPCI (Unfractionated Heparin Versus Bivalirudin in Primary Percutaneous Coronary Intervention) trial, 1,829 patients from a single center with ST-segment elevation myocardial infarction (STEMI) referred for primary PCI were randomized to heparin (70 U/kg bolus) or bivalirudin, with GP IIb/IIIa inhibitor only used for bail out (15.5% vs. 13.5%, p = NS) (4). The majority of the PCI (,80%) were performed transradially. Nearly all patients (99.6%) were pre-loaded with dual antiplatelet therapy; 60% of patients received ...
Platelet Glycoprotein IIb / IIIa Inhibition and its Clinical Use | Bentham SciencePlatelet Glycoprotein IIb / IIIa Inhibition and its Clinical Use | Bentham Science
Keywords: platelet, IIIa antagonist, abciximab, eptifibatide, tirofiban, lamifiban, thrombocytopenia, angioplasty. Abstract: The activation of platelets and the resultant aggregation have been shown to play important role in the pathogenesis of cardiovascular, cerebrovascular and peripheral vascular diseases and in acute coronary syndromes. Hence platelet adhesion and aggregation have been identified as promising targets for the development of anti-thrombotic drugs. Glycoprotein (GP) IIb / IIIa antagonism exerts a strong anti-platelet effect, because this interference inhibits the final common pathway of platelet aggregation and is not dependent on a single activation pathway. Three GPIIb / IIIa antagonists have been approved by the US Food and Drug administration. They include abciximab (the chimeric monoclonal antibody 7E3 Fab fragment), eptifibatide (the cyclic heptapeptide based on the KGD amino acid sequence) and tirofiban (a nonpeptide tyrosine derivative). In addition, nonpeptide oral ...
Revista Argentina de Cardioangiología IntervencionistaRevista Argentina de Cardioangiología Intervencionista
High residual platelet reactivity (HRPR) on clopidogrel treatement is associated with an increased risk of adverse events after percutaneous coronary intervention (PCI) and the three REsponsiveness to CLopidogrel and Stent Thrombosis (RECLOSE) studies showed this relationship, the futility of a tailored therapy with increasing dose of clopidogrel, and that nonresponsiveness to clopidogrel is a modifiable risk factor.. RECLOSE-1 1,2. This study is based on a cohort of of 804 patients who had successful sirolimus- or paclitaxel-eluting stent implantation. All patients received a loading dose of 600 mg of clopidogrel, and residual platelet reactivity was assessed by light transmittance aggregometry (LAT) using 10 µmol of adenosine diphosphate as agonist. Patients with platelet aggregation by 10 µmol ADP ≥70% were defined as nonresponders. All patients received chronic dual antiplatelet treatment (aspirin 325 mg and clopidogrel 75 mg daily) for 6 months. The primary end point was the incidence ...
Initial platelet activity may predict efficacy after chronic oral glycoprotein IIb/IIIa blockade: should we still consider...Initial platelet activity may predict efficacy after chronic oral glycoprotein IIb/IIIa blockade: should we still consider...
Initial platelet activity may predict efficacy after chronic oral glycoprotein IIb/IIIa blockade: should we still consider uniform treatment regimens?
Platelet glycoprotein IIb/IIIa should be blocked before stenting | The Scientist Magazine®Platelet glycoprotein IIb/IIIa should be blocked before stenting | The Scientist Magazine®
Eptifibatide, a platelet glycoprotein IIb/IIIa inhibitor substantially reduces ischemic complications in coronary stent interventions and could become a routine pre-treatment in stent coronary implantation, concludes a study published in 16 December Lancet (Lancet 2000 356:2037).In a prospective study, Dr James Tcheng and colleagues from Duke University Medical Centre in North Carolina recruited 2064 patients who were undergoing coronary stent implantation. Immediately before the procedure, pati
No More Financial Assistance for Plavix from Bristol-Myers But Are Generics Really the Same?No More Financial Assistance for Plavix from Bristol-Myers But Are Generics Really the Same?
Bristol-Myers Squibb (NYSE: BMY) is no longer offering its $37-a-month Plavix® Co-Pay Discount Card. And some patients are not happy about this. Additionally, according to the companys web site for "Patient Assistance Programs," the company is no longer making this life-saving drug available to patients who cannot afford it. This, of course, has something to do with the fact that brand-name Plavix has gone off patent and generic versions have been available since May 2012. (See our Patient Alert: How to Get the Best Price on New Generic Plavix.) But are the generic versions of clopidogrel really the same?. Plavix (clopidogrel) is a critical component of all drug-eluting stent implantations. One year of Dual AntiPlatelet Therapy or DAPT (aspirin plus clopidogrel or prasugrel or ticagrelor or even the older ticlopidine) is a package deal with drug-eluting stents: you cant have one without the other. Thats why "Financial Assistance for Plavix" has been one of the most popular topics in ...
Glycoprotein iib/iiia antagonists - from bench to practiceGlycoprotein iib/iiia antagonists - from bench to practice
The central role played by the alphaIIb beta3 receptor in platelet aggregation, and hence in platelet thrombosis, has led to the development of a number of parenteral and oral glycoprotein (GP) IIb/IIIa inhibitors for use in cardiovascular disease states, such as acute coronary syndromes and stroke. The predominant effect of these agents is to inhibit platelet aggregation, although studies of alphaIIb beta3 receptor function and various GP IIb/IIIa inhibitors have demonstrated the potential for these agents to produce effects on other aspects of platelet function, in addition to non-platelet effects. Overall, clinical studies have demonstrated an impressive beneficial effect for parenteral agents in reducing ischemic complications following percutaneous intervention, and a more modest beneficial effect in the treatment of patients with acute coronary syndromes. Trials with oral GP IIb/IIIa inhibitors in similar patient populations have demonstrated toxicity, manifested by an increased mortality ...
Risk of early adverse events after Clopidogrel discontinuation in patients undergoing short-term Dual Antiplatelet Therapy: An...Risk of early adverse events after Clopidogrel discontinuation in patients undergoing short-term Dual Antiplatelet Therapy: An...
The study sought to evaluate the presence of a clinically relevant rebound phenomenon after dual antiplatelet therapy discontinuation in randomized trials.
CHAPTER 131 ANTIPLATELET THERAPY | Free Medical TextbookCHAPTER 131 ANTIPLATELET THERAPY | Free Medical Textbook
CHAPTER 131 ANTIPLATELET THERAPY Williams Hematology CHAPTER 131 ANTIPLATELET THERAPY HARVEY J. WEISS Antiplatelet Drugs Aspirin Inhibitors of Thromboxane A2 Synthesis or Binding Prostaglandin I2 and Analogues Dipyridamole Ticlopidine and Clopidogrel Inhibitors of the Platelet GPIIB/IIIA Receptor Other Antiplatelet Agents Antiplatelet Drugs in Clinical Medicine Ischemic Heart Disease Valvular Heart Disease Cerebrovascular Disease Peripheral Vascular…
ASPIRIN AND EXTENDED-RELEASE DIPYRIDAMOLE (capsule) | Top Interaction Warnings | Healthgrades.comASPIRIN AND EXTENDED-RELEASE DIPYRIDAMOLE (capsule) | Top Interaction Warnings | Healthgrades.com
Interactions for ASPIRIN AND EXTENDED-RELEASE DIPYRIDAMOLE (capsule) explain how Aspirin and Extended-Release Dipyridamole works in concert with other medications and substances. This section outlines the advice given to doctors and pharmacists when prescribing and dispensing Aspirin and Extended-Release Dipyridamole
Effect of On-Admission Antiplatelet Treatment on Patients with Cerebral HemorrhageEffect of On-Admission Antiplatelet Treatment on Patients with Cerebral Hemorrhage
Background: Antiplatelet treatment remains the first choice for primary and secondary prevention of vascular diseases; even so, expected benefits may be offset by risk of bleeding, particularly cerebral hemorrhage. The aim of this study was to assess the influence of antiplatelet treatment on clinical outcome at hospital discharge. Materials and Methods: Consecutive patients with first-ever stroke due to a primary intraparenchymal hemorrhage were prospectively identified over a 4-year period (2000â€"2003). Data on hemorrhage location, vascular risk factors, and antiplatelet and anticoagulant treatment were collected. At discharge, outcome was measured using the modified Rankin Scale (disabling stroke ≥3). Patients treated with anticoagulant therapy were excluded from the study. Results: Of 457 consecutive patients with cerebral hemorrhage, 94 (20.5%) had been taking antiplatelet agents. The treated patients (mean age for antiplatelet group 78.9 ± 9.0 years) were older than the ...
Prasugrel as Antiplatelet Therapy in Patients With Acute Coronary Syndromes or Undergoing Percutaneous Coronary InterventionPrasugrel as Antiplatelet Therapy in Patients With Acute Coronary Syndromes or Undergoing Percutaneous Coronary Intervention
The article discusses the therapy for patients with acute coronary syndromes (ACS). It provides information on prasugrel, a new antiplatelet agent which offers an alternative pharmacological treatment and was recently cleared for marketing by the U.S. Food and Drug Administration. It also notes that by inhibiting platelet activation, the thienopyridine antiplatelet agents play a crucial role in the adjunctive treatment of patients with ACS ...
Interactions between heparins, glycoprotein IIb/IIIa antagonists, and coronary intervention. The Global Registry of Acute...Interactions between heparins, glycoprotein IIb/IIIa antagonists, and coronary intervention. The Global Registry of Acute...
Interactions between heparins, glycoprotein IIb/IIIa antagonists, and coronary intervention. The Global Registry of Acute Coronary Events (GRACE).
Download Platelet Glycoprotein Iib Iiia Inhibitors In Cardiovascular Disease (Contemporary Cardiology) 2Nd Edition 2003Download Platelet Glycoprotein Iib Iiia Inhibitors In Cardiovascular Disease (Contemporary Cardiology) 2Nd Edition 2003
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Platelet ADP Receptor AntagonistPlatelet ADP Receptor Antagonist
This page includes the following topics and synonyms: Platelet ADP Receptor Antagonist, Adenosine Receptor Antagonist, P2Y12 Receptor Antagonist, P2Y Receptor Antagonist, P2Y Receptor Inhibitor, Thienopyridine, Clopidogrel, Plavix, Thiophene, Prasugrel, Effient, Brilinta, Ticagrelor.
Discontinuation of low dose aspirin and risk of myocardial infarction: case-control study in UK primary care | The BMJDiscontinuation of low dose aspirin and risk of myocardial infarction: case-control study in UK primary care | The BMJ
A major strength of this study is that use of The Health Improvement Network enabled analysis of an extensive sample that was representative of the UK primary care population and had age and sex distributions similar to those in the national population. Also, the network includes all patients in participating practices who have been diagnosed as having a primary cardiovascular event and prescribed low dose aspirin to prevent a secondary event in primary care, supporting the broad external validity of these findings. Moreover, we observed the increased risk of non-fatal myocardial infarction in patients who were truly non-adherent but not in those who were found to be taking over the counter aspirin, which reinforces the internal validity of this study.. A potential limitation of the study is that use of aspirin might have been misclassified in some cases. For example, the recording of a prescription for low dose aspirin in The Health Improvement Network does not necessarily mean that the patient ...
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Platelet Aggregation InhibitorsPlatelet AggregationCrotalid VenomsSalivary Proteins and PeptidesDisintegrinsSalivary GlandsBlood PlateletsAmino Acid SequenceMolecular Sequence DataCongo RedPlatelet AdhesivenessPlatelet CountAmyloid beta-PeptidesPlatelet Membrane GlycoproteinsAdenosine DiphosphatePeptide FragmentsPlatelet Function TestsPlatelet Glycoprotein GPIIb-IIIa ComplexBleeding TimeThrombinCell AggregationPeptidesFibrinogenThromboxane A2Platelet ActivationPlatelet Factor 4Platelet Activating FactorPlatelet Glycoprotein GPIb-IX ComplexAspirinCollagenThrombosisReceptors, Purinergic P2Y12Thromboxane B2Platelet TransfusionRistocetinApyrasevon Willebrand FactorP-SelectinSerotoninBlood CoagulationEpoprostenolThromboxanesBlood Platelet DisordersThrombocytopeniaAntigens, Human Platelet15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidErythrocyte AggregationHemostasisProstaglandin Endoperoxides, SyntheticEpinephrineTiclopidineThrombastheniaPlatelet Factor 3Platelet Membrane Glycoprotein IIbMegakaryocytesImmunoglobulin Fab FragmentsReceptors, ThromboxaneArachidonic AcidDose-Response Relationship, DrugRabbitsReceptors, ThrombinArachidonic AcidsCalciumAntibodies, MonoclonalBlood Coagulation FactorsReceptors, Thromboxane A2, Prostaglandin H2HemorheologyReceptors, Purinergic P2Y1KineticsBlood Coagulation TestsPurinergic P2Y Receptor AntagonistsOligopeptidesDual Specificity Phosphatase 2Protein BindingThromboxane-A SynthasePlatelet-Rich PlasmaCarotid Artery ThrombosisHydrazines
Novel anticoagulants and antiplatelet agents; a guide for the urologist. - NextBio articleNovel anticoagulants and antiplatelet agents; a guide for the urologist. - NextBio article
Riva-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.comRiva-Clopidogrel - Uses, Side Effects, Interactions - MedBroadcast.com
platelet aggregation inhibitor (CHEBI:50427)platelet aggregation inhibitor (CHEBI:50427)
Platelet Aggregation Inhibitors - DrugBankPlatelet Aggregation Inhibitors - DrugBank
Novel platelet aggregation inhibitor for the treatment and prophylaxis of cardiovascular diseasesNovel platelet aggregation inhibitor for the treatment and prophylaxis of cardiovascular diseases
Platelet aggregation inhibitor | definition of Platelet aggregation inhibitor by Medical dictionaryPlatelet aggregation inhibitor | definition of Platelet aggregation inhibitor by Medical dictionary
Search of: Atrial Fibrillation | Recruiting, Not yet recruiting, Available Studies | Platelet Aggregation Inhibitors - List...Search of: Atrial Fibrillation | Recruiting, Not yet recruiting, Available Studies | 'Platelet Aggregation Inhibitors' - List...
Indications for platelet aggregation inhibitors after venous stentsIndications for platelet aggregation inhibitors after venous stents
Potent inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. A proposal on the nature of...Potent inhibitors of platelet aggregation based upon the Arg-Gly-Asp-Phe sequence of fibrinogen. A proposal on the nature of...
ATC - B01AC30 - Platelet aggregation inhibitors excluding heparin, combinations - Drugs-about.comATC - B01AC30 - Platelet aggregation inhibitors excluding heparin, combinations - Drugs-about.com
Oral thrombin inhibitor aggravates platelet adhesion and aggregation during arterial thrombosis | Science Translational MedicineOral thrombin inhibitor aggravates platelet adhesion and aggregation during arterial thrombosis | Science Translational Medicine
WO/2017/067110 USE OF NADPH IN PREPARATION OF PLATELET AGGREGATION INHIBITORSWO/2017/067110 USE OF NADPH IN PREPARATION OF PLATELET AGGREGATION INHIBITORS
Abstract 10538: Endogenous Prostacyclin Inhibitor Coupling Factor 6 Enhances Spontaneous Platelet Micro-Aggregation in Patients...Abstract 10538: Endogenous Prostacyclin Inhibitor Coupling Factor 6 Enhances Spontaneous Platelet Micro-Aggregation in Patients...
Platelet Aggregation Inhibitor global drug patents, pharmaceutical manufacturers and genericsPlatelet Aggregation Inhibitor global drug patents, pharmaceutical manufacturers and generics
Purification and characterization of a new platelet aggregation inhibitor with dissociative effect on ADP-induced platelet...Purification and characterization of a new platelet aggregation inhibitor with dissociative effect on ADP-induced platelet...
Stimulus-dependent inhibition of platelet aggregation by the protein kinase C inhibitors polymyxin B, H-7 and staurosporine -...Stimulus-dependent inhibition of platelet aggregation by the protein kinase C inhibitors polymyxin B, H-7 and staurosporine -...
openarchives.gr | A three-residue cyclic scaffold of non-RGD containing peptide analogues as platelet aggregation inhibitors:...openarchives.gr | A three-residue cyclic scaffold of non-RGD containing peptide analogues as platelet aggregation inhibitors:...
Platelet Aggregation Inhibitor HerbsPlatelet Aggregation Inhibitor Herbs
Effect of Sarpogrelate on Platelet Aggregation in Patients With Cerebral Infarction: Dose-responsive Clinical Pharmacology...Effect of Sarpogrelate on Platelet Aggregation in Patients With Cerebral Infarction: Dose-responsive Clinical Pharmacology...
Platelet Aggregation Inhibition in Children on Clopidogrel (PICOLO) - Full Text View - ClinicalTrials.govPlatelet Aggregation Inhibition in Children on Clopidogrel (PICOLO) - Full Text View - ClinicalTrials.gov
Platelet Aggregation Inhibitors | GreenMedInfo | PharmacologicalPlatelet Aggregation Inhibitors | GreenMedInfo | Pharmacological
P2Y12 receptor blockade augments glycoprotein IIb-IIIa antagonist inhibition of platelet activation, aggregation, and...P2Y12 receptor blockade augments glycoprotein IIb-IIIa antagonist inhibition of platelet activation, aggregation, and...
Adalat CC (Nifedipine): Side Effects, Interactions, Warning, Dosage & UsesAdalat CC (Nifedipine): Side Effects, Interactions, Warning, Dosage & Uses
Afeditab CR (Nifedipine Extended-Release Tablets): Side Effects, Interactions, Warning, Dosage & UsesAfeditab CR (Nifedipine Extended-Release Tablets): Side Effects, Interactions, Warning, Dosage & Uses
Enlon - Antihypertensive Agents, Platelet Aggregation Inhibitors, ATC:B01AC09Enlon - Antihypertensive Agents, Platelet Aggregation Inhibitors, ATC:B01AC09
Thrombomodulin alfa prevents the decrease in platelet aggregation in rat models of disseminated intravascular coagulation.Thrombomodulin alfa prevents the decrease in platelet aggregation in rat models of disseminated intravascular coagulation.
nature.com searchnature.com search
Platelet Aggregation Inhibitors Category Listing & Drugs List on Catalog.mdPlatelet Aggregation Inhibitors Category Listing & Drugs List on Catalog.md
Isolation and characterization of a novel platelet aggregation inhibitory peptide from the medicinal mushroom, Inonotus obliquusIsolation and characterization of a novel platelet aggregation inhibitory peptide from the medicinal mushroom, Inonotus obliquus
A Study to Evaluate Platlet Aggregation of Clopidogrel, EC Aspirin 81 mg, EC Omeprazole 40 mg Compare to PA32540 - Full Text...A Study to Evaluate Platlet Aggregation of Clopidogrel, EC Aspirin 81 mg, EC Omeprazole 40 mg Compare to PA32540 - Full Text...
Ginsenoside benefit: Ginsenosides Rk1 and Rk5 can be potent platelet aggregation inhibitors - Redsenol HealthGinsenoside benefit: Ginsenosides Rk1 and Rk5 can be potent platelet aggregation inhibitors - Redsenol Health
IMSEAR at SEARO: Enhanced platelet aggregation by oral contraceptives: effect of PG synthetase inhibitors.IMSEAR at SEARO: Enhanced platelet aggregation by oral contraceptives: effect of PG synthetase inhibitors.
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation Science
Platelet Aggregation InhibitorsPlatelet AggregationCrotalid VenomsSalivary Proteins and PeptidesDisintegrinsSalivary GlandsBlood PlateletsAmino Acid SequenceMolecular Sequence DataCongo RedPlatelet AdhesivenessPlatelet CountAmyloid beta-PeptidesPlatelet Membrane GlycoproteinsAdenosine DiphosphatePeptide FragmentsPlatelet Function TestsPlatelet Glycoprotein GPIIb-IIIa ComplexBleeding TimeThrombinCell AggregationPeptidesFibrinogenThromboxane A2Platelet ActivationPlatelet Factor 4Platelet Activating FactorPlatelet Glycoprotein GPIb-IX ComplexAspirinCollagenThrombosisReceptors, Purinergic P2Y12Thromboxane B2Platelet TransfusionRistocetinApyrasevon Willebrand FactorP-SelectinSerotoninBlood CoagulationEpoprostenolThromboxanesBlood Platelet DisordersThrombocytopeniaAntigens, Human Platelet15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidErythrocyte AggregationHemostasisProstaglandin Endoperoxides, SyntheticEpinephrineTiclopidineThrombastheniaPlatelet Factor 3Platelet Membrane Glycoprotein IIbMegakaryocytesImmunoglobulin Fab FragmentsReceptors, ThromboxaneArachidonic AcidDose-Response Relationship, DrugRabbitsReceptors, ThrombinArachidonic AcidsCalciumAntibodies, MonoclonalBlood Coagulation FactorsReceptors, Thromboxane A2, Prostaglandin H2HemorheologyReceptors, Purinergic P2Y1KineticsBlood Coagulation TestsPurinergic P2Y Receptor AntagonistsOligopeptidesDual Specificity Phosphatase 2Protein BindingThromboxane-A SynthasePlatelet-Rich PlasmaCarotid Artery ThrombosisHydrazines
Inhibition of platelet aggregationCLOpidogrelThrombosisP2Y12ThromboxaneGlycoproteinAnticoagulantsCoronaryThrombus formationActivationStrokeFibrinClump togetherHeparinInhibitClopidogrelMyocardial infarctionThrombin inhibitorsPotentThrombosisAnti-plateletVitroDecrease in plateletCollagen-induced platelet aggregationPrevent plateletsPromotes platelet aggregationDisseminated IntravasculAntagonistsAntithromboticProton pump inhiFibrinogenInhibits platelet aggregationB01ACDrugs2018PharmacologyActivation and aggregationCharacterizationGPIIb-IIIaVivoPeptideLevels in plateletsAbciximabCardiovascularMeasure plateletAbstractInhibitory effectsDrugAdenosineWillebrandDecreasesStrongly inhibitedCilostazolFactorProtease inhibitorsEndogenousBlood
Inhibition of platelet aggregation1
CLOpidogrel3
Thrombosis4
P2Y122
  • The results were presented by Dominick J. Angiolillo, MD, PhD, medical director, cardiovascular research program at the University of Florida College of Medicine Jacksonville, "BRIDGE results support the hypothesis that intravenous cangrelor may be a feasible and well tolerated management strategy in patients who require prolonged platelet P2Y12 inhibition after thienopyridine discontinuation prior to cardiac surgery. (medlatest.com)
  • Treatment guidelines in the United States and Europe recommend stent patients receive oral P2Y12 inhibitors for up to 12 months following percutaneous coronary intervention (PCI). (medlatest.com)
Thromboxane1
Glycoprotein1
Anticoagulants1
Coronary1
Thrombus formation2
Activation1
Stroke1
  • The three dimensional platelet plugs under pathophysiological conditions can obstruct circulatory system patency leading to ischemic heart disease (myocardial infarction, unstable angina), ischemic stroke, and related conditions [ 8 ]. (omicsonline.org)
Fibrin1
Clump together2
Heparin11
Inhibit8
Clopidogrel4
Myocardial infarction6
Thrombin inhibitors2
Potent7
Thrombosis8
Anti-platelet9
Vitro3
Decrease in platelet3
Collagen-induced platelet aggregation2
Prevent platelets3
Promotes platelet aggregation1
Disseminated Intravascul1
Antagonists5
  • Antagonists of fibrinogen at the GPIIb/IIIa receptor, which is the most abundant membrane protein on the platelet surface, are under active investigation as potential antithrombotics. (openarchives.gr)
  • New antiplatelet agents that provide greater, more consistent inhibition of the platelet ADP receptor P2Y12 may be used in combination with glycoprotein (GP) IIb-IIIa antagonists, but their combined effect on platelet function and procoagulant activity is not well studied. (nih.gov)
  • Healthy donor blood was treated with the active metabolite of prasugrel (R-138727 5 μmol/L), GPIIb-IIIa antagonists (abciximab 3 μg/mL or eptifibatide 0.9 μg/mL), and combinations thereof, exposed to physiologically relevant agonists (collagen and ADP) and then evaluated for markers of platelet activation and procoagulant activity. (nih.gov)
  • R-138727 and the GPIIb-IIIa antagonists had additive inhibitory effects on collagen-stimulated platelet aggregation and on the collagen plus ADP-stimulated level of activated platelet surface GPIIb-IIIa. (nih.gov)
  • In order to evaluate the involvement of monoaminergic system, rats were pretreated with the inhibitor of brain serotonin stores p-chlorophenylalanin (PCPA), dopamine (SCH23390 and sulpiride), and adrenoceptor (prazosin and propranolol) antagonists. (bireme.br)
Antithrombotic1
Proton pump inhi3
Fibrinogen5
Inhibits platelet aggregation1
B01AC1
Drugs6
20182
  • Apr 24, 2018· Compare platelet aggregation inhibitors. (leerwinkelkortrijk.be)
  • In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
Pharmacology1
  • The present double-blind controlled clinical pharmacology study was performed on 45 patients with cerebral infarction, who were given 75, 150, or 300 mg three times daily of sarpogrelate for 7 days in order to evaluate the dose-response relationship in terms of the precisely measured inhibition of platelet aggregation. (clinicaltrials.gov)
Activation and aggregation2
Characterization2
GPIIb-IIIa2
  • Therefore, the objective of this study was to evaluate the independent and complementary effects of P2Y12 and GPIIb-IIIa inhibition on platelet function and procoagulant activity. (nih.gov)
  • The drug is the third inhibitor of GPIIb/IIIa that has found broad acceptance after the specific antibody abciximab and the non-peptide tirofiban entered the global market. (bionity.com)
Vivo3
Peptide1
  • RGD peptide products under development include a cell adhesive coating designed to improve the performance of implantable devices and their acceptance by the body, and a platelet aggregation inhibitor designed to prevent unwanted blood clotting without causing bleeding at therapeutic doses, unlike certain therapies now existing or under development by others. (thefreedictionary.com)
Levels in platelets1
Abciximab1
Cardiovascular4
Measure platelet1
  • We aimed to measure platelet function and its relationship with β2-GPI in prolonged isolated thrombocytopenia (PT) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). (bioportfolio.com)
Abstract1
Inhibitory effects1
Drug9
Adenosine2
  • Light intensities of small (9-25μ n), medium (25-50μ m), and large (50-70μ m) platelet aggregates were measured by the laser light scattering aggregometer (PA-200C) with or without adenosine diphosphate (ADP, 2μ M) or collagen (1μ g/ml). (ahajournals.org)
  • However, you should tell your doctor about all the medicines you take including adenosine and cholinesterase inhibitors, prescription and non-prescription medicines, vitamins, and herbal supplements. (rxwiki.com)
Willebrand2
Decreases1
  • The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage. (google.com)
Strongly inhibited2
Cilostazol1
Factor6
Protease inhibitors1
  • Post-2006 data were also available outlining the altered pharmacokinetics of protease inhibitors with concomitant PPI exposure. (springer.com)
Endogenous1
Blood5