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PubMed1999

[Platelet aggregation inhibitors in diabetes mellitus].

Major cardiovascular complications and ischemic events occur more frequently in diabetic than nondiabetic patients. Platelets of diabetic patients are found in a permanent prethrombotic state. Platelet activation and aggregation with resultant arterial thrombus formation, are the central mechanisms in the pathophysiology of acute coronary syndromes. Over the past two decades aspirin was the leading antithrombotic agent for reduction of thrombotic events and efficacy was proven in many studies. The main study concerning the aspirin question was the "Antiplatelet Trialist's Collaboration-Study", where a successful risk reduction for vascular events of 25%-34% was observed with daily dosis between 75 and 325 mg. In the last years some new, very effective drugs have been developed. Clopidogrel, a thienopyridine was studied in the CAPRIE trial and compared with aspirin. A small advantage could be proved for clopidogrel. The development of inhibitors of fibrinogen, binding to the platelet glykoprotein IIb/IIIa receptor has expanded the therapeutic spectrum for the treatment of thrombotic disorders. Especially in diabetic patients a significant benefit of these new drugs was demonstrated in various clinical indications. The newest results show the clear advantage of combining thrombolytic agents with the glycoprotein IIb/IIIa receptor antagonists in reperfusion after myocardial infarction. In conclusion the main message is, that diabetic patients do need antithrombotic therapy earlier than nondiabetic patients, that efficient drugs are available and that a primary prevention should be considered in this special patient group.

Aspirin↗
PubMed1993

Platelet aggregation inhibitors in a Bhutanese medicinal plant, shug chher.

The 90% methanol-soluble fraction of a Bhutanese medicinal plant, Shug Chher, exhibited inhibition of platelet aggregation induced by platelet activating factor. Bioassay-directed fractionation led to the isolation of four new labdane diterpenoids, 3 alpha, 15-dihydroxy-labda-8(17), 13E-diene (5), 3 alpha-hydroxy-labda-8(17), 13E-dien-15-oic acid (6), 3 alpha-hydroxy-labda-8(17), 12E, 14-trien-19-oic acid (7), and 3 alpha-acetoxyisocupressic acid (8) and four known diterpenoids, manool (1), 3 alpha-hydroxymanool (2), 3 alpha-hydroxy-12, 13E-biformene (3), and isocupressic acid (4). The structures of the new compounds were determined spectroscopically. Compounds 2, 3, and 5 inhibited platelet aggregation.

Bhutan↗
PubMed1985

Cyclic guanidines. 17. Novel (N-substituted amino)imidazo[2,1-b]quinazolin-2 ones: water-soluble platelet aggregation inhibitors.

A series of novel 1,2,3,5-tetrahydroimidazo[2,1-b]quinazolin-2-one derivatives substituted with a secondary amino group has been prepared and tested for the activities of inhibiting platelet aggregation in rats in vitro and ex vivo. Most of the compounds were found to be the potent inhibitors of platelet aggregation. Some of the active compounds were soluble in water and effective via iv infusion in rats. Structure-activity relationships have indicated that a lipophilic secondary amino group located at position 6 or 7 contributed to retention of potent activity. Among the compounds studied, 7-piperidino-1,2,3,5-tetrahydroimidazo[2,1-b]quinazolin-2- one (13 g,DN-9693) was the most favorable compound.

Animals↗
PubMed1992

Platelet aggregation inhibitors and inotropic constituents in Pyrolae herba.

The chloroform-soluble and n-butyl alcohol-soluble fractions of water extract of Pyrolae Herba inhibited platelet aggregation induced by arachidonic acid and showed a positive inotropic effect. A new naphthoquinone and a new tetralone derivative and known chimaphilin, acetovanillon, and toluhydroquinone were isolated as active constituents. Three new tetralone derivatives were also obtained from an active fraction. The structures of the new compounds were elucidated.

Animals↗
PubMed2006

A classical QSAR study on some platelet aggregation inhibitors.

Cardiovascular diseases are still the main cause of morbidity and mortality in the world. Anti-platelet drugs have found clinical application in the secondary prevention of vascular events including acute myocardial infarction, stroke and cardiovascular death. In the present review, we have developed sixteen quantitative structure-activity relationships (QSAR) for different sets of compounds that are X-phenols (I), X-catechols (II), caffeic acid amides (III), X-alcohols (IV), 1,4-naphthoquinones (V), tetrahydronaphthalenes (VI), phenoxyacetaldehyde guanylhydrazones (VII), pyrrolobenzylisoquinolines (VIII) and phosphonic acids (IX) with respect to their anti-platelet activities. QSAR results have shown that the anti-platelet activities of these compounds are largely dependent not only on their hydrophobicity, but also on the influence of their molar refractivity.

Humans↗
PubMed2003

[Platelet aggregation inhibitors and vitamin K antagonists in stomatology and maxillo-facial surgery].

Anti-thrombin, anti-platelet and anti-vitamin K agents are common treatments given for the prevention of thrombotic or embolic events. In oral or maxillofacial surgery, the question is whether oral anticoagulants or anti-platelets should be discontinued or not: temporary interruption could limit the risk of bleeding, but would increase the risk of thrombosis, and inversely. The best risk/benefit ratio must be achieved, but in many cases anti-platelet agents or even anti-vitamin K agents can be continued. In case of "potentially hemorrhagic" oral surgery, anti-platelet agents should be interrupted about ten days before the intervention. Anti-vitamin K agents should be interrupted four days before surgery and if required, replaced by low-molecular weight heparin at preventive or curative doses. In the very large majority of patients however, surgery (avulsion for example) can be performed without interrupting anticoagulation. Data in the literature have demonstrated that despite the theoretical risk of hemorrhage, bleeding is minimal and can be easily controlled by local treatments; the risk of thrombotic or thromboembolic events after discontinuing anticoagulation is much greater. A close collaboration between the dentist, the stomatologist, and the clinician is required to determine whether anti-thrombosis prevention should be continued and whether the anticoagulation level is adapted to the thrombotic risk. Good surgical technique and local anti-hemorrhagic treatment are essential in oral surgery, particularly in patients taking anti-platelets or oral anticoagulants.

Administration, Oral↗
PubMed2001

Studies on new platelet aggregation inhibitors 1. Synthesis of 7-nitro-3,4-dihydroquinoline-2(1H)-one derivatives.

A series of 6-cyclic aliphatic amino-7-nitro-3,4-dihydroquinoline-2(1H)-ones were prepared and tested for platelet aggregation inhibitory effect, cardiotonic activity and chronotropic activity. These compounds appeared to show selective inhibitory activity against platelet aggregation. Among them, 6-(4-ethoxycarbonylpiperidino)-7-nitro-3,4-dihydroquinoline-2(1H)-one (22f) showed the most potent inhibitory activity and high selectivity. A divergent synthetic route to 6-cyclic aliphatic amino-7-nitro-3,4-dihydroquinoline-2(1H)-one derivatives has also been investigated.

Acetylation↗
PubMedDate not supplied

[Efficacy of clopidogrel as ADP-dependent platelet aggregation inhibitor. Study on individuals with coronary artery disease].

Acetyl-salicylic acid inhibits thromboxane A2 production and reduces the risk of vascular occlusive events by 20 to 25%. Ticlopidine inhibits ADP-dependent platelet aggregation and reduces the same risk by 30 to 35%, but produces some adverse effects. Clopidogrel is a ticlopidin-derived antiplatelet-drug, with the same mechanism of action; reduces the expression of the glycoprotein IIb/IIIa, the fibrinogen receptor on the platelet surface. Clopidogrel has the same clinical efficacy of ticlopidin and lowers the incidence of adverse effects. In this study, we evaluated the effects of one daily dosis of 75 mg of clopidogrel on platelet function in 33 subjects with coronary artery disease. Before treatment and after the 6th and 12th week, the following parameters were evaluated: 5 microM-ADP and 20 micrograms/mL collagen-induced platelet aggregation, bleeding time and fibrinogen concentration. In basal and in the 6th and 12th week samples, ADP-induced platelet aggregation was 90.7% +/- 13.2, 54.6% +/- 23.2 and 49.2% +/- 23.7 respectively, that represents a significant reduction of 38.6% and 44.4%. Reduction of collagen-induced platelet aggregation was not significative. Plasmatic fibrinogen did not suffer variation during treatment. Bleeding time was significant prolonged from 4.1 minutes to 15.4 and 14.6 minutes (3.7-3.5 times compared with the test before treatment). There were no haemorrhagic complications, only digestive discomfort in fewer than 3% of patients. We concluded that clopidogrel is a safe and efficacious drug for patients, it efficiently reduces ADP-induced platelet aggregation and prolongs bleeding time.

Adenosine Diphosphate↗