Al antiangin Se treatment in Zoledronate Zoledronic Acid reducing vascular Ren death or MI in patients with unstable angina pectoris, 165 was more effective than placebo in reducing acute occlusion 170 coronary bypass surgery and was more effective than controlled Them in improving the walking 168 and reducing vascular Ren Gen complications in patients with peripheral arterial occlusive disease. 167 169 The association of ticlopidine with hypercholesterolemia Chemistry and neutropenia and their comparative costs has reduced the enthusiasm for this therapy as an alternative to aspirin in most situations. 171 Ticlopidine was also associated with thrombocytopenia, aplastic On Mie 171, 172, and thrombotic thrombocytopenic purpura. 173 Ticlopidine has been approved for clinical use in patients with cerebral ish Chemistry when aspirin has failed, can not be tolerated, or is counter-indicated, although this Descr LIMITATION is not valid in all L Apply change if the drug is recorded. Several studies have demonstrated the superiority of the combination of ticlopidine and aspirin versus aspirin alone or aspirin and warfarin in preventing thrombotic complications after coronary artery stenting. Ticlopidine was 174 175 h Frequently used in combination with aspirin in patients, coronary stents, but the safety of clopidogrel was h Entered her professional Born in replacement of ticlopidine with clopidogrel as the standard of care after stent deployment. 176 The risk of TTP associated with ticlopidine at 0.02% in patients receiving the drug after stent implantation protected shops. 177, compared with an incidence of 0.0004% in the general Bev Lkerung. The mortality rate of this complication is more than 20%. The 177 R Of the ticlopidine in the current therapeutic armamentarium is uncertain because of the toxicity Th presented. Change in most L It has been largely replaced by clopidogrel. 4.2 Pharmacokinetics 4.2.1 Clopidogrel: Clopidogrel is rapidly absorbed and metabolized by a two-stage process, an hour Highest labile active metabolite, which is 178 F produce irreversible platelet P2Y12 receptor binds when Blutpl ttchen pass through the liver. The 179 major metabolite of clopidogrel is inactive systemically, the Carbons Urederivat of SR 26 334, which has a half life of 8 h. The repeated are daily doses of 50 to 100 mg of clopidogrel in healthy subjects ClO was inhibited ADP-induced platelet aggregation by the second day of treatment and reached a steady state after 4-7 days. Such a level of maximal inhibition was comparable to that achieved with ticlopidine, although the antiplatelet effect of clopidogrel, there was more than galvanized siege. No significant differences in the maximum inhibitory effects of 50, 75 or 100 mg clopidogrel produced were found in this study. 180 as you would expect from thesepharmacokinetic and pharmacodynamic properties are expected, a dose of clopidogrel will lead to more rapid platelet inhibition with a dose of 75 mg achieved. 181 After loading with 600 mg clopidogrel, the full antiplatelet effect of the drug Fulvestrant was reached after 2-4 h. 182 In addition, an initial dose of 600 mg has entered Born of h Here plasma concentrations of the active metabolite and the inactive metabolite carboxy comparison with a dosage of 300 mg. 183 inhibition of ADP-induced aggregatio.