Antithrombotic Therapy in Prevention of Ischemic Stroke by Richard C Becker, Frederick A Spencer

By Richard C Becker, Frederick A Spencer

Stroke is the most typical explanation for grownup mortality within the usa. Antithrombotic brokers shape the mainstay of stroke prevention. Aspirin produces a modest aid within the possibility of moment stroke and brief ischemic assault (TIA, mini-stroke) and is greatly instructed for preliminary treatment. The thienopyridines (Ticlid) and clopodogrel (Plavix) are choices for secondary prevention in sufferers who don't reply to or can't take aspirin. they're not more powerful than aspirin and feature been linked to thrombotic thrombocytopenic purpura. the combo of aspirin and extended-release dipyridamole (Aggrenox) has a number of mechanisms of motion and an additive impact on lowering stroke hazard in comparison with both agent on my own. A 2-fold elevate in chance relief and favorable safeguard profile recommend that the combo can function first-line prophylaxis opposed to a moment stroke. This quantity, as a part of the Oxford American Pocket Note sequence, offers the clinician wtih updated details at the instructions, and healing concepts in recurrent stroke/TIA prevention. beneficial good points comprise therapy algorithms, illustrations, medicine tables, charts and figures to permit either the professional and the first supplier to make sure the easiest innovations to their sufferers with a purpose to hinder the reocurrence of stroke/TIA.

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Extra info for Antithrombotic Therapy in Prevention of Ischemic Stroke

Example text

The Clopidogrel versus Aspirin in Patients at Risk for Ischemic Events (CAPRIE) study32 was designed to test the hypothesis that clopidogrel (75 mg daily) would reduce vascular events in high-risk patients by approximately 15% compared with aspirin (325 mg daily). The study population consisted of patients with atherosclerotic vascular disease manifested as recent ischemic stroke, recent MI, or symptomatic peripheral arterial occlusive disease. A total of 19,185 patients were enrolled in the international trial.

Dose-dependent inhibition of platelet aggregation is observed approximately 4 hours after a single oral dose of clopidogrel, with a slightly more rapid and robust degree 23 OAPN Intestinal absorption Clopidogrel bisulfate CYP P450 conversion Prasugrel Thrombin/ collagen Gq Gq Active metabolite G12 AZD6140, cangrelor ADP P2Y1 T×A2 TP Inactive metabolite Hydrolysis Gq ADP G12 G12 Activation PLC␤ Membrane phospholipids Ca++ AA mobilization COX-1 ASA TxA2 Granule secretion Rho kinase Shape change P13K Rap1b Akt Gi P2Y12 Adenylyl cyclase ↓cAMP ↓VASP-P ADP Integrin ␣lb␤3 activation Figure 7 Mechanism of action of clopidogrel and prasugrel.

Thrombotic thrombocytopenic purpura associated with ticlopidine. A review of 60 cases. Ann Intern Med 1998;128:541–4. 39. Antman EM, Wiviott SD, Murphy SA, et al. Early and late benefits of prasugrel in patients with acute coronary syndromes 43 OAPN undergoing percutaneous coronary intervention: a TRITONTIMI 38 (TRial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet InhibitioN with PrasugrelThrombolysis In Myocardial Infarction) analysis. J Am Coll Cardiol 2008;51(21):2028–33.

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