Antiplatelet Therapy in Cardiovascular Disease by Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.

By Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.

Edited by way of one of many world's best interventional cardiologists and educators, this new booklet is created with a watch on giving the reader a high-quality, functional and clinically-focused realizing of this significant type of substances, from easy technological know-how to a clear-headed dialogue of complicated subject matters akin to mixture remedies, drug-drug interactions, and platelet resistance.

This vital new book:

  • Begins with a concise yet thorough dialogue of platelet biology and pathophysiology in order that readers know the way those treatments paintings and why they could additionally produce one of these diverse diversity of issues, from minor gastrointestinal dissatisfied, to probably life-threatening stipulations comparable to neutropenia, a severe scarcity of white blood cells.
  • Thoroughly covers platelet functionality trying out, together with new, novel techniques.
  • Clarifies present best-practices in regards to the use of antiplatelet brokers in either persistent and acute cardiovascular disease
  • Reviews of every kind of antiplatelet brokers – from aspirin to lately licensed medicinal drugs – together with symptoms, scientific results, and facet effects/complications

Written by way of a global who's-who of specialists within the box, Antiplatelet remedy additionally comprises a complete part masking using antiplatelet medicines in PCIs, together with percutaneous valve fix, which makes this article really necessary to Interventional Cardiologists.

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Some studies demonstrated that pharmacological blockade of P2Y12 receptors reduces the ability of platelets to produce TXA2; however, the platelet TXA2 production is normal in patients with P2Y12 deficiency [4]. P2Y12 amplifies the mobilization of cytoplasmic Ca2+ mediated by P2Y1 and other receptors and regulates diacylglycerol-mediated signaling [4]. 2). Early studies demonstrated the important role of P2Y12 in shear-induced platelet aggregation long before its molecular identification, by using platelets from individuals treated with the antithrombotic drug ticlopidine or from a patient with congenital P2Y12 deficiency [4].

GPIIb/IIIa receptor antagonists act by inhibiting this final common pathway of platelet aggregation. Platelet aggregation phase Platelet activation causes modifications in the shape of platelets and conformational changes in the GPIIb/IIIa receptor, transforming it from a ligand-unreceptive to a ligand-receptive state. The GPIIb/IIIa receptors on most platelet surfaces are presented as deactivated forms that require activation by thrombin, collagen, or TXA2; platelet aggregation begins when an aggregating agent interacts with its receptor(s) on the platelet surface.

Et al. (2002) An additional mechanism of action of abciximab: dispersal of newly formed platelet aggregates. Thrombosis and Haemostasis, 87, 1020–1025. , Soria, J. et al. (2001) Disaggregation of in vitro platelet-rich clots by abciximab increases fibrinogen exposure and promotes fibrinolysis. Arteriosclerosis, Thrombosis, and Vascular Biology, 21, 142–148. , Obonska, K. et al. (2012) Clinical efficacy and safety of intracoronary vs. intravenous abciximab administration in STEMI patients undergoing primary percutaneous coronary intervention: a meta-analysis of randomized trials.

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