By Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.
Edited by way of one of many world's major interventional cardiologists and educators, this new ebook is created with an eye fixed on giving the reader a fantastic, sensible and clinically-focused figuring out of this crucial classification of substances, from easy technological know-how to a clear-headed dialogue of advanced issues corresponding to blend treatments, 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 the sort of diverse variety of issues, from minor gastrointestinal disappointed, to possibly life-threatening stipulations akin 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 continual and acute cardiovascular disease
- Reviews of every kind of antiplatelet brokers – from aspirin to lately licensed medicines – together with symptoms, medical results, and facet effects/complications
Written through a world who's-who of specialists within the box, Antiplatelet treatment additionally contains a whole part overlaying using antiplatelet medications in PCIs, together with percutaneous valve fix, which makes this article relatively necessary to Interventional Cardiologists.
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Extra resources for Antiplatelet Therapy in Cardiovascular Disease
24 Antiplatelet Therapy in Cardiovascular Disease “Inside-out” and “outside-in” GPIIb/IIIa signaling phenomenon GPIIb/IIIa receptor expression and function are dynamic and responsive to the state of internal activation of platelets. “Inside-out” GPIIb/IIIa signaling has been described to trigger platelet activation and increase receptor expression and binding affinity . First platelet–platelet contacts that initiate aggregation occur after fibrinogen and vWF binding to the GPIIb/IIIa receptor.
Journal of Physiology and Pharmacology, 50, 661–667. , Udelhoven, M. et al. (2004) Cyclooxygenase COX-2a, a novel COX-2 mRNA variant, in platelets from patients after coronary artery bypass grafting. Thrombosis and Haemostasis, 92, 925–928. , Paolini, C. et al. (2007) Alternative splicing of platelet cyclooxygenase-2 mRNA in patients after coronary artery bypass grafting. Thrombosis and Haemostasis, 98, 1309–1315. A. A. (1987) Inhibition of thromboxane formation in vivo and ex vivo: implications for therapy with platelet inhibitory drugs.
29 30 Antiplatelet Therapy in Cardiovascular Disease Protease-activated receptor 1 (PAR1) The serine protease thrombin is the most potent platelet activator and plays a critical role in thrombosis and in the maintenance of hemostasis following vascular injury . As direct thrombin inhibitors block thrombin-mediated cleavage of fibrinogen, targeting the downstream platelet thrombin receptors instead should theoretically result in a safer bleeding profile. 1) and can form heterodimers on the platelet surface, which together account for the entire thrombin signal in platelets .
Antiplatelet Therapy in Cardiovascular Disease by Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.