By Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.
Edited through one of many world's top interventional cardiologists and educators, this new e-book is created with an eye fixed on giving the reader an outstanding, sensible and clinically-focused knowing of this crucial category of substances, from simple technology to a clear-headed dialogue of complicated subject matters corresponding to blend cures, drug-drug interactions, and platelet resistance.
This very important new book:
- Begins with a concise yet thorough dialogue of platelet biology and pathophysiology in order that readers know how those remedies paintings and why they could additionally produce any such diverse variety of problems, from minor gastrointestinal disappointed, to possibly life-threatening stipulations resembling neutropenia, a serious scarcity of white blood cells.
- Thoroughly covers platelet functionality trying out, together with new, novel techniques.
- Clarifies present best-practices concerning the use of antiplatelet brokers in either power and acute cardiovascular disease
- Reviews of every kind of antiplatelet brokers – from aspirin to lately authorized medicines – together with symptoms, medical results, and part effects/complications
Written by means of a global who's-who of specialists within the box, Antiplatelet treatment additionally contains a whole part overlaying using antiplatelet medicines in PCIs, together with percutaneous valve fix, which makes this article really necessary to Interventional Cardiologists.
Read Online or Download Antiplatelet Therapy in Cardiovascular Disease PDF
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Extra resources for Antiplatelet Therapy in Cardiovascular Disease
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.
1) and can form heterodimers on the platelet surface, which together account for the entire thrombin signal in platelets . Thrombin activates the PARs by cleaving a specific peptide bond in the receptor extracellular domain: R41–S42 for PAR1 and R47–G48 for PAR4 . The signal from the high-affinity PAR1 thrombin receptor is fast and transient , whereas the lower-affinity PAR4  evokes a prolonged signal that contributes to irreversible platelet aggregation [11, 13, 14]. PAR1 is the major receptor for thrombin in human platelets and has become an intensively studied antiplatelet target in clinical trials.
1881) Su di un nuovo elemento morfologico del sangue dei mammiferi e della sua importanza nellatrombosie nella coagulazione. L’Osservatore, 17, 785–787. V. (1962) Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature, 194, 927–929. A. S. (2010) Combination antithrombotic therapies. Circulation, 121, 569–583. A. S. (2012) Do platelet function testing and genotyping improve outcome in patients treated with antithrombotic agents? Platelet function testing and genotyping improve outcome in patients treated with antithrombotic agents.
Antiplatelet Therapy in Cardiovascular Disease by Ron Waksman, Paul A. Gurbel, Michael A. Gaglia Jr.