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

Edited by means of one of many world's major interventional cardiologists and educators, this new ebook is created with an eye fixed on giving the reader an effective, functional and clinically-focused figuring out of this significant classification of substances, from uncomplicated technology to a clear-headed dialogue of advanced issues akin to mix cures, 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 remedies paintings and why they could additionally produce this kind of various variety of issues, from minor gastrointestinal disappointed, to very likely 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 concerning the use of antiplatelet brokers in either power and acute cardiovascular disease
  • Reviews of all kinds of antiplatelet brokers – from aspirin to lately authorized medicines – together with symptoms, medical 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 protecting using antiplatelet medicinal drugs in PCIs, together with percutaneous valve fix, which makes this article really necessary to Interventional Cardiologists.

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Additional info for Antiplatelet Therapy in Cardiovascular Disease

Example text

The PCI cohort also received unfractionated heparin, low-molecular-weight heparin, or bivalirudin and a loading dose of clopidogrel (300–600 mg) and aspirin (162–325 mg oral or IV 150–500 mg). 5 mg, or placebo). After 60 days of maintenance of vorapaxar, greater than 80% platelet inhibition to TRAP was seen at all three doses. Patients were evaluated at 60 days for safety (primary end point TIMI major/minor bleeding) and efficacy (MACE – nonfatal MI, nonfatal stroke, hospitalization for recurrent ischemia, or urgent coronary revascularization).

1986) Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. Circulation, 73, 418–427. 10 Glover, C. R. (2000) Pathophysiological insights from studies of retrieved coronary atherectomy tissue. Seminars in Interventional Cardiology, 5, 167–173. M. et al. (2010) A 2-step mechanism of arterial thrombus formation induced by human atherosclerotic plaques. Journal of the American College of Cardiology, 55, 1147–1158. , Falk, E. et al. (1994) Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture.

Pharmacogenetics and Genomics, 17, 145–160. C. (2008) Cyclooxygenase polymorphisms and risk of cardiovascular events: the Atherosclerosis Risk in Communities (ARIC) study. Clinical Pharmacology and Therapeutics, 83, 52–60. , and Sharma, P. (2008) Pharmacogenetics of aspirin resistance: a comprehensive systematic review. British Journal of Clinical Pharmacology, 66, 222–232. , and Schrör, K. (1999) Cyclooxygenase-2 in human platelets as a possible factor in aspirin resistance. Lancet, 353, 900. , and Morita, I.

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