Skip to main content Accessibility help
×
Hostname: page-component-8448b6f56d-sxzjt Total loading time: 0 Render date: 2024-04-24T20:19:55.959Z Has data issue: false hasContentIssue false

23 - Antiplatelet therapies in cardiology

Published online by Cambridge University Press:  15 October 2009

Robert A. Harrington
Affiliation:
Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA
Paolo Gresele
Affiliation:
Università degli Studi di Perugia, Italy
Valentin Fuster
Affiliation:
Mount Sinai School of Medicine, New York
Jose A. Lopez
Affiliation:
Seattle University
Clive P. Page
Affiliation:
King's College London
Jos Vermylen
Affiliation:
Katholieke Universiteit Leuven, Belgium
Get access

Summary

INTRODUCTION

Antiplatelet therapies are the mainstay in the treatment of acute coronary syndromes (ACSs) as well as in the chronic primary and secondary prevention of acute coronary events. This chapter describes the established antiplatelet agents in cardiology and introduces the novel drugs currently in advanced development.

ASPIRIN

Acetylsalicylic acid, known as aspirin, is an inhibitor of the production of prostaglandins and thromboxanes.

Mechanism of action

The prostaglandin (PG) endoperoxide H synthases-1 and -2, or cyclooxygenase (COX)-1 and -2, catalyze the conversion of arachidonic acid to PGH2, the first reaction of prostanoids synthesis. PGH2 is the immediate precursor of PGD2, PGE2, PGF, PGI2, and thromboxane (Tx) A2. Aspirin permanently inactivates COX-1 and COX-2. COX-1 is a constitutive enzyme of platelets and is 50- to 100-fold more sensitive to aspirin than COX-2 (which is predominantly expressed in response to inflammatory stimuli by monocytes/macrophages). Aspirin inhibits the synthesis of TxA2, a potent platelet-aggregating agonist and vasoconstrictor agent that is primarily produced by platelets from PGH2 and of PGI2 (prostacyclin), a platelet inhibitor and vasodilator agent that is produced by vascular endothelial cells. TxA2 is mainly produced by the COX-1 of platelets and therefore is most sensitive to the effect of aspirin, whereas PGI2 can be produced by both COX-1 and COX-2.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2007

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×