ReviewAspirin, Clopidogrel, and Ticagrelor in Acute Coronary Syndromes
Section snippets
Aspirin
Aspirin mediates its cardioprotective effects through the irreversible inhibition of cyclooxygenase (COX)-1 in the arachidonic acid pathway, subsequently blocking the production of thromboxane A2, a platelet agonist, thereby reducing thrombus formation.11, 12
The use of aspirin has been shown unequivocally to reduce vascular morbidity and mortality in patients with ACS both in the acute13 and long-term clinical settings.14 In a meta-analysis of 16 secondary prevention trials comparing long-term
Thienopyridines
The thienopyridines, clopidogrel and prasugrel, selectively inhibit the P2Y12 purinoreceptor and block platelet activation for the lifespan of the platelet because of their irreversible binding to the receptor.19, 20 Both compounds are prodrugs, requiring biotransformation into their active form by hepatic cytochrome P450 (CYP) enzymes, particularly the CYP3A4 isozyme.20, 21
The Evolution of Aspirin Dosing for Secondary Prevention of Events in ACS
The use of aspirin for the prevention of vascular morbidity and mortality has evolved over many years. The original tablet version of aspirin was developed in 1900 and sold in the United States as a 5-grain pill (∼325 mg)—the genesis of the “higher cardiovascular” dose commonly used today.17 An 81-mg tablet for children was arbitrarily selected as a quarter of the adult dose and became available in 1922.17 Given the long-term use of aspirin as an antiplatelet therapy and its inclusion in many
Clopidogrel and Aspirin
An overview of real-world treatment practice showed that high aspirin doses were commonly used in North America.50 Furthermore, a cross-country evaluation of CURE also demonstrated that use of high aspirin doses was common in North America, with 86% of patients receiving ≥200 mg, whereas low aspirin doses were commonly used in Europe (>50% of patients in both Western and Eastern Europe received doses of ≤100 mg/day). In addition to the previously mentioned analysis by aspirin dose of the CURE
Ticagrelor and Aspirin
In the PLATO trial investigating ticagrelor plus aspirin versus clopidogrel plus aspirin for the prevention of cardiovascular events in patients with ACS, it was recommended that all patients receive a maintenance aspirin dose of 75 to 100 mg/day (325 mg for 6 months was permitted in those who received a stent).36 As mentioned above, prespecified subgroup analyses from the PLATO trial indicated that the efficacy of ticagrelor plus aspirin was less compared with clopidogrel with aspirin for 3 of
Acknowledgment
The author acknowledges the assistance of Josh Collis and Jackie Phillipson, PhD, of Gardiner-Caldwell Communications in drafting the review article. Views expressed in this review represent those of the author.
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Prasugrel
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The metabolism of clopidogrel is catalyzed by human cytochrome P450 3A and is inhibited by atorvastatin
Drug Metab Dispos
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2022, JACC: Basic to Translational ScienceElectrocatalytic determination of clopidogrel using Bi<inf>2</inf>O<inf>3</inf>-Pp-AP/GCE by differential pulse voltammetry in pharmaceutical productions
2017, Journal of Electroanalytical ChemistryCitation Excerpt :The medical properties, pharmacodynamics, pharmacokinetics and various aspect of this compound, have been published in both books and research papers [1–5]. This compound is an oral thienopyridine derivative which is used to inhibit blood clot formation in coronary artery diseases, peripheral vascular diseases and so on [6,7]. Clopidogrel is a prodrug that is absorbed in the intestine and activated in the liver.
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2017, Journal of Diabetes and its ComplicationsPrevalence and predictors of high-on treatment platelet reactivity with ticagrelor in ACS patients undergoing stent implantation
2016, Vascular PharmacologyCitation Excerpt :In addition, due to its peculiar adenosine-like structure, it may display potential pleiotropic effects [18–20] that may contribute to explain the significant benefits in mortality obtained with ticagrelor, but not with prasugrel, as compared to clopidogrel [21,22]. Even though recent evidence has emerged on the impact of circulating and genetic factors on the response to ticagrelor [23,24], no study has so far extensively attempted to evaluate the prevalence and predictors of HRPR with ticagrelor, that was, therefore, the aim of the present study. We included patients admitted for acute coronary syndromes to the Division of Cardiology, “Maggiore della Carità” Hospital, Eastern Piedmont University in Novara, Italy, from September 2013 to September 2014 and undergoing percutaneous coronary revascularization.
HAS-BLED score predicts risk of in-hospital major bleeding in patients with acute non-ST segment elevation myocardial infarction
2015, Thrombosis ResearchCitation Excerpt :Acute non-ST segment elevation myocardial infarction (NSTEMI) is a disease characterized by atherosclerotic plaque rupture-related acute thrombosis. The use of powerful anti-thrombotic therapy has been reported to reduce the ischemic complications seen in these patients [1–3]. However, this strategy increases the likelihood of bleeding, especially in high-risk patients [4–6].
The author did not receive any financial compensation for authoring this article. Medical writing support was funded by AstraZeneca.
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