Comparison of Triflusal with Aspirin in the Secondary Prevention of Atherothrombotic Events; Α Randomised Clinical Trial.


Journal

Current vascular pharmacology
ISSN: 1875-6212
Titre abrégé: Curr Vasc Pharmacol
Pays: United Arab Emirates
ID NLM: 101157208

Informations de publication

Date de publication:
2019
Historique:
received: 01 01 2018
revised: 07 04 2018
accepted: 01 06 2018
pubmed: 6 6 2018
medline: 9 6 2020
entrez: 6 6 2018
Statut: ppublish

Résumé

Triflusal has demonstrated an efficacy similar to aspirin in the prevention of vascular events in patients with acute myocardial infarction (ΜΙ) and ischaemic stroke but with less bleeding events. We performed a randomised, multicentre, phase 4 clinical trial to compare the clinical efficacy and safety of triflusal versus aspirin, administered for 12 months in patients eligible to receive a cyclooxygenase-1 (COX-1) inhibitor. Patients with stable coronary artery disease or with a history of non-cardioembolic ischaemic stroke were randomly assigned to receive either triflusal 300 mg twice or 600 mg once daily or aspirin 100 mg once daily for 12 months. The primary efficacy endpoint was the composite of: (a) ΜΙ, (b) stroke (ischaemic or haemorrhagic), or, (c) death from vascular causes for the entire follow-up period. The primary safety endpoints were the rate of bleeding events as defined by Bleeding Academic Research Consortium (BARC) criteria. At 12-month follow-up, an equivalent result was revealed between the triflusal (n=559) and aspirin (n=560) in primary efficacy endpoint. Specifically, the combined efficacy outcome rate (i.e. MI, stroke or death from vascular causes) difference was equal to -1.3% (95% confidence interval -1.1 to 3.5) and lied within the a-priori defined equivalence interval (p<0.001). Regarding the primary safety endpoints, patients on triflusal treatment were 50% less likely to develop bleeding events according to the BARC criteria, and especially any clinically overt sign of haemorrhage that requires diagnostic studies, hospitalisation or special treatment (BARC type 2). The efficacy of triflusal in the secondary prevention of vascular events is similar to aspirin when administered for 12 months. Importantly, triflusal significantly reduced the incidence of ΜΙ and showed a better safety profile compared with aspirin. (ASpirin versus Triflusal for Event Reduction In Atherothrombosis Secondary prevention, ASTERIAS trial; Clinical Trials.gov Identifier: NCT02616497).

Sections du résumé

BACKGROUND
Triflusal has demonstrated an efficacy similar to aspirin in the prevention of vascular events in patients with acute myocardial infarction (ΜΙ) and ischaemic stroke but with less bleeding events.
OBJECTIVE
We performed a randomised, multicentre, phase 4 clinical trial to compare the clinical efficacy and safety of triflusal versus aspirin, administered for 12 months in patients eligible to receive a cyclooxygenase-1 (COX-1) inhibitor.
METHODS
Patients with stable coronary artery disease or with a history of non-cardioembolic ischaemic stroke were randomly assigned to receive either triflusal 300 mg twice or 600 mg once daily or aspirin 100 mg once daily for 12 months. The primary efficacy endpoint was the composite of: (a) ΜΙ, (b) stroke (ischaemic or haemorrhagic), or, (c) death from vascular causes for the entire follow-up period. The primary safety endpoints were the rate of bleeding events as defined by Bleeding Academic Research Consortium (BARC) criteria.
RESULTS
At 12-month follow-up, an equivalent result was revealed between the triflusal (n=559) and aspirin (n=560) in primary efficacy endpoint. Specifically, the combined efficacy outcome rate (i.e. MI, stroke or death from vascular causes) difference was equal to -1.3% (95% confidence interval -1.1 to 3.5) and lied within the a-priori defined equivalence interval (p<0.001). Regarding the primary safety endpoints, patients on triflusal treatment were 50% less likely to develop bleeding events according to the BARC criteria, and especially any clinically overt sign of haemorrhage that requires diagnostic studies, hospitalisation or special treatment (BARC type 2).
CONCLUSION
The efficacy of triflusal in the secondary prevention of vascular events is similar to aspirin when administered for 12 months. Importantly, triflusal significantly reduced the incidence of ΜΙ and showed a better safety profile compared with aspirin. (ASpirin versus Triflusal for Event Reduction In Atherothrombosis Secondary prevention, ASTERIAS trial; Clinical Trials.gov Identifier: NCT02616497).

Identifiants

pubmed: 29866011
pii: CVP-EPUB-90919
doi: 10.2174/1570161116666180605090520
doi:

Substances chimiques

Cyclooxygenase Inhibitors 0
Platelet Aggregation Inhibitors 0
Salicylates 0
triflusal 1Z0YFI05OO
Aspirin R16CO5Y76E

Banques de données

ClinicalTrials.gov
['NCT02616497']

Types de publication

Clinical Trial, Phase IV Comparative Study Equivalence Trial Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

635-643

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Kallirroi I Kalantzi (KI)

Department of Cardiology, University Hospital of Ioannina, Ioannina, Greece.
Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Ioannis V Ntalas (IV)

Department of Cardiology, University Hospital of Ioannina, Ioannina, Greece.
Department of Cardiology, Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom.

Vasileios G Chantzichristos (VG)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Maria E Tsoumani (ME)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Dimitrios Adamopoulos (D)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Christos Asimakopoulos (C)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Adamantios Bourdakis (A)

Internal Medicine, Diabetes and Metabolism Unit, Trikala General Hospital, Trikala, Greece.

Petros Darmanis (P)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Alexandra Dimitriadou (A)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Stefanos Gkiokas (S)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Konstantinos Ipeirotis (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Kyriaki Kitikidou (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Ioannis Klonaris (I)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Aglaia Kostaki (A)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Dimitrios Logothetis (D)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Konstantinos Mainas (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Theodoros Mais (T)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Athanasios Maragiannis (A)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Konstantina Martiadou (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Konstantinos Mavronasos (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Ioannis Michelongonas (I)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Dimitrios Mitropoulos (D)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Georgios Papadimitriou (G)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Achilleas Papadopoulos (A)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Miltiadis Papaioakeim (M)

Department of Internal Medicine, General Hospital of Komotini, Komotini, Greece.

Kosmas Sofillas (K)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Sotiria Stabola (S)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Emmanouil Stefanakis (E)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Dimitrios Stergiou (D)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Maria Thoma (M)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Alexandros Zenetos (A)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

Stergios Zisekas (S)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

John A Goudevenos (JA)

Department of Cardiology, University Hospital of Ioannina, Ioannina, Greece.

Demosthenes B Panagiotakos (DB)

School of Health Science & Education, Harokopio University, Athens, Greece.

Alexandros D Tselepis (AD)

Department of Chemistry, Atherothrombosis Research Centre, University of Ioannina, Ioannina, Greece.

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