Randomized controlled clinical trials versus real-life atrial fibrillation patients treated with oral anticoagulants. Do we treat the same patients?
non-valvular atrial fibrillation
oral anticoagulation
randomized trial
real-world study
Journal
Cardiology journal
ISSN: 1898-018X
Titre abrégé: Cardiol J
Pays: Poland
ID NLM: 101392712
Informations de publication
Date de publication:
2020
2020
Historique:
received:
16
04
2018
accepted:
11
10
2018
revised:
06
11
2018
pubmed:
9
11
2018
medline:
18
8
2021
entrez:
9
11
2018
Statut:
ppublish
Résumé
The aim of the study was to compare clinical characteristics of real-life atrial fibrillation (AF) patients with populations included in randomized clinical trials (ROCKET AF and RE-LY). The analysis included 3528 patients who are participants of the ongoing, multicentre, retrospective CRAFT study. The study is registered in ClinicalTrials.gov: NCT02987062. The study is based on a retrospective analysis of hospital records of AF patients treated with vitamin K antagonists (VKAs) (acenocoumarol, warfarin) and non-vitamin K oral anticoagulants (NOACs) (dabigatran, rivaroxaban). CHADS2 score was used for risk of stroke stratification. VKA was prescribed in 1973 (56.0%), while NOAC in 1549 (44.0%), including dabigatran - 504 (14.3%) and rivaroxaban - 1051 (29.8%), of the 3528 patients. VKA patients in the CRAFT study were at significantly lower risk of stroke (CHADS2 1.9 ± 1.3), compared with the VKA population from the RE-LY (2.1 ± 1.1) and the ROCKET-AF (3.5 ± 1.0). Patients in the CRAFT study treated with NOAC (CHADS2 for patients on dabigatran 150 mg - 1.3 ± 1.2 and on rivaroxaban - 2.2 ± 1.4) had lower risk than patients from the RE-LY (2.2 ± 1.2) and the ROCKET AF (3.5 ± 0.9). Real-world patients had a lower risk of stroke than patients included in the RE-LY and ROCKET AF trials.
Sections du résumé
BACKGROUND
The aim of the study was to compare clinical characteristics of real-life atrial fibrillation (AF) patients with populations included in randomized clinical trials (ROCKET AF and RE-LY).
METHODS
The analysis included 3528 patients who are participants of the ongoing, multicentre, retrospective CRAFT study. The study is registered in ClinicalTrials.gov: NCT02987062. The study is based on a retrospective analysis of hospital records of AF patients treated with vitamin K antagonists (VKAs) (acenocoumarol, warfarin) and non-vitamin K oral anticoagulants (NOACs) (dabigatran, rivaroxaban). CHADS2 score was used for risk of stroke stratification.
RESULTS
VKA was prescribed in 1973 (56.0%), while NOAC in 1549 (44.0%), including dabigatran - 504 (14.3%) and rivaroxaban - 1051 (29.8%), of the 3528 patients. VKA patients in the CRAFT study were at significantly lower risk of stroke (CHADS2 1.9 ± 1.3), compared with the VKA population from the RE-LY (2.1 ± 1.1) and the ROCKET-AF (3.5 ± 1.0). Patients in the CRAFT study treated with NOAC (CHADS2 for patients on dabigatran 150 mg - 1.3 ± 1.2 and on rivaroxaban - 2.2 ± 1.4) had lower risk than patients from the RE-LY (2.2 ± 1.2) and the ROCKET AF (3.5 ± 0.9).
CONCLUSIONS
Real-world patients had a lower risk of stroke than patients included in the RE-LY and ROCKET AF trials.
Identifiants
pubmed: 30406937
pii: VM/OJS/J/58091
doi: 10.5603/CJ.a2018.0135
pmc: PMC8078963
doi:
Substances chimiques
Angiotensin Receptor Antagonists
0
Angiotensin-Converting Enzyme Inhibitors
0
Anticoagulants
0
Vitamin K
12001-79-5
Banques de données
ClinicalTrials.gov
['NCT02987062']
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
590-599Références
Kardiol Pol. 2016;74(5):418-24
pubmed: 26502939
Pulm Pharmacol Ther. 2014 Apr;27(2):129-38
pubmed: 24468677
Kardiol Pol. 2016;74(3):251-61
pubmed: 26365943
J Am Coll Cardiol. 2010 Feb 23;55(8):725-31
pubmed: 20170808
Biomed Res Int. 2014;2014:567026
pubmed: 25133166
Pol Arch Intern Med. 2018 Mar 17;128(5):274-279
pubmed: 29549695
Cardiol J. 2019;26(3):260-264
pubmed: 29297178
Kardiol Pol. 2018;76(5):889-898
pubmed: 29350386
N Engl J Med. 2009 Sep 17;361(12):1139-51
pubmed: 19717844
Br J Clin Pharmacol. 2007 Sep;64(3):292-303
pubmed: 17506785
Clin Res Cardiol. 2016 Nov;105(11):912-920
pubmed: 27245329
Lancet. 1989 Jan 28;1(8631):175-9
pubmed: 2563096
Eur Heart J. 2016 Apr 7;37(14):1145-53
pubmed: 26330425
Heart. 2017 Sep;103(17):1331-1338
pubmed: 28286333
Eur J Clin Pharmacol. 2005 Dec;61(12):873-80
pubmed: 16328318
Am Heart J. 2009 May;157(5):805-10, 810.e1-2
pubmed: 19376304
N Engl J Med. 1990 Nov 29;323(22):1505-11
pubmed: 2233931
Kardiol Pol. 2015;73(2):85-93
pubmed: 25179482
J Am Heart Assoc. 2013 Feb 19;2(1):e000067
pubmed: 23525418
Pharmacoepidemiol Drug Saf. 2015 Dec;24(12):1297-303
pubmed: 26419506
Kardiol Pol. 2016;74(4):362-71
pubmed: 26365937
Europace. 2016 Nov;18(11):1609-1678
pubmed: 27567465
Int Angiol. 2015 Dec;34(6):552-61
pubmed: 25410296
Cardiovasc Ther. 2015 Aug;33(4):177-83
pubmed: 25930214
Pol Arch Med Wewn. 2016;126(3):138-48
pubmed: 27000745
Int J Cardiol. 2016 Jan 15;203:882-4
pubmed: 26605688
Thromb J. 2014 Jun 24;12:14
pubmed: 25024644
N Engl J Med. 2011 Sep 8;365(10):883-91
pubmed: 21830957
Thromb Haemost. 2016 Jan;115(1):152-60
pubmed: 26354766