Dual therapy with oral anticoagulation and single antiplatelet agent versus monotherapy with oral anticoagulation alone in patients with atrial fibrillation and stable ischemic heart disease: a systematic review and meta-analysis.


Journal

Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing
ISSN: 1572-8595
Titre abrégé: J Interv Card Electrophysiol
Pays: Netherlands
ID NLM: 9708966

Informations de publication

Date de publication:
Mar 2023
Historique:
received: 13 07 2022
accepted: 12 08 2022
pubmed: 10 9 2022
medline: 4 3 2023
entrez: 9 9 2022
Statut: ppublish

Résumé

In patients with atrial fibrillation (AF) and stable ischemic heart disease, recent guidelines recommend oral anticoagulant (OAC) monotherapy in preference to OAC + single antiplatelet agent (SAPT) dual therapy. However, these data are based on the results of only two randomized controlled trials (RCTs) and a relatively small group of patients. Thus, the safety and efficacy of this approach may be underpowered to detect a significant difference. We hypothesized that OAC monotherapy will have a reduced risk of bleeding, but similar all-cause mortality and ischemic outcomes as compared to dual therapy (OAC + SAPT). A systematic search of PubMed/MEDLINE, EMBASE, and Scopus was conducted. Safety outcomes included total bleeding, major bleeding, and others. Efficacy outcomes included all-cause mortality, cardiovascular mortality, myocardial infarction, stroke, and major adverse cardiovascular events (MACE). RCTs and observational studies were pooled separately (study design stratified meta-analysis). Subgroup analyses were performed for vitamin K antagonists and direct oral anticoagulants (DOACs). Pooled risk ratios (RR) with corresponding 95% confidence intervals (CI) were calculated using the Mantel-Haenszel method. Meta-analysis of 2 RCTs comprising a total of 2905 patients showed that dual therapy (OAC + SAPT) vs. OAC monotherapy was associated with a statistically significant increase in major bleeding (RR 1.51; 95% CI [1.10, 2.06]). There was no significant reduction in MACE (RR 1.10; [0.71, 1.72]), stroke (RR 1.29; [0.85, 1.95]), myocardial infarction (RR 0.57; [0.28, 1.16]), cardiovascular mortality (RR 1.22; [0.63, 2.35]), or all-cause mortality (RR 1.18 [0.52, 2.68]). Meta-analysis of 20 observational studies comprising 47,451 patients showed that dual therapy (OAC + SAPT) vs. OAC monotherapy was associated with a statistically significant higher total bleeding (RR 1.50; [1.20, 1.88]), major bleeding (RR = 1.49; [1.38, 1.61]), gastrointestinal bleeding (RR = 1.62; [1.15, 2.28]), and myocardial infarction (RR = 1.15; [1.05, 1.26]), without significantly lower MACE (RR 1.10; [0.97, 1.24]), stroke (RR 0.93; [0.73, 1.19]), cardiovascular mortality (RR 1.11; [0.95, 1.29]), or all-cause mortality (RR 0.93; [0.78, 1.11]). Subgroup analysis showed similar results for both vitamin K antagonists and DOACs, except a statistically significant higher intracranial bleeding with vitamin K antagonist + SAPT vs. vitamin K antagonist monotherapy (RR 1.89; [1.36-2.63]). In patients with AF and stable ischemic heart disease, OAC + SAPT as compared to OAC monotherapy is associated with a significant increase in bleeding events without a significant reduction in thrombotic events, cardiovascular mortality, and all-cause mortality.

Sections du résumé

BACKGROUND BACKGROUND
In patients with atrial fibrillation (AF) and stable ischemic heart disease, recent guidelines recommend oral anticoagulant (OAC) monotherapy in preference to OAC + single antiplatelet agent (SAPT) dual therapy. However, these data are based on the results of only two randomized controlled trials (RCTs) and a relatively small group of patients. Thus, the safety and efficacy of this approach may be underpowered to detect a significant difference. We hypothesized that OAC monotherapy will have a reduced risk of bleeding, but similar all-cause mortality and ischemic outcomes as compared to dual therapy (OAC + SAPT).
METHODS METHODS
A systematic search of PubMed/MEDLINE, EMBASE, and Scopus was conducted. Safety outcomes included total bleeding, major bleeding, and others. Efficacy outcomes included all-cause mortality, cardiovascular mortality, myocardial infarction, stroke, and major adverse cardiovascular events (MACE). RCTs and observational studies were pooled separately (study design stratified meta-analysis). Subgroup analyses were performed for vitamin K antagonists and direct oral anticoagulants (DOACs). Pooled risk ratios (RR) with corresponding 95% confidence intervals (CI) were calculated using the Mantel-Haenszel method.
RESULTS RESULTS
Meta-analysis of 2 RCTs comprising a total of 2905 patients showed that dual therapy (OAC + SAPT) vs. OAC monotherapy was associated with a statistically significant increase in major bleeding (RR 1.51; 95% CI [1.10, 2.06]). There was no significant reduction in MACE (RR 1.10; [0.71, 1.72]), stroke (RR 1.29; [0.85, 1.95]), myocardial infarction (RR 0.57; [0.28, 1.16]), cardiovascular mortality (RR 1.22; [0.63, 2.35]), or all-cause mortality (RR 1.18 [0.52, 2.68]). Meta-analysis of 20 observational studies comprising 47,451 patients showed that dual therapy (OAC + SAPT) vs. OAC monotherapy was associated with a statistically significant higher total bleeding (RR 1.50; [1.20, 1.88]), major bleeding (RR = 1.49; [1.38, 1.61]), gastrointestinal bleeding (RR = 1.62; [1.15, 2.28]), and myocardial infarction (RR = 1.15; [1.05, 1.26]), without significantly lower MACE (RR 1.10; [0.97, 1.24]), stroke (RR 0.93; [0.73, 1.19]), cardiovascular mortality (RR 1.11; [0.95, 1.29]), or all-cause mortality (RR 0.93; [0.78, 1.11]). Subgroup analysis showed similar results for both vitamin K antagonists and DOACs, except a statistically significant higher intracranial bleeding with vitamin K antagonist + SAPT vs. vitamin K antagonist monotherapy (RR 1.89; [1.36-2.63]).
CONCLUSIONS CONCLUSIONS
In patients with AF and stable ischemic heart disease, OAC + SAPT as compared to OAC monotherapy is associated with a significant increase in bleeding events without a significant reduction in thrombotic events, cardiovascular mortality, and all-cause mortality.

Identifiants

pubmed: 36085242
doi: 10.1007/s10840-022-01347-1
pii: 10.1007/s10840-022-01347-1
doi:

Substances chimiques

Platelet Aggregation Inhibitors 0
Anticoagulants 0
Fibrinolytic Agents 0
Vitamin K 12001-79-5

Types de publication

Meta-Analysis Systematic Review Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

493-506

Subventions

Organisme : Academy of Teaching Scholars, University of Oklahoma Health Sciences Center
ID : ATS

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Aamina Shakir (A)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA.

Arsalan Khan (A)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA.

Siddharth Agarwal (S)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA.

Shari Clifton (S)

Robert M Bird Health Sciences Library, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.

Jessica Reese (J)

Department of Biostatistics and Epidemiology, Hudson College of Public Health, Oklahoma City, OK, USA.

Muhammad Bilal Munir (MB)

Section of Electrophysiology, Division of Cardiology, University of California Davis, Sacramento, CA, USA.

Usama Bin Nasir (UB)

Baystate Medical Center, Springfield, MA, USA.

Safi U Khan (SU)

Houston Methodist Hospital, Houston, TX, USA.

Rakesh Gopinathannair (R)

Kansas City Heart Rhythm Institute, Overland Park, MO, USA.

Christopher V DeSimone (CV)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.

Abhishek Deshmukh (A)

Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.

Warren M Jackman (WM)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA.

Stavros Stavrakis (S)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA.

Zain Ul Abideen Asad (ZUA)

Department of Medicine, University of Oklahoma Health Sciences Center, 800 Stanton L. Young Blvd, AAT 5400, Oklahoma City, OK, 73104, USA. drzainasad@gmail.com.

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