Device-detected Atrial FibrillationDDAF-HEVNCT07713615
Blood Clotting Markers and Heart Ultrasound in People With Device-Detected Atrial Fibrillation
An observational study of Device-detected Atrial Fibrillation and Subclinical Atrial Fibrillation, run by Andreas Sjøholm-Christensen at 1 site in Denmark.
Trial summary
The purpose of this observational study is to investigate whether blood tests related to blood clotting are associated with established clinical stroke risk scores, the total amount of device-detected atrial fibrillation recorded by an implanted cardiac device, and ultrasound measurements of the heart in people with… Read more about this study
- Who is it for?
- Ages 50 years and older
- Conditions the study is for
- Device-detected Atrial Fibrillation, Subclinical Atrial Fibrillation, Atrial High Rate Episodes
- How many people
- 222 participants
- Where
- 1 siteDenmark
- Study dates
- 27 Feb 2026to Sep 2037
- How long will I take part?
- 10 Years
- Phase
- Observational
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 50 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Participants will be recruited from the Department of Cardiology, Esbjerg and Grindsted Hospital, University Hospital of Southern Denmark. The study population comprises adults with implanted cardiac devices undergoing routine outpatient device interrogation or home monitoring. The device-detected atrial fibrillation cohort will include participants with at least one episode of device-detected atrial fibrillation lasting ≥30 seconds identified during either during routine device interrogation within the previous 12 months or through home monitoring. The control cohort will comprise participants without device-detected atrial fibrillation during the previous 4 years, recruited from the same outpatient population and matched on age, sex, and indication for cardiac device implantation. All participants will be enrolled consecutively from a single-center cardiology outpatient clinic.
Who may be able to join
- Age > 50 years at inclusion
- Presence of a cardiac implanted electronic device, either:
- A pacemaker or internal cardiac defibrillator with an atrial lead
- An implantable cardiac monitor
- ≥1 episode of device-detected atrial fibrillation lasting ≥30 seconds within the previous 12 months, indentified:
- During routine cardiac implantable electronic device interrogation for patients with a pacemaker or implantable cardiac defibrillator.
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- Through remote monitoring for patients with an implantable cardiac monitor
- The longest episode of device-detected atrial fibrillation must be confirmed by the investigator by review of the stored intracardiac electrogram (EGM) for pacemakers and implantable cardiac defibrillators or review of the single-lead electrogardiogram for implantable cardiac monitors.
- Written informed consent obtained prior to inclusion
Who cannot join
- History of ECG-documented atrial fibrillation at any time prior to inclusion
- Use of oral anticoagulation or dual antiplatelet therapy within 6 months prior to inclusion, irrespective of indication
- Current treatment with oral contraceptives or hormone replacement therapy
- Pregnancy or breastfeeding
- End-stage renal disease (creatinine clearance <15 mL/min, calculated using the Cockcroft-Gault equation)
- Active malignancy, defined as cancer diagnosis not followed by curative treatment within 6 months of diagnosis
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- Major surgery within the last 3 months
- Connective tissue disease requiring treatment
- Acute coronary syndrome, stroke/transient ischemic attack, or venous thromboembolism within 3 months prior to inclusion
- Known thrombophilia
- Clinically significant hepatic or hematological disease requiring treatment and/or specialist follow-up
- Mechanical heart valve, moderate-to-severe mitral stenosis, or other valvular disease requiring intervention
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
Denmark1 site, 1 recruiting
- Recruiting
Department of Cardiology, Esbjerg and Grindsted Hospital, Southwest Denmark
Esbjerg, 6700
Andreas Sjøholm-Christensen, MD, +45 71776422, andreas.sjoholm-christensen@rsyd.dk
Andreas Sjøholm-Christensen, MD
About this study
Official title: Device-Detected Atrial Fibrillation - Haemostatic Profile and Echocardiographic Variables
The purpose of this observational study is to investigate whether blood tests related to blood clotting are associated with established clinical stroke risk scores, the total amount of device-detected atrial fibrillation recorded by an implanted cardiac device, and ultrasound measurements of the heart in people with device-detected atrial fibrillation. The study will also evaluate whether these baseline measurements are associated with future clinical outcomes and may improve future stroke risk assessment.
Device-detected atrial fibrillation is an irregular heart rhythm detected by implanted cardiac devices such as pacemakers, implantable cardiac monitors, and implantable defibrillators. It is often brief and does not cause symptoms. Although it increases the risk of stroke and systemic embolism, the risk is lower than in people with clinically diagnosed atrial fibrillation. As a result, it remains difficult to identify which patients are most likely to benefit from blood-thinning medication, which reduces the risk of stroke but also increases the risk of bleeding.
Read more
The study will include 222 participants with implanted cardiac devices, including 111 participants with device-detected atrial fibrillation and 111 age-, sex-, and cardiac device indication-matched control participants without device-detected atrial fibrillation. At baseline, participants will undergo blood sampling, ultrasound examination of the heart, and routine device interrogation. Information on medical history and established clinical stroke risk factors will also be collected. The implanted cardiac device will be used to determine the total amount of device-detected atrial fibrillation recorded since the last device interrogation.
The baseline analyses will investigate whether established clinical stroke risk scores, the total amount of device-detected atrial fibrillation, and heart ultrasound findings are associated with changes in blood clotting that may indicate an increased tendency to form blood clots. The study will evaluate both primary and additional blood clotting markers to improve the understanding of the biological mechanisms underlying thromboembolic risk in device-detected atrial fibrillation.
Participants will subsequently be followed for 10 years to determine whether baseline blood clotting markers, the total amount of device-detected atrial fibrillation, heart ultrasound findings, and clinical stroke risk scores are associated with future clinical outcomes, including stroke, systemic embolism, hospitalization, death, progression to clinically diagnosed atrial fibrillation, and initiation of oral anticoagulant therapy.
The findings may improve the understanding of thromboembolic risk in people with device-detected atrial fibrillation and support the development of more individualized approaches to future stroke risk assessment and treatment.
Read the detailed description
Scientific Rationale Device-detected atrial fibrillation (DDAF) is associated with an increased risk of stroke and systemic embolism, although the risk is lower than in patients with clinically diagnosed atrial fibrillation. Consequently, it remains challenging to identify which patients are most likely to benefit from oral anticoagulant therapy while minimizing the risk of bleeding. Current stroke risk assessment in patients with device-detected atrial fibrillation relies primarily on clinical risk scores and does not incorporate haemostatic biomarkers, the burden of device-detected atrial fibrillation, or echocardiographic markers of atrial remodeling that may contribute to thromboembolic risk. This study aims to improve the understanding of thromboembolic risk in patients with DDAF and to evaluate whether integrating clinical stroke risk scores, DDAF burden, advanced echocardiographic variables, and haemostatic biomarkers may improve future stroke risk assessment.
Study Design This is a prospective, single-center observational cohort study conducted at the Department of Cardiology, Esbjerg and Grindsted Hospital, University Hospital of Southern Denmark, in collaboration with the Unit for Thrombosis Research, Department of Clinical Diagnostics.
The study consists of a single prospective observational cohort with three prespecified baseline analyses followed by a prospective 10-year longitudinal follow-up. A total of 222 participants will be enrolled, including 111 participants with device-detected atrial fibrillation and 111 control participants matched for age, sex, and indication for cardiac device implantation.
Baseline Assessments At baseline, all participants will undergo standardized blood sampling, comprehensive transthoracic echocardiography, and collection of demographic and clinical information. Device interrogation will be performed to quantify the burden of device-detected atrial fibrillation. Clinical thromboembolic risk will be assessed using the CHA₂DS₂-VASc score. In addition, the ABC-stroke score will be calculated to evaluate its associations with haemostatic biomarkers and subsequent clinical outcomes in participants with device-detected atrial fibrillation.
Independent variables in the prespecified baseline analyses include the CHA₂DS₂-VASc score, the ABC-stroke score, burden of device-detected atrial fibrillation, and advanced echocardiographic variables.
The baseline analyses are designed to address three prespecified objectives. Together, these analyses are intended to determine whether established clinical stroke risk scores, burden of device-detected atrial fibrillation, and cardiac structural and functional abnormalities are associated with a more prothrombotic haemostatic profile.
- To investigate whether the primary haemostatic biomarkers, endogenous thrombin potential (ETP) and von Willebrand factor antigen, differ between participants with device-detected atrial fibrillation and matched controls and whether they are associated with the CHA₂DS₂-VASc and ABC-stroke risk scores. Secondary analyses will evaluate associations between additional haemostatic biomarkers and the clinical stroke risk scores.
- To investigate whether the primary haemostatic biomarkers are associated with the burden of device-detected atrial fibrillation. Secondary analyses will evaluate associations between DDAF burden and additional haemostatic biomarkers.
- To investigate whether the primary haemostatic biomarkers are associated with advanced echocardiographic variables, including left atrial size and function. Secondary analyses will evaluate associations between echocardiographic variables and additional haemostatic biomarkers.
The primary cross-sectional outcome measures are endogenous thrombin potential (ETP) and von Willebrand factor antigen. Secondary cross-sectional outcome measures comprise additional biomarkers of coagulation and fibrinolysis.
Longitudinal Follow-up Participants will subsequently be followed for 10 years through electronic health records, routine device interrogation reports, and Danish national health registries. Follow-up data will be collected every second year to evaluate whether baseline primary and secondary haemostatic biomarkers, DDAF burden, clinical stroke risk scores, and echocardiographic findings are associated with subsequent stroke, systemic embolism, hospitalization, death, progression to clinically diagnosed atrial fibrillation, and initiation of oral anticoagulant therapy.
Statistical Analysis The sample size was calculated to provide 80% statistical power at a two-sided significance level of 5% to detect the expected differences in endogenous thrombin potential and von Willebrand factor antigen between predefined CHA₂DS₂-VASc stroke risk groups, based on previously published effect sizes.
Continuous variables will be assessed for normality using histograms and Q-Q plots. Variables with skewed distributions will be logarithmically transformed where appropriate. Homogeneity of variances will be assessed before parametric analyses. Continuous variables will be summarized as mean ± standard deviation or median with interquartile range according to data distribution, whereas categorical variables will be summarized as frequencies and percentages.
Baseline comparisons between participants with device-detected atrial fibrillation and matched controls will be performed using appropriate parametric or non-parametric statistical methods according to data distribution. Multivariable regression models will be adjusted for predefined confounding variables as appropriate.
The prespecified baseline analyses will primarily be performed using multivariable linear regression models with endogenous thrombin potential and von Willebrand factor antigen as the primary dependent variables. Secondary analyses will evaluate associations with additional haemostatic biomarkers. Regression models will be adjusted for prespecified confounding variables. Continuous predictors will be assessed for approximate linearity, and the assumptions underlying the linear regression models will be evaluated before interpretation of the results. Sensitivity analyses will be performed to evaluate the robustness of the primary findings. Adjustment for multiple testing will be performed using the Holm-Bonferroni procedure.
Longitudinal analyses will evaluate whether baseline haemostatic biomarkers, burden of device-detected atrial fibrillation, clinical stroke risk scores, and echocardiographic findings are associated with subsequent clinical outcomes. Time-to-event analyses will be performed using Cox proportional hazards regression models when appropriate. Hazard ratios with 95% confidence intervals will be reported. Statistical significance will be defined as a two-sided p-value <0.05.
- Conditions
- Device-detected Atrial Fibrillation, Subclinical Atrial Fibrillation, Atrial High Rate Episodes
- Keywords
- Stroke risk, Thromboembolism, ABC-stroke score, Haemostasis, Thrombin generation, von Willebrand factor, Echocardiography, Left atrial function, Cardiac implantable electronic devices, Oral anticoagulation, Biomarkers, Atrial fibrillation burden, CHA₂DS₂-VASc, CHA₂DS₂-VA
- Medical subject headings
- Thromboembolism
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Device-detected atrial fibrillation | Patients with implanted cardiac devices with at least one episode of device-detected atrial fibrillation lasting ≥ 30 seconds within the preceding year, identified during routine device interrogation visits or through remote monitoring. | |
| Matched controls without device-detected atrial fibrillation | Patients with implanted cardiac devices without device-detected atrial fibrillation in the preceding four years, matched 1:1 to cases on age, sex, and indication for device implantation, identified during routine device follow-up visits or through home monitoring. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Thrombin generation assessed by endogenous thrombin potential
Thrombin generation plays a pivotal role in blood clotting and thus serve as primary outcome measure. Thrombin generation will be assessed through measurement of endogenous thrombin potential (nmol/L x min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Levels of von Willebrand factor (vWF) antigen
von Willebrand factor plays an important role in platelet plug formation. von Willebrand factor antigen (%) will be measured using an in-house immunoassay.
Measured: Baseline
Secondary outcomes (50)
Plasma P-selectin Concentration
Plasma concentration of soluble P-selectin antigen (ng/ml) measured using an enzyme-linked immunosorbent assay (ELISA). P-selectin will only be measured in participants with elevated von Willebrand factor antigen concentrations.
Measured: Baseline
Thrombin generation assessed by lag time
Thrombin generation plays a pivotal role in blood clotting. Thrombin generation will be assessed through measurement of lag time (min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline.
Thrombin generation assessed by peak thrombin concentration
Thrombin generation plays a pivotal role in blood clotting. Thrombin generation will be assessed through measurement of peak thrombin concentration (nmol/L), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Thrombin generation assessed by time to peak
Thrombin generation plays a pivotal role in blood clotting. Thrombin generation will be assessed through measurement of time to peak (min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Kallikrein generation assessed by lag time
Kallikrein generation plays an important role in the contact activation system of the secondary hemostasis. Kallikrein generation will be assessed through measurement of lag time (min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
High-sensitivity Cardiac Troponin T (hs-cTnT) Concentration
Plasma concentration of high-sensitivity cardiac troponin T (hs-cTnT) in ng/L measured at baseline
Measured: Baseline
Kallikrein generation assessed by peak kallikrein concentration
Kallikrein generation plays an important role in the contact activation system of the secondary hemostasis. Kallikrein generation will be assessed through measurement of peak kallikrein concentration (nmol/L), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Kallikrein generation assessed by time to peak
Kallikrein generation plays an important role in the contact activation system of the secondary hemostasis. Kallikrein generation will be assessed through measurement of time to peak (min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Kallikrein generation assessed by endogenous kallikrein potential
Kallikrein generation plays an important role in the contact activation system of the secondary hemostasis. Kallikrein generation will be assessed through measurement of endogenous kallikrein potential (nmol/L*min), using the calibrated automated thrombography (CAT) method.
Measured: Baseline
Concentrations of prothrombin fragment 1 + 2
Activation of the inactive prothrombin to the active thrombin will be estimated from concentrations of prothrombin fragment 1 + 2 (pmol/L), using a commercial enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of cleaved high-molecular weight kininogen (cHK)
cHK is an essential component of the contact activation system of the coagulation cascade. cHK (µg/ml) will be measured with the help of enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of coagulation factor XII (FXII)
FXII is an essential component of the contact activation system of the coagulation cascade. FXII (µg/ml) will be measured with the help of enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of prekallikrein
Prekallikrein is an essential component of the contact activation system of the coagulation cascade. Prekallikrein (µg/ml) will be measured with the help of enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of high-molecular weight kininogen (HK)
HK plays a key role in the contact activation system of the coagulation cascade. HK (%) will be measured using enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of C1-inhibitor
C1-inhibitor is the main regulator of the contact activation system. Concentration of C1-inhibitor (g/L) will be measured using nephelometry.
Measured: Baseline
Concentration of coagulation factor VII (FVII)
FVII plays an important role in the secondary hemostasis. Concentration of FVII (%) will be measured using clot assay.
Measured: Baseline
Concentration of coagulation factor X (FX)
FX plays an important role in the secondary hemostasis. Concentration of FX (%) will be measured using clot assay.
Measured: Baseline
Concentration of coagulation factor II (FII)
FII plays an important role in the secondary hemostasis. Concentration of FII (%) will be measured using clot assay.
Measured: Baseline
Concentration of protein C
Protein C is essential for the regulation of the blood coagulation cascade. Concentration of protein C (%) will be measured using chromogenic assay.
Measured: Baseline
Concentration of protein S
Protein S is essential for the regulation of the blood coagulation cascade. Concentration of protein S (%) will be measured using turbidity.
Measured: Baseline
Concentration of antithrombin (AT)
Antithrombin is essential for the regulation of the blood coagulation cascade. Concentration of antithrombin (%) will be measured using chromogenic assay.
Measured: Baseline
Concentration of tissue factor pathway inhibitor (TFPI)
TFPI is important in the regulation of the blood coagulation system. TFPI (pg/ml) will be measured using enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Fibrin turnover assessed by maximum lysis velocity (Vmax)
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of Vmax (optical density (OD)/min) will be conducted.
Measured: Baseline
Fibrin turnover assessed by peak optical density (OD)
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of peak OD (OD) will be conducted.
Measured: Baseline
Fibrin turnover assessed by clot lysis
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of clot lysis (%) will be conducted.
Measured: Baseline
Fibrin turnover assessed by overall hemostatic potential (OHP)
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of OHP (OD x min) will be conducted.
Measured: Baseline
Fibrin turnover assessed by fiber diameter
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of fiber diameter (µm) will be conducted.
Measured: Baseline
Fibrin turnover assessed by fiber density
Fibrin turnover will be assessed through fibrin clot lysis, where measurement of fiber density (x 10^6 Da/cm^3) will be conducted.
Measured: Baseline
Concentration of fibrinogen
Conversion of fibrinogen to fibrin, in which thrombin plays a key role, is essential for blood coagulation. Concentrations of fibrinogen (µmol/L) will be measured using nephelometry.
Measured: Baseline
Concentration of D-dimer
D-dimer is a fibrin degradation product that reflects the fibrinolysis process (the breakdown of fibrin network), which plays a crucial role in preventing blood clots from causing complications. D-dimer (mg/L) will be measured using immunoassay.
Measured: Baseline
Concentration of tissue-type plasminogen activator (t-PA)
t-PA is a protein that stimulates the breakdown of blood clots. It helps convert plasminogen into its active form, plasmin, the major enzyme responsible for the breakdown of blood clots. Concentration of t-PA (ng/ml) will be measured using enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Concentration of plasminogen activator inhibitor 1 (PAI-1)
PAI-1 functions as the inhibitor of t-PA, which will stimulate the formation of blood clots. Concentration of PAI-1 (ng/ml) will be measured using enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
Levels of plasminogen
Plasminogen is the inactive form of plasmin, the major enzyme that breaks down blood clots. Levels of plasminogen (%) will be measured using chromogenic assay.
Measured: Baseline
Levels of coagulation factor XIII (FXIII)
FXIII plays a key role in stabilizing the blood clots. Levels of FXIII will be measured using immunoassay.
Measured: Baseline
Levels of plasmin inhibitor (PI)
PI is the major inhibitor of plasmin. Levels of PI (%) will be measured using chromogenic assay.
Measured: Baseline
Levels of thrombin activatable fibrinolysis inhibitor (TAFI)
TAFI is an enzyme that is activated by thrombin, which downregulates fibrinolysis, stimulating blood clot formation. Levels TAFI will be measured using enzyme-linked immunosorbent assay (ELISA).
Measured: Baseline
ADAMTS13 Antigen Concentration
Plasma concentration of ADAMTS13 antigen (ng/mL) measured using an enzyme-linked immunosorbent assay (ELISA). ADAMTS13 will only be measured in participants with elevated von Willebrand factor antigen concentrations.
Measured: Baseline
N-terminal Pro-B-type Natriuretic Peptide (NT-proBNP) Concentration
Plasma concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in ng/L measured at baseline.
Measured: Baseline
Stroke
Clinical stroke verified with imaging e.g. CT or MR.
Measured: Up to 10 years.
Transient Ischemic Attack
Transient Ischemic Attack verified with imaging e.g. CT or MR
Measured: Up to 10 years
Systemic embolism
Systemic embolism verified with imaging e.g. CT, MR or ultrasound
Measured: Up to 10 years
Hospitalizations
All cause hospitalizations
Measured: Up to 10 years
Heart failure hospitalizations
New onset or worsening of heart failure leading to hospitalization or urgent visit heart failure clinic
Measured: Up to 10 years
All-cause mortality
All-cause mortality
Measured: Up to 10 years
Cardiovascular death
Cardiovascular death
Measured: Up to 10 years
Progression to clinically diagnosed atrial fibrillation or atrial flutter
Atrial fibrillation or flutter verified by a 12-lead ECG or ambulatory ECG monitoring
Measured: Up to 10 years
Progression to >24 hours device-detected atrial fibrillation
Progression to >24 hours device-detected atrial fibrillation at a scheduled out-of hospital or acute cardiac device interrogation
Measured: Up to 10 years.
Initiation of oral anticoagulant therapy
Initiation of oral anticoagulant therapy with minimum 3 months treatment duration.
Measured: Up to 10 years
Pulmonary embolism
Pulmonary embolism verified with imaging e.g. CT or V/Q scan
Measured: Up to 10 years
Deep venous thrombosis
Deep venous thrombosis verified with radiology e.g. ultrasound or CT
Measured: Up to 10 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted20 Jul 2026
- Study start27 Feb 2026
- Primary completionFeb 2029 (estimated)
- Study completionSep 2037 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Device-detected Atrial FibrillationStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 222 participants (estimated)
- Target duration
- 10 Years
Sponsor and investigators
- Lead sponsor
- Andreas Sjøholm-Christensen
- Sponsor type
- University, hospital or other
- Collaborators
- Sydvestjysk Kardiologisk Fond, Grosserer L.F. Foghts Foundation, Region of Southern Denmark, Karola Jørgensens Foundation and Foundation for Cardiology in Southwest Denmark., The A.P. Moeller Foundation, Odense Patient Data Explorative Network, The Simon Spies Foundation, The foundation of Fam. Kjærsgaard, Sunds
- Responsible party
- Sponsor-investigator, Andreas Sjøholm-Christensen, University of Southern Denmark
- Investigators
- Andreas Sjøholm-Christensen, MD, Principal investigator, Region of Southern Denmark
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07713615
- Sponsor's protocol ID
- 116655
- Acronym
- DDAF-HEV
- Status last verified
- Oct 2026
- First submitted
- 8 Jul 2026
- Last updated
- 15 Oct 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: Individual participant data will not be shared publicly due to privacy regulations and ethical restrictions. Aggregated data will be reported in publications.
Publications
Hijazi Z, Lindback J, Alexander JH, Hanna M, Held C, Hylek EM, Lopes RD, Oldgren J, Siegbahn A, Stewart RA, White HD, Granger CB, Wallentin L; ARISTOTLE and STABILITY Investigators. The ABC (age, biomarkers, clinical history) stroke risk score: a biomarker-based risk score for predicting stroke in atrial fibrillation. Eur Heart J. 2016 May 21;37(20):1582-90. doi: 10.1093/eurheartj/ehw054. Epub 2016 Feb 25.
PubMed 26920728Thomas L, Hoy M, Byth K, Schiller NB. The left atrial function index: a rhythm independent marker of atrial function. Eur J Echocardiogr. 2008 May;9(3):356-62. doi: 10.1016/j.euje.2007.06.002. Epub 2007 Aug 7.
PubMed 17689293Glowicki B, Matusik PT, Plens K, Undas A. Prothrombotic State in Atrial Fibrillation Patients With One Additional Risk Factor of the CHA2DS2-VASc Score (Beyond Sex). Can J Cardiol. 2019 May;35(5):634-643. doi: 10.1016/j.cjca.2019.01.014. Epub 2019 Jan 30.
PubMed 30955928Kundrick J, Saba KI, Naniwadekar A, Singla V, Mulukutla S, Thoma F, Bhonsale A, Kancharla K, Voigt A, Shalaby AA, Estes Iii NAM, Jain S, Saba S. Diastolic Dysfunction and the Risk of Stroke and Major Bleeding. Stroke. 2024 Dec;55(12):2856-2862. doi: 10.1161/STROKEAHA.124.048287. Epub 2024 Nov 11.
PubMed 39523999Suwa Y, Miyasaka Y, Taniguchi N, Harada S, Nakai E, Shiojima I. Atrial fibrillation and stroke: importance of left atrium as assessed by echocardiography. J Echocardiogr. 2022 Jun;20(2):69-76. doi: 10.1007/s12574-021-00561-6. Epub 2022 Jan 23.
PubMed 35066798Alonso A, Tang W, Agarwal SK, Soliman EZ, Chamberlain AM, Folsom AR. Hemostatic markers are associated with the risk and prognosis of atrial fibrillation: the ARIC study. Int J Cardiol. 2012 Mar 8;155(2):217-22. doi: 10.1016/j.ijcard.2010.09.051. Epub 2010 Oct 20.
PubMed 20965585Wu N, Chen X, Cai T, Wu L, Xiang Y, Zhang M, Li Y, Song Z, Zhong L. Association of inflammatory and hemostatic markers with stroke and thromboembolic events in atrial fibrillation: a systematic review and meta-analysis. Can J Cardiol. 2015 Mar;31(3):278-86. doi: 10.1016/j.cjca.2014.12.002. Epub 2014 Dec 9.
PubMed 25746020Undas A. Altered fibrin clot properties and fibrinolysis in patients with atrial fibrillation: practical implications. Europace. 2020 Feb 1;22(2):185-194. doi: 10.1093/europace/euz271.
PubMed 31625555Becher N, Toennis T, Bertaglia E, Blomstrom-Lundqvist C, Brandes A, Cabanelas N, Calvert M, Camm AJ, Chlouverakis G, Dan GA, Dichtl W, Diener HC, Fierenz A, Goette A, de Groot JR, Hermans ANL, Lip GYH, Lubinski A, Marijon E, Merkely B, Mont L, Ozga AK, Rajappan K, Sarkozy A, Scherr D, Schnabel RB, Schotten U, Sehner S, Simantirakis E, Vardas P, Velchev V, Wichterle D, Zapf A, Kirchhof P. Anticoagulation with edoxaban in patients with long atrial high-rate episodes >/=24 h. Eur Heart J. 2024 Mar 7;45(10):837-849. doi: 10.1093/eurheartj/ehad771.
PubMed 37956458McIntyre WF, Benz AP, Healey JS, Connolly SJ, Yang M, Lee SF, Field TS, Alings M, Benezet-Mazuecos J, Boriani G, Nielsen JC, Gold MR, Pergolini F, Glotzer TV, Granger CB, Lopes RD. Risk of Stroke or Systemic Embolism According to Baseline Frequency and Duration of Subclinical Atrial Fibrillation: Insights From the ARTESiA Trial. Circulation. 2024 Nov 26;150(22):1747-1755. doi: 10.1161/CIRCULATIONAHA.124.069903. Epub 2024 Sep 4.
PubMed 39229707Van Gelder IC, Healey JS, Crijns HJGM, Wang J, Hohnloser SH, Gold MR, Capucci A, Lau CP, Morillo CA, Hobbelt AH, Rienstra M, Connolly SJ. Duration of device-detected subclinical atrial fibrillation and occurrence of stroke in ASSERT. Eur Heart J. 2017 May 1;38(17):1339-1344. doi: 10.1093/eurheartj/ehx042.
PubMed 28329139McIntyre WF, Benz AP, Becher N, Healey JS, Granger CB, Rivard L, Camm AJ, Goette A, Zapf A, Alings M, Connolly SJ, Kirchhof P, Lopes RD. Direct Oral Anticoagulants for Stroke Prevention in Patients With Device-Detected Atrial Fibrillation: A Study-Level Meta-Analysis of the NOAH-AFNET 6 and ARTESiA Trials. Circulation. 2024 Mar 26;149(13):981-988. doi: 10.1161/CIRCULATIONAHA.123.067512. Epub 2023 Nov 12.
PubMed 37952187Schnabel RB, Benezet-Mazuecos J, Becher N, McIntyre WF, Fierenz A, Lee SF, Goette A, Atar D, Bertaglia E, Benz AP, Chlouverakis G, Birnie DH, Dichtl W, Blomstrom-Lundqvist C, Camm AJ, Erath JW, Simantirakis E, Kutyifa V, Lip GYH, Mabo P, Marijon E, Rivard L, Schotten U, Alings M, Sehner S, Toennis T, Linde C, Vardas P, Granger CB, Zapf A, Lopes RD, Healey JS, Kirchhof P. Anticoagulation in device-detected atrial fibrillation with or without vascular disease: a combined analysis of the NOAH-AFNET 6 and ARTESiA trials. Eur Heart J. 2024 Dec 7;45(46):4902-4916. doi: 10.1093/eurheartj/ehae596.
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