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Atrial fibrillation (AF) can be newly detected in approximately one-fourth of patients with ischemic stroke and transient ischemic attack without previously recognized AF. We present updated evidence supporting that AF detected after stroke or transient ischemic attack (AFDAS) may be a distinct clinical entity from AF known before stroke occurrence (known atrial fibrillation). Data suggest that AFDAS can arise from the interplay of cardiogenic and neurogenic forces. The embolic risk of AFDAS can be understood as a gradient defined by the prevalence of vascular comorbidities, the burden of AF, neurogenic autonomic changes, and the severity of atrial cardiopathy. The balance of existing data indicates that AFDAS has a lower prevalence of cardiovascular comorbidities, a lower degree of cardiac abnormalities than known atrial fibrillation, a high proportion (52%) of very brief (<30 seconds) AF paroxysms, and is more frequently associated with insular brain infarction. These distinctive features of AFDAS may explain its recently observed lower associated risk of stroke than known atrial fibrillation. We present an updated ad-hoc meta-analysis of randomized clinical trials in which the association between prolonged cardiac monitoring and reduced risk of ischemic stroke was nonsignificant (incidence rate ratio, 0.90 [95% CI, 0.71–1.15]). These findings highlight that larger and sufficiently powered randomized controlled trials of prolonged cardiac monitoring assessing the risk of stroke recurrence are needed. Meanwhile, we call for further research on AFDAS and stroke recurrence, and a tailored approach when using prolonged cardiac monitoring after ischemic stroke or transient ischemic attack, focusing on patients at higher risk of AFDAS and, more importantly, at higher risk of cardiac embolism.

Graphical Abstract

Approximately 7.8 million incident ischemic strokes occur worldwide each year.1 Around 20% to 30% of patients with ischemic stroke and transient ischemic attack (TIA) have known atrial fibrillation (KAF) diagnosed before their stroke.2,3 Among the remaining 70% to 80% without known arrhythmias, up to 24% can be newly diagnosed with atrial fibrillation (AF) after intensive cardiac monitoring (Figure 1A), yielding a rough estimate of 1.3 to 1.5 million new cases of AF detected after stroke or TIA (AFDAS) globally each year.4–6 These estimates are derived from Western populations and may not entirely represent the reality of other regions. Also, while KAF is a well-established cause of ischemic stroke, the role of AFDAS as a definite causal mechanism is disputed in specific circumstances.7
Figure 1. Relative frequency of heart rhythms in acute ischemic stroke and transient ischemic attack. A, Proportions of heart rhythms among patients with ischemic stroke. B, Characteristics and outcomes of atrial fibrillation detected after stroke (AFDAS) relative to known atrial fibrillation before stroke (KAF), *Charts were created from estimates from the meta-analysis of Fridman et al.19 Percentages are derived from odds ratios (ORs) for dichotomic variables and standardized mean differences (SMD) for continuous variables evaluating the association between patients characteristics or outcomes and AFDAS relative to KAF. †Estimates for insular cortex involvement were not available. The higher frequency of insular involvement was observed in 2 studies.21,22 AF indicates atrial fibrillation; CAD, coronary artery disease; CHF, congestive heart failure; LV, left ventricular; MI, myocardial infarction; PAD, peripheral artery disease; and PCM, prolonged cardiac monitoring.
Age is consistently associated with increased risk of AFDAS and is included in almost all scores developed for predicting AFDAS (Table S2).8 The adjusted incidence of AFDAS after controlling for cardiovascular comorbidities and risk factors may be higher in White patients compared with Hispanic or Black patients.9 Racial differences in the risk of AFDAS might be explained by a smaller left atrial size10 and a lower prevalence of left atrial cardiopathy11 among Hispanic and Black individuals with cryptogenic stroke. Data from the Ontario Stroke Registry suggest that women are 49% more likely to be diagnosed with AFDAS (unadjusted odds ratio, 1.49 [95% CI, 1.26-1.76]).3 However, in a recent study of cryptogenic ischemic stroke individuals with implantable loop recorders (ILR), sex was not associated with increased AFDAS risk.12


Terms currently used when reporting the incident detection of AF in individuals with ischemic stroke or TIA do not accurately reflect the nature of AFDAS. “Post-stroke AF” implies that AF episodes occurred only after the stroke, which is not entirely accurate since AF paroxysms may have been present before stroke occurrence.13,14 “Occult,” “Silent,” “Covert,” and “Subclinical” AF may be misleading terms, as suggested in a recent Position Statement of the American Heart Association proposing that despite the absence of AF-specific symptoms, subjects with otherwise subclinical AF who develop a stroke should no longer be considered as having asymptomatic AF.15 “Newly diagnosed AF” is more technically correct but nonspecific and frequently used in the general population, and does not acknowledge the relationship between the AF and the stroke or TIA. “Paroxysmal AF” portrays an intermittent AF pattern and is ambiguous regarding the timing of AF diagnosis relative to stroke occurrence and the type of patients (eg, general population versus stroke patients).16 AFDAS was introduced in 2017 as a new term to acknowledge that this specific AF is detected after stroke or TIA occurrence, can be either paroxysmal or permanent, prevalent or incident, and has distinctive clinical and prognostic characteristics.17

Classification of Cardiac Rhythm in Patients With Stroke and TIA

We have previously proposed that heart rhythm in patients with stroke and TIA should be grouped under 3 categories: (a) no-AF (including sinus rhythm and other non-AF rhythms); (b) known AF (KAF)—AF diagnosed before stroke onset; and (c) AFDAS.17 AFDAS is defined as a newly detected AF after ischemic stroke or TIA in patients without KAF. In the past, any AF detected on admission ECG, inpatient cardiac monitoring, or outpatient AF screening technologies in patients with ischemic stroke or TIA without KAF was considered AFDAS. AFDAS detected on admission ECG are likely high burden, resembling KAFs. For future research, we suggest not considering AFs detected on admission ECG as AFDAS, since it is unclear if they represent newly diagnosed AFs or a KAFs that was undiagnosed before the stroke.18
The distinction between KAF and AFDAS is based on different detection time frames and clinical and prognostic characteristics. Patients with AFDAS have a lower CHA2DS2-VASc score, lower prevalence of vascular comorbidities, a higher left ventricular ejection fraction, and smaller mean atrial diameter than those with KAF (Figure 1B).19 Furthermore, the risk of stroke recurrence was found to be lower than KAF, possibly because of the overall lower burden of cardiovascular comorbidities (Figure 1B). Together, these data suggest that, on average, AFDAS cases have less abnormal cardiac substrate than KAF, although early atrial cardiopathy not evident on standard echocardiography has not been rigorously compared in these groups. Involvement of the insular cortex, a trigger for neurogenic cardiac changes,20 is associated with AFDAS detection,8 and more frequent in AFDAS than KAF.21,22 As such, in contrast with KAF, AFDAS may also occur in stroke and TIA patients with less severe vascular profiles, apparently structurally healthier hearts, and sometimes triggered by neurogenic phenomena (eg, involvement of the insular cortex).

Cardiogenic and Neurogenic Pathophysiology

Conceptually, AFDAS can be thought to arise from the interplay of 2 forces: cardiogenic and neurogenic (Figure 2, graphic abstract).
Figure 2. Gradient of embolic risk in known atrial fibrillation before stroke (KAF) and atrial fibrillation detected after stroke (AFDAS), underlying atrial cardiopathy progresses with age and increasing burden of cardiovascular risk factors, leading to increased embolic risk and higher risk of atrial fibrillation (AF). Poststroke neurogenic mechanisms, including stroke-induced heart injury (SIHI), autonomic surges, and inflammation, contribute to increasing the severity of atrial cardiopathy and the burden of AF, and can trigger incident AF paroxysms.

Cardiogenic and Neurogenic Factors

Patients with cardiogenic risk factors leading to AFDAS likely have a substantial degree of atrial cardiopathy and systemic vascular risk factors.23 They may have had undiagnosed episodes of AF before stroke onset, with the AF remaining undiagnosed until patients underwent prolonged cardiac monitoring (PCM) poststroke.
Neurogenic AFDAS mechanisms have been recognized as part of the recently described Stroke-Heart Syndrome.24,25 Neurogenic factors involve autonomic and inflammatory mechanisms24,26 triggering focal ectopic firing at the ganglionated plexi and, at a later stage, reentry mechanisms related to stroke-induced heart injury (eg, subendocardial hemorrhage).7,27 A rat model has demonstrated the development of left atrial endothelial dysfunction, inflammation, and fibrosis early after the induction of selective right and left insular stroke.28 Significant differences relative to control rats in left atrial fibrosis were observed as early as 14 days after stroke.28 Importantly, an average of 5% to 6% of the left atrium showed fibrosis already at 28 days poststroke, and the extent of tissue scarring correlated with the severity of stroke-related microglia activation. Thus, the development of neurogenic AF poststroke not only has a physiological component (autonomic dysfunction and inflammation) but also seems to be explained by a stroke-related sudden increase in the severity of left atrial substrate, which has been described as stroke-induced heart injury or SIHI (Figure 2, graphic abstract).24,28 It has been proposed that AFDAS can occur in the absence of clinically or echocardiographically evident structural heart disease, as a consequence of neurogenic mechanisms.7,29 However, more subtle features of subclinical atrial cardiopathy that are not yet routinely measured in clinical practice such as left atrial strain likely contribute to lowering the arrhythmogenesis threshold in the presence of neurogenic mechanisms.30 This is reinforced by sham rats showing a mild degree of age-related atrial fibrosis in the absence of cerebrovascular events.28 Patients with a predominance of neurogenic mechanisms and less severe atrial cardiopathy would be expected to have a lower burden of AFDAS. The high proportion of very low burden AF31 and the frequent involvement of the insular cortex in AFDAS compared with KAF19 support this concept.

Finding AFDAS

Predictors of AFDAS

The lack of benefit of oral anticoagulants relative to aspirin in recent clinical trials of patients with embolic stroke of undetermined source requires a refinement of PCM strategies.32 The best screening strategy for AFDAS in patients with ischemic stroke and TIA is yet to be determined. Identifying patients more likely to be diagnosed with AFDAS on PCM is crucial for the efficient use of resources and for ensuring that high-risk patients receive and adhere to PCM. The biomarkers most consistently associated with the diagnosis of AFDAS are age,33 left atrial enlargement,34 increased cardiac natriuretic peptides,33 and premature atrial complexes.35 Measuring cardiac troponin is recommended in stroke prevention guidelines and is done as part of the regular workup in most stroke centers.36 An elevation of >20% in cardiac troponin in the days after the baseline measurement performed on admission has been described as the “rise and fall” pattern, which is associated with insular cortex involvement.37 Several other biomarkers for AFDAS detection have been described less consistently. Additionally, over 20 scores have been developed for predicting AFDAS occurrence or detection, and only a few of them have been validated externally (Table S2). Comprehensive head-to-head comparisons of available scores are lacking.
In summary, natriuretic peptides and chronic elevation of cardiac troponin are biomarkers of cardiogenic factors contributing to AFDAS pathophysiology, whereas cardiac troponin’s “rise and fall” pattern constitutes a promising candidate biomarker for differentiating neurogenic versus cardiogenic contributions to AFDAS.

Minimum AF Duration Threshold for the Diagnosis of AFDAS

Cardiac arrhythmias with electrocardiographic characteristics of AF should last ≥30 seconds to be considered AF.38 This threshold was established in a consensus conference and has been carried forward for over 14 years in clinical guidelines and randomized controlled trials.38 However, it has not been sufficiently validated and has not been widely accepted among stroke physicians.39 Stroke physicians are 2x more prone to accept a <30 second-AF paroxysm as proof of AF39 because detecting very short-lasted AFs in stroke patients may not entail the same stroke risk as 30-second AFs in the general population. Furthermore, most evidence on AF duration and its association with stroke risk comes from studies performed in patients with cardiac implantable electronic devices and considerable underlying heart disease, not representing the overall stroke population.40
Importantly, AFDAS lasting <30 seconds is highly prevalent among stroke patients.31 In our updated meta-analysis (Supplemental Methods) including 18 studies and 4782 patients, AFDAS lasting <30 seconds comprised 52% (95% CI, 36%–66%) of all newly detected AFs (Figure S2). The burden of vascular comorbidities, clinical characteristics, and risk of recurrent stroke of AFDAS lasting <30 seconds and ≥30 seconds have not been compared.

Duration of Cardiac Monitoring

A recent meta-analysis of ILR studies has shown an independent association between duration of PCM and AFDAS detection yield.41 Randomized controlled trials have proven that, relative to usual care, AFDAS detection rates are 6x higher with 6-month ILR and 5x higher with 30-day external event-triggered recorders.4,5 The relative yield of both technologies was recently compared in the Post-Embolic Rhythm Detection with Implantable Versus External Monitoring (PER DIEM) randomized clinical trial, which showed a 3x higher AFDAS detection rate with ILR than with 30-day external loop recorders at 12 months.42

AFDAS After Noncryptogenic Stroke

In the STROKE-AF (Stroke of Known Cause and Underlying Atrial Fibrillation) study, patients with strokes caused by large- or small-vessel disease showed an AFDAS detection rate of 12.1% at 12 months on ILR.43 This high detection rate in noncryptogenic strokes indicates that AFDAS can be frequently detected even in settings where it likely did not play a direct causative embolic role in the stroke being invested. Its significance in this setting lies in its potential embolic risk for future stroke.

AFDAS and Risk of Stroke Recurrence, Death, and Dementia

Embolic Risk Spectrum of AFDAS

Like KAF, AFDAS comprises a spectrum of phenotypes with varying degrees of embolic risk. Conceptually, the embolic risk of AFDAS can be understood as a gradient defined by the prevalence of vascular comorbidities and the severity of atrial cardiopathy (Figure 2, graphic abstract). Indeed, elevated natriuretic peptides44 and left atrial enlargement,45 reliable markers of advanced atrial cardiopathy, are strong predictors of stroke risk in patients with AF. The contribution of noncardioembolic mechanisms such as carotid atherosclerosis or small vessel disease may also play a role in patients with high-risk AFDAS who have a higher burden of risk factors. The burden of AFDAS is the total amount of time spent on AF during PCM and may reflect the severity of underlying atrial cardiopathy.44,45 It is unknown to what extent AFDAS burden increases embolic risk beyond the severity of atrial substrate and whether there is a specific threshold defining high or low risk of embolism.44,45
Quantifying the embolic risk of AFDAS based on biomarkers, genetics, neuroimaging patterns, and cardiovascular comorbidities is needed for a more efficient and tailored diagnostic and therapeutic approach. Although some AFDAS may entail a relatively low risk of stroke recurrence, their detection requires close follow-up and the medical management of risk factors to prevent its progression to higher-risk AF.

AFDAS and Risk of Stroke Recurrence

In a recent meta-analysis, AFDAS had a significantly lower risk of stroke recurrence than KAF.19 Whether AFDAS has a different risk of stroke recurrence than no-AF is less known. We therefore pooled data from 5 observational studies with 71 714 patients reporting the adjusted risk of stroke recurrence in AFDAS versus no-AF (Supplemental Methods). We did not include studies without adjusted time-to-event analyses, given the possibility of confounding and the need to account for the use of oral anticoagulants whenever possible. In this ad-hoc meta-analysis, AFDAS was associated with doubled risk of stroke recurrence than no-AF (HR, 1.98 [95% CI, 1.50−2.59]; Figure 3A).
Figure 3. Adjusted risk of recurrent stroke and death in atrial fibrillation detected after stroke (AFDAS) relative to no-atrial fibrillation (AF). A, Risk of stroke recurrence. B, Risk of death. References for each study are provided in the Supplemental Material. Kamel et al: adjusted for age, sex, and previous ischemic stroke. Ntaios at al. adjusted for age and days of hospitalization. Lip et al: adjusted for CHA2DS2-VASc score, type of event (stroke vs transient ischemic attack [TIA]), and setting (inpatient vs emergency department visit). Sposato et al: adjusted for age, sex, stroke severity, systemic hypertension, diabetes, congestive heart failure, coronary artery disease, prior history of stroke, prior history of TIA, history of dementia, modified Rankin Scale score at discharge, and prescription of oral anticoagulants at discharge. Yang et al.: adjusted for age, sex, stroke severity, systemic hypertension, diabetes, congestive heart failure, coronary artery disease, peripheral artery disease, myocardial infarction, prior history of stroke or transient ischemic attack, and prescription of anticoagulants at discharge. Bhatla et al: adjusted for age, sex, race, hypertension, diabetes, obesity, prevalent heart failure, prevalent coronary artery disease, chronic kidney disease, vascular disease, and anticoagulant and antiplatelet medications considered as time-dependent covariates. Bhatla et al: ≤6 mo, AFDAS detected within 6 mo after stroke; >6 mo, AFDAS detected after 6 mo poststroke.

AFDAS and Risk of Death

The risk of death in patients with AFDAS is similar to KAF, as shown in a meta-analysis of 7 studies and 9246 patients (odds ratio, 0.87 [95% CI, 0.56–1.37]).19 We performed an ad-hoc meta-analysis including 3 studies and 4040 patients to compare the risk of death between AFDAS and no-AF (Supplemental Methods). We found a 60% higher risk of death in AFDAS relative to no-AF (HR, 1.60 [95% CI, 1.38−1.85]; Figure 3B).

AFDAS and Risk of Dementia

Compared with no-AF, AFDAS is associated with increased risk of dementia, regardless of whether it is diagnosed during stroke admission (HR, 1.78 [95% CI, 1.51–2.10]) or in the outpatient setting (HR, 1.74 [95% CI, 1.47–2.05]).46

Role of Oral Anticoagulation in Patients With AFDAS

Anticoagulation in AFDAS Detected With Unselected Diagnostic Methods

In a retrospective, population-based, observational study based on administrative claims, oral anticoagulants were associated with 41% lower adjusted risk of stroke recurrence and 29% lower adjusted risk of death in patients with AFDAS, without differences in the incidence of intracerebral hemorrhage (Hsu et al. Asian Oceanian Congress of Neurology 2021. Available at Accessed on October 2, 2021). Oral anticoagulants have also been associated with a 40% lower adjusted risk of incident dementia in first-ever ischemic stroke patients with AFDAS.46 The abovementioned studies included cohorts of unselected AFDAS patients in which the diagnosis of AF was made based on the retrospective analysis of administrative data. Indeed, a study based on the same population of one of these studies showed that <1% of the stroke population received at least >48 hours of Holter monitoring at 30 days post-discharge.47 As such, the association between anticoagulants use and lower risk of stroke and dementia in these populations is likely driven by non-PCM-detected AFDAS, which are likely high burden and associated with more cardiovascular comorbidities.48 The role of anticoagulants for reducing the risk of stroke recurrence in PCM-detected AFDAS (generally lower burden, as shown above) is less clear, as discussed in the next section.

Anticoagulation in PCM-Detected AFDAS

Secondary analyses from randomized controlled trials suggest that individuals undergoing PCM are more likely to be started on oral anticoagulants than those receiving standard of care at 90 days (18.6% versus 11.1%, P=0.01),4 6 months (10.1% versus 4.6%, P=0.04),5 and 12 months (14.7% versus 6.0%, P=0.007).5 Similar estimates were derived from 2 recent meta-analyses showing higher anticoagulation initiation rates among patients undergoing PCM relative to usual care.12,49
Although PCM is associated with increased use of oral anticoagulants, whether higher PCM-related anticoagulation rates result in fewer recurrent strokes remains unclear. In other words, are all patients with PCM-detected AFDAS suitable candidates for anticoagulation? A recent meta-analysis including 1102 patients from 2 observational studies and 2 randomized controlled trials found a significant 55% lower relative risk of stroke recurrence associated with PCM use.49 Since a relatively large number of articles were published after this work, we updated this meta-analysis by including 4 observational studies and 6 randomized controlled trials of PCM versus standard of care to pool incidence rate ratios for the recurrence of ischemic stroke. We additionally investigated other secondary end points, including ischemic stroke or TIA, any stroke (ischemic or hemorrhagic), and any stroke or TIA associated with the use of PCM versus standard of care (Supplemental Methods). The incidence rate ratio for recurrent ischemic stroke associated with PCM in randomized controlled trials was 0.90 (95% CI, 0.71–1.15). Results were similar for all other end points (Figure 4; Figures S5, S7, S9, and S11) and did not change significantly in sensitivity analyses including a study comparing 2 different-duration PCM modalities (Figures S6, S8, S10, and S12).42 It must be noted that duration of cardiac monitoring in one of the studies was only 72 hours in the PCM and the control groups.50 Regardless, the associations between PCM and lower risk of stroke recurrence may have been stronger if limited to AFDAS cases with a high associated risk of future cardiac embolism, underscoring the need for a more personalized selection of patients who are most likely to benefit from oral anticoagulation (eg, high prevalence of atrial cardiopathy). Identifying these patients could contribute to lessening the risk of unnecessary anticoagulation and related hemorrhages in lower-risk patients, especially for those who require antiplatelet therapy (eg, coronary stents or intracranial atherosclerosis).
Figure 4. Prolonged cardiac monitoring and risk of recurrent cerebrovascular events. References for each study are provided in the Supplemental Material. IRR indicates incidence rate ratio; and TIA, transient ischemic attack. *Primary end point.
The results of ongoing randomized controlled trials evaluating the effect of PCM on the risk of recurrent strokes are not yet available. The Intensive Rhythm Monitoring to Decrease Ischemic Stroke and Systemic Embolism (FIND-AF2) Trial compares 7-day Holter monitoring, ILR, and standard of care (URL:; Unique identifier: NCT04371055). The primary efficacy end point is recurrent ischemic stroke or systemic embolism. The Home-Based Solution for Remote Atrial Fibrillation Screening to Prevent Recurrence Stroke Trial (HUA-TUO AF Trial) compares remote cardiac monitoring with a handheld single-lead ECG recorder versus usual care (URL:; Unique identifier: NCT04523649). The primary efficacy end point is AFDAS detection, whereas secondary end points are recurrent stroke and recurrent TIA. Post hoc analyses of these trials may help identify AFDAS phenotypes more likely to benefit from oral anticoagulation. The ARCADIA trial (Atrial Cardiopathy and Antithrombotic Drugs in Prevention After Cryptogenic Stroke Randomized)51 is comparing apixaban versus aspirin in patients with embolic stroke of undetermined source and atrial cardiopathy. If ARCADIA proves that apixaban is better than aspirin, it may pave the way toward more of a focus on the underlying atrial substrate to guide anticoagulation.


Evidence suggests that AFDAS is different from KAF and possibly bears an overall lower risk of stroke. The relatively more benign prognosis of AFDAS is explained by a gradient of embolic risk determined by the interplay of cardiogenic and neurogenic factors. Future research should focus on characterizing AFDAS phenotypes and their associated risk of stroke. For now, the prevailing practice pattern is for AFDAS patients to receive oral anticoagulants unless contraindicated.36 To date, there is no proof that applying PCM leads to fewer stroke recurrences. Available evidence does not indicate that PCM has an impact on the risk of recurrent ischemic stroke, although existing studies are underpowered and more research is needed. Patients with embolic strokes of undetermined source, especially those with other biomarkers (eg, enlarged left atrium, intraatrial block, high burden premature atrial complexes), should be considered for AF screening until the results of ongoing clinical trials are available.51 We acknowledge that conducting a randomized controlled trial comparing antiplatelet agents versus direct oral anticoagulants in patients with PCM-detected AFDAS would be challenging. The vast majority of clinicians currently prescribe anticoagulation for patients with AFDAS, perhaps partly because current clinical guidelines strongly recommend the use of oral anticoagulants in patients with AF and a recent ischemic stroke, without discriminating between KAF and AFDAS. Two ongoing trials, ARTESiA (URL:; Unique identifier: NCT01938248) and NOAH (URL:; Unique identifier: NCT02618577), are comparing anticoagulation versus antiplatelet therapy for patients with device-detected subclinical AF. Although they are not focused on patients with recent stroke, their findings will nevertheless help shed some light on this issue. In the meantime, we hope that the present work will contribute to highlighting the unique characteristics of AFDAS and the need for better individualizing prevention strategies among these patients.

Article Information

Supplemental Material

Supplemental Methods
Tables S1–S7
Figures S1–S17
Reference 60


We thank Dr Juan Camilo Vargas Gonzalez for performing the statistical analyses and data-extraction, and Dr Amado Jimenez-Ruiz for his participation in the systematic search.


Nonstandard Abbreviations and Acronyms

atrial fibrillation
atrial fibrillation detected after stroke or transient ischemic attack
Atrial Cardiopathy and Antithrombotic Drugs in Prevention After Cryptogenic Stroke Randomized
implantable loop recorder
known atrial fibrillation
odds ratio
prolonged cardiac monitoring
Stroke of Known Cause and Underlying Atrial Fibrillation
transient ischemic attack

Supplemental Material

File (str_stroke-2021-034777_supp2.pdf)


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Published online: 5 January 2022
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  1. atrial fibrillation
  2. brain infarction
  3. incidence
  4. ischemic attack, transient
  5. prevalence




Departments of Clinical Neurological Sciences, Epidemiology and Biostatistics and Anatomy and Cell Biology; Schulich School of Medicine and Dentistry (L.A.S.), Western University, London, Canada.
Heart & Brain Laboratory (L.A.S.), Western University, London, Canada.
Robarts Research Institute (L.A.S.), Western University, London, Canada.
Lawson Health Research Institute, London, Canada (L.A.S.).
Department of Neurology & Stroke Program, University of Maryland School of Medicine, Baltimore (S.C.).
Department of Neurology, Tainan Sin Lau Hospital, Taiwan (C.-Y.H.).
Libin Cardiovascular Institute, Department of Cardiac Sciences, University of Calgary, AB, Canada (C.A.M.).
Clinical and Translational Neuroscience Unit, Feil Family Brain and Mind Research Institute and Department of Neurology, Weill Cornell Medicine, New York (H.K.).


The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
Supplemental Material is available at Supplemental Material.
For Sources of Funding and Disclosures, see page e101.
Correspondence to: Luciano A. Sposato, MD, MBA, 339 Windermere Rd, London, Ontario N6A 5A5, Canada. Email [email protected]


Dr Sposato is speaker, consulting honoraria, and research grants from Boehringer Ingelheim, Pfizer, Bayer, Gore, Daiichi Sankyo; Chair, WSO Brain & Heart Task Force; Member, Editorial Board of NEUROLOGY, STROKE, and JAHA. Neurocardiology section editor, STROKE. Associate Guest Editor, JAHA. Dr Chaturvedi is Associate Editor, Stroke. Editorial board member: Neurology and Journal of Stroke & Cerebrovascular Disease. Dr Morillo participates in CRYSTAL-AF Steering Committee, ASSERT Steering committee. Consultant for Abbott Canada, Medtronic USA, Novartis Foundation (Grant/Contract). Dr Kamel is PI for the NIH-funded ARCADIA trial (NINDS U01NS095869), which receives in-kind study drug from the BMS-Pfizer Alliance for Eliquis and ancillary study support from Roche Diagnostics. Deputy Editor, JAMA Neurology. Steering committee member, Medtronic’s Stroke-AF trial. Trial executive committee for Janssen. End point adjudication committee for a trial of empagliflozin for Boehringer-Ingelheim.

Sources of Funding

Dr Sposato is supported by the Kathleen & Dr Henry Barnett Research Chair in Stroke Research (Western University, London, Canada) and the Edward and Alma Saraydar Neurosciences Fund (London Health Sciences Foundation, London, Canada). None of these funding sources had a role in the design or results of this study.

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  1. Cardiocerebrovascular benefits of early rhythm control in patients with atrial fibrillation detected after stroke: a systematic review and meta-analysis, Frontiers in Cardiovascular Medicine, 11, (2024).
  2. Predictors of atrial fibrillation detection in embolic stroke of undetermined source patients with implantable loop recorder, Frontiers in Cardiovascular Medicine, 11, (2024).
  3. Heart–brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential, Frontiers in Cardiovascular Medicine, 11, (2024).
  4. Plateauing atrial fibrillation burden in acute ischemic stroke admissions in the United States from 2010 to 2020, International Journal of Stroke, 19, 5, (547-558), (2024).
  5. A Patient‐Centered Approach to Cardiac Monitoring After Cryptogenic Stroke: A Review, Stroke: Vascular and Interventional Neurology, 4, 2, (2024)./doi/10.1161/SVIN.123.001126
  6. Performance of Different Risk Scores for the Detection of Atrial Fibrillation Among Patients With Cryptogenic Stroke, Stroke, 55, 2, (454-462), (2024)./doi/10.1161/STROKEAHA.123.044961
  7. Subclinical Atrial Fibrillation and Stroke Risk: Time to Put the Horse Back in Front of the Cart?, Journal of the American Heart Association, 13, 3, (2024)./doi/10.1161/JAHA.123.033349
  8. Atrial Fibrillation Detection and Ischemic Stroke Recurrence in Cryptogenic Stroke: A Retrospective, Multicenter, Observational Study, Journal of the American Heart Association, 13, 3, (2024)./doi/10.1161/JAHA.123.031508
  9. Prevalence and Characteristics of Known versus Newly Detected Atrial Fibrillation in Ischemic Stroke: A Population-Based Study, Neuroepidemiology, (1-8), (2024).
  10. Prevalence, risk factors and prognostic value of atrial fibrillation detected after stroke after haemorrhagic versus ischaemic stroke, Stroke and Vascular Neurology, (svn-2023-002974), (2024).
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Atrial Fibrillation Detected After Stroke and Transient Ischemic Attack: A Novel Clinical Concept Challenging Current Views
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