CONTEMPORARY REVIEW

Clinical significance of atrial fibrillation detected by cardiac implantable electronic devices Anthony E. DeCicco, MD, Jonathan B. Finkel, MD, Arnold J. Greenspon, MD, Daniel R. Frisch, MD From the Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. The detection of atrial fibrillation (AF) by a cardiac implantable electronic device (CIED) in patients without a prior history of AF is increasing. This trend is the result of the increased number of CIEDs being implanted in a population whose multiple medical comorbidities are known to predispose to AF. Cardiac implantable electronic device–detected atrial fibrillation (CDAF) is independently associated with the development of ischemic stroke, and the annual risk may depend on both total AF burden and individual risk factors. No data evaluating the benefit of oral anticoagulation in this population are available, which makes the decision to initiate anticoagulation challenging. This review analyzes the available data on CDAF and the associated risk of ischemic stroke, and it presents a rationale for the use of long-term oral anticoagulation in this population.

KEYWORDS Atrial fibrillation; Cardiac implantable electronic device; Pacemaker; Implantable cardioverter-defibrillator; Cardiac resynchronization therapy; Anticoagulation

Cardiac implantable electronic device population and cardiac implantable electronic device–detected atrial fibrillation

to 2% annually and up to 10% over 3 years in patients with congestive heart failure (HF).12 The discrepancy might be accounted for in part by 2 explanations: (1) the CIED population is unique, and these patients have comorbidities that place them at higher risk for AF than the general population; and (2) in many patients AF likely was present before implantation but was discovered only after implantation because CIEDs have increased sensitivity compared with conventional diagnostic methods. We have considered that the presence of intravascular hardware or AV dyssynchronous pacing may themselves be proarrhythmic. However, across the spectrum of pacing options (single chamber, dual chamber, CRT), the proarrhythmic effect appears to be insufficient to explain the high incidence observed.13,14

Cardiac implantable electronic devices and atrial fibrillation incidence The use of permanent pacemakers (PMs), implantable cardioverter-defibrillators (ICDs), and cardiac resynchronization therapy (CRT) with or without defibrillation capability is increasing both in North America and globally.1,2 Patients with cardiac implantable electronic devices (CIEDs) constitute a growing and unique population. Device interrogation in these patients frequently leads to the discovery of arrhythmias, most commonly atrial fibrillation (AF), despite a lack of any associated clinical symptoms.1,3–11 Rates can reach 10% by 3 months and 35% by 30 months.1,3–5,7,9,11 A summary of studies that have documented cardiac implantable electronic device–detected atrial fibrillation (CDAF) in patients (both with and without a clinical history of AF) is given in Table 1. The reported incidence of CDAF is significantly higher than previous estimates of AF diagnosed by conventional methods (hereafter, AF), which have been estimated at 0.1% Address reprint requests and correspondence: Dr. Daniel Frisch, Jefferson Heart Institute, 925 Chestnut St, Philadelphia, PA 19107. E-mail address: [email protected].

1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.

ABBREVIATIONS AF ¼ atrial fibrillation; AHRE ¼ atrial high-rate episode; AVB ¼ atrioventricular block; CDAF ¼ cardiac implantable electronic device–detected atrial fibrillation; CIED ¼ cardiac implantable electronic device; CRT ¼ cardiac resynchronization therapy; DM ¼ diabetes mellitus; HF ¼ heart failure; HR ¼ hazard ratio; HTN ¼ hypertension; ICD ¼ implantable cardioverterdefibrillator; ICH ¼ intracranial hemorrhage; PM ¼ pacemaker; SND ¼ sinus node dysfunction; TIA ¼ transient ischemic attack (Heart Rhythm 2014;11:719–724) I 2014 Heart Rhythm Society. All rights reserved.

CIED population The high incidence of CDAF likely reflects the underlying predisposing conditions in the population of patients who receive CIEDs. Devices typically are implanted in patients with sinus node dysfunction (SND), atrioventricular block (AVB), or both, and often in the presence of other significant comorbidities. In the CIED studies presented here, SND was documented in 42% to 100%, AVB in 17% to 53%, HF in 1% to 60%, hypertension (HTN) in 38% to 100%, and diabetes mellitus (DM) in 15% to 32%.1,3,4,7–10 Each of these http://dx.doi.org/10.1016/j.hrthm.2014.01.001

720

Heart Rhythm, Vol 11, No 4, April 2014

Table 1

Comparison of CDAF incidence and/or prevalence according to clinical history of AF and device type

Study

Device type

Population

No. of patients

History of AF

CDAF duration

CDAF incidence (%)

Followup

Healey1

PPM/ICD

2580

No

46 min

35%

2.5 y

Mittal4 Cheung7 Jons5

PPM PPM ILR

1482 262 271

No No No

45 min 45 min 416 beats

10% 29% 39%

6 mo 2y 2y

Ziegler11

PPM/ICD/ CRT PPM/ICD/ CRT PPM

Age Z65 years, hypertension Variable CHADS2 Variable CHADS2 Variable CHADS2, post-MI infarction, ejection fraction o40% Age Z65 years, CHADS2 Z1

1368

No

45 min

30%

1.1 y

Age Z65 years, CHADS2 Z1

1988 498 124 188 568 725

No Yes No Yes Yes Yes

420 s

45% N/A* 25% 69% 79% 74%

17 mo

Glotzer9 Glotzer3 8

Botto Capucci10

PPM PPM

Age 421 years, variable CHADS2 Variable CHADS2 Variable CHADS2

45 min *

N/A N/A*

27 mo 1y 22 mo

AF ¼ atrial fibrillation; CDAF ¼ cardiac implantable electronic device–detected atrial fibrillation; CRT ¼ cardiac resynchronization therapy; ICD ¼ implantable cardioverter-defibrillator; ILR ¼ implantable loop recorder; PPM ¼ permanent pacemaker. * N/A indicates that a study used devices with CDAF detection algorithms, and thus CDAF detection was independent of AHRE duration. Medtronic AT500 pacemakers were used in the studies by Botto et al and Capucci et al.

comorbidities is known to correlate with the development of AF. Major trials have demonstrated AF in 410% of patients with HF and in as many as 50% of patients with class III or IV New York Heart Association symptoms.12 Other authors have demonstrated an increase in AF among patients with SND, HTN, and DM.12,15

Accuracy and sensitivity of AF detection by CIEDs CIEDs are sensitive and specific for diagnosing AF, particularly compared with conventional methods. Some devices continuously track atrial activity and record episodes in which the sensed atrial rate either exceeds a predefined cutoff or deviates from a running average or sensor-based physiologic rate.1,4,6 The positive predictive value of such atrial high-rate episodes (AHREs) varies considerably over a given range of atrial rates and/or event durations. For example, when comparing all AHREs in ASSERT (Asymptomatic Atrial Fibrillation and Stroke Evaluation in Pacemaker Patients and the Atrial Fibrillation Reduction Atrial Pacing Trial) with adjudicated electrograms, the authors demonstrated that the positive predictive value of AHREs (all 4190 bpm) was only 48% if lasting o6 minutes but was 83% if 46 minutes and 97% if 46 hours.16 The ASSERT analysis also showed that the positive predictive value of AHREs (46 minutes, minimum) improved from 82.7% to 89.9% as the rate cutoff increased from 4190 to 4250 bpm. The inaccuracy of the short-duration episodes may be partly explained by inappropriately labeling AF (e.g., when nonreentrant ventricularatrial synchrony is present). Regardless, slower rates and/or shorter duration episodes should be confirmed as AF by electrogram review.17 Other devices use different diagnostic algorithms to increase accuracy (e.g., noncompetitive atrial pacing). Use of such device-specific algorithms can increase the sensitivity and specificity to 495%.8–10,18 An additional potential advantage of continuous monitoring is sensitivity. Although clinicians routinely interpret

conventional studies that diagnose AF (e.g., physical examination, ECGs, mobile cardiac outpatient telemetry monitoring), these studies may miss episodes of AF.3,8 Botto et al8 presented a direct comparison between CIED monitoring and conventional methods. The authors analyzed 1 year of continuous rhythm data from a post-PM cohort and diagnosed AF with a previously validated device-specific algorithm. They compared continuous monitoring with periods of simulated Holter monitoring, the latter performed at varying intervals to minimize the effect of random sampling. For any AF episode lasting 45 minutes, the sensitivity of 24-hour, 1-week, and 1-month Holter-monitoring was 44%, 50%, and 65%, respectively. Furthermore, even for AF episodes lasting 448 hours, 1-month Holter monitoring had a negative predictive value of only 73%. In aggregate, CIEDs have the ability to detect correctly the presence of AF in a more comprehensive and inclusive manner than conventional approaches. Generally, CIED accuracy exceeds 85%, although correct detection improves with longer episodes and may vary from manufacturer to manufacturer. The question remains, however, regarding the extent to which CDAF affects patient outcomes.

CIEDs and stroke AF is known to increase the risk of stroke up to 5-fold and is responsible for as many as 15% of all strokes.1,12 Consequently, timely diagnosis and implementation of appropriate anticoagulation are essential. Although AF may present with clinical symptoms of palpitations, chest pain, dyspnea, or lightheadedness, asymptomatic episodes of AF actually occur more frequently.3 The majority of CDAF also is asymptomatic.1,3,7 The advantage of early detection afforded by CIEDs theoretically could allow for earlier initiation of anticoagulation, assuming that CDAF imparts a stroke risk similar to AF.

DeCicco et al

Atrial Fibrillation and Cardiac Devices

721

ASSERT was a prospective, multicenter observational trial designed to examine the relationship between CDAF and ischemic stroke.1 Investigators enrolled 2580 patients all aged 465 years with comorbid HTN and all with recent PM (n ¼ 2451) or ICD (n ¼ 159) implantation. Patients with a history of known AF and those taking oral anticoagulation for any reason were excluded. The cohort was monitored over 3 months for subclinical AF (i.e., CDAF), and then was followed for an average of 2.5 years to assess the primary outcome of ischemic stroke or systemic embolism. AHREs with rate 4190 bpm lasting 46 minutes were considered CDAF. In total, 261 patients (10.1%) experienced CDAF within the first 3 months. Among these patients, the primary endpoint occurred at a rate of 1.69% annually, with ischemic stroke occurring at 1.59%. Early CDAF predicted ischemic stroke or systemic embolism during follow-up (hazard ratio [HR] 2.49), and remained predictive even after adjustment for other risk factors. Interestingly, early CDAF also predicted a subsequent diagnosis of AF by office ECG (HR 5.56), although none of the 51 patients who experienced the primary outcome were diagnosed with AF during the first 3 months, including the 11 patients with CDAF.1 TRENDS (Prospective Study of the Clinical Significance of Atrial Arrhythmias Detected by Implanted Device Diagnostics) was a similar prospective, multicenter observational study that addressed a slightly different question.9 Investigators enrolled 2486 patients after CIED implantation, all aged 465 years with Z1 risk factor for stroke based on guidelines from 2001, which are encompassed by the CHADS2 score (congestive HF, HTN, age 475 age, DM, and prior thromboembolism). Patients with and without prior AF were included. CDAF was defined as any AHRE with rate 4175 bpm lasting Z20 seconds and was refined further by devicespecific algorithms.18 Patients were followed over an average of 1.4 years, and rolling windows of 30 days were used to track AF. Windows were divided into subsets of zero, low, or high CDAF burden based on the longest total duration of AT/AF (i. e., CDAF) recorded on any 1 day in the full 30-day period. A cutoff of 5.5 hours (the median duration of all recorded CDAF episodes) was used to delineate low and high CDAF burden. Investigators then analyzed the relationship between CDAF Table 2

burden and the primary outcome, a composite of ischemic stroke, transient ischemic attack (TIA), and systemic embolism (collectively referred to as thromboembolic events). In TRENDS, CDAF was diagnosed in 45% of the 1988 patients without a documented history of AF and in 24% of all 30-day windows. For windows that included any CDAF (both the low- and high-burden subsets), the yearly rate of thromboembolic events was 1.8%, or 1.5% when excluding TIAs. There was no difference in the rate of thromboembolic events between windows with zero or low CDAF burden (HR 0.98). By comparison, thromboembolic events were more common in 30-day windows with high CDAF burden (HR 1.8). The risk remained increased after adjustment for other risk factors, including prior thromboembolic events, DM, HTN, HF, and oral anticoagulation use (HR 2.2). Data from ASSERT and TRENDS are supported by several smaller prospective trials that have also examined the relationship between CDAF and embolic events (Table 2). Interestingly, in these studies, 14% to 36% of patients were on anticoagulation. Moreover, as noted in the study by Capucci et al,10 the distribution of anticoagulation among patients typically was not uniform, and providers often prescribed therapy to those patients at higher levels for risk.1,8–10 As a result, the incidence of embolic events is likely underestimated.

Clinical benefit of oral anticoagulation in CDAF The increasing prevalence of patients with CIEDs, in combination with CDAF and its associated stroke risk, presents a novel challenge to clinicians. The effectiveness of oral anticoagulation for stroke prevention in AF is well documented, but no data on similar strategies in patients with CDAF are available.19–21 To date, the only prospective, randomized trial to address this question was the IMPACT study, which was stopped early and is unpublished.22 In a 2012 focused update of the European Society of Cardiology (ESC) guidelines for the management of AF, the initiation of anticoagulation in patients with a CHA2DS2 VASc score Z2 is a class I recommendation based on level A data.23 This recommendation, likely to be reinforced in

Association between CDAF and TE, including effect of CDAF burden on overall risk TE*†

Study 1

Healey Glotzer9 Capucci10 Glotzer3 Botto8

Population size

Follow-up

AHREs

Annual rate

Risk

2580 2486 725 312 568

2.5 years 1.4 years 22 mo 27 mo 1 years

6 min 5.5 h 24 h 5 min 24 h (if CHADS 41) 5 min (if CHADS Z2)

1.5% 1.8% 1.9% 1.6% 5.0%

HR 2.52 (95% CI 1.28–4.85) HR 2.20 (95% CI 0.96–5.05) OR 3.1 (95% CI 1.1–10.5) HR 2.79 (95% CI 1.51–5.15) OR 5.0 (P ¼ .035)

TE included transient ischemic attack, ischemic stroke, or systemic embolism; in Glotzer 2003, death or ischemic stroke; and in Healey 2012, ischemic stroke only. AHRE ¼ atrial high-rate event; CI ¼ confidence interval; HR ¼ hazard ratio; OR ¼ odds ratio; TE ¼ thromboembolic event. * Data include only TE among patients with CDAF. †End-points constituting TE varied across trials; in Glotzer 2009, Capucci 2005, and Botto 2009.

722 future American Heart Association/American College of Cardiology (AHA/ACC) guidelines, points toward a purposeful expansion of anticoagulation in AF, in part supported by data from two large-scale registries.24 In these registries, investigators calculated the net clinical benefit of warfarin in AF (oral factor Xa and direct thrombin inhibitors were not studied) by subtracting the on-treatment increase in intracranial hemorrhage (ICH) from the decrease in ischemic strokes.20,21 In both studies, the stroke risk increased commensurate with increasing CHADS2 scores whereas the ICH risk increased only slightly. This observation shows amplification of the benefit of anticoagulation as the CHADS2 score increases. In the study by Singer et al,20 benefit was achieved for patients with CHADS2 Z2, for whom the annual stroke rate without warfarin was Z2.54%. In the report by Friberg et al,21 benefit was achieved for all patients with CHADS2 Z1 and an annual stroke rate Z3.0%. Although the annual stroke rate is increased in CIED patients with documented CDAF, published studies report a lower rate than that associated with AF.1,3–11 In ASSERT the annual rate of systemic embolism was 1.59% compared with 2.29% in the study by Singer et al20 and 4.5% in the study by Friberg et al.21 Furthermore, the average CHADS2 score of patients not on anticoagulation therapy was 1.96 in the report by Friberg et al and o1 in the study by Singer et al. In contrast, in ASSERT the average score was 2.3 and in TRENDS was 2.2. Although a higher CHADS2 score is associated with an increased risk of major bleeding, including ICH, compared with all-comers with AF, patients with CDAF appear to be at lower risk for ischemic stroke.22 As a result, the net clinical benefit of anticoagulation in CDAF may be reduced. Significant heterogeneity exists within the CDAF population, as it does in patients with conventionally recognized AF.19–21 Stratification of patients into subsets with different risk profiles could allow clinicians to selectively offer anticoagulation to appropriate patients.

Heart Rhythm, Vol 11, No 4, April 2014 demonstrate a significant increase in markers of hypercoagulability. These changes occurred after as few as 15 minutes in AF.25,26 In another study using transesophageal echocardiography, the authors documented the presence of left atrial thrombus in 14% of patients with acute-onset AF (mean duration 1.6 days, all o3 days). Left atrial thrombus was then documented in 27% of patients with longstanding persistent AF (mean duration 890 days, all 43 days).12 These data suggest that a thrombus can develop early during an AF episode and that the overall risk may correlate with AF duration.

CDAF duration, burden, and stroke: what we have learned from CDAF CIED studies have provided additional insight on the issue of AF burden and stroke risk and are notable for their ability to quantify CDAF duration. In TRENDS, windows with zero and low CDAF burden were not associated with thromboembolic events, whereas those in which CDAF exceeded 5.5 hours/day showed a significant increase in the incidence of thromboembolic events.9 In a separate analysis of TRENDS, however, the temporal relationship of AF and thromboembolic events were less clearly linked. This is an area of uncertainty but reiterates the concept that CIED patients may be at higher risk for stroke from mechanisms other than cardiac thromboembolism.27 In ASSERT, when patients with any CDAF were stratified into quartiles based on the duration of their longest episode, only CDAF 417.72 hours significantly increased the risk of stroke or systemic embolism.1 In the study by Capucci et al,10 episodes of CDAF lasting 45 minutes did not increase embolic risk, whereas episodes lasting 424 hours did (odds ratio 3.1). In all of these studies, CDAF o48 hours was independently associated with thromboembolism, including ischemic stroke. Furthermore, there was a clear difference in embolic risk that became apparent only when CDAF duration exceeded certain thresholds.1,9,10 Future studies are required to determine the minimum burden of AF that increases risk for thromboembolic events.

CDAF duration, burden, and stroke: What we know Investigators have evaluated a number of variables for their contribution to stroke risk in CDAF, including CDAF duration, total CDAF burden, and individual risk factors. However, the correlation between AF duration and stroke has not been definitively determined. The 2006 ACC/AHA/ ESC guidelines recommend a transesophageal echocardiogram to look for intraatrial thrombus or 3 to 4 weeks of anticoagulation before electrical cardioversion of AF when the AF duration exceeds 48 hours. Although previous studies have suggested that thrombus formation is unlikely in AF o48 hours, these data are based on symptomatic AF.12 Authors of the 2006 guidelines acknowledged that the consensus on this cutoff was not strong (level of evidence C) and that conflicting data exist.12 More recently, in 2 separate studies, investigators induced AF and then sampled blood directly from the left atrium to

CDAF, individual risk factors, and stroke Risk stratification based on the presence of established highrisk comorbidities has been repeatedly validated in patients with AF.19–21 Investigators studying CDAF have documented similar results when applying the CHADS2 score. In the report by Capucci et al,10 CHADS2 variables were analyzed (although ischemic heart disease was used as a surrogate for congestive HF), and the authors demonstrated a graded increase in the annual rate of arterial embolism (ischemic stroke, TIA, or peripheral embolism). As the number of risk factors increased from 0 to Z4, arterial thromboembolism increased from 0% to 11.66%.10 In ASSERT, the annual risk of stroke or systemic embolism was 0.56% for a CHADS2 score of 1, 1.29% for CHADS2 score of 2, and 3.78% for CHADS2 score Z3. HR for stroke or systemic embolism for early CDAF compared

DeCicco et al

Atrial Fibrillation and Cardiac Devices

with no CDAF was 2.11, 1.83, and 3.93, respectively; however, the overall trend did not meet criteria for significance (P ¼ .35).1 TRENDS did not present a specific analysis of CHADS2 and stroke risk, but the overall annualized thromboembolic rate of 1.8% for a population with an average CHADS2 score of 2.2 was similar to that of ASSERT and the study by Capucci et al.10 Together these data suggest that CHADS2 scoring can provide prognostic information with regard to stroke risk in CDAF. A comprehensive evaluation would combine episode duration and/or CDAF burden with CHADS2 scoring. Botto et al8 analyzed this method by following 568 patients for the first year after PM implantation. All patients had a history of paroxysmal AF, although their individual AF burden varied considerably during follow-up ( 1/3 had no CDAF,  1/3 CDAF o24 hours,  1/3 CDAF 424 hours). After 1 year, authors stratified patients using a combination of CDAF burden and CHADS2 scoring and then calculated the thromboembolic rates among the different groups. Separate populations with distinctly different stroke risks emerged. In both patients with a CHADS2 score of 1 and CDAF 424 hours and in those with CHADS2 score Z2 and CDAF 45 minutes, there was a significantly increased risk of stroke ( 5% annually) compared to patients with a lower CHADS2 score and/or lower CDAF burden ( 1% annually).8

Net clinical benefit of oral anticoagulation in CDAF Five prospective, observational studies have analyzed CDAF and associated embolic risk.1,3,8–11 In particular, both ASSERT and the study by Botto et al8 have provided an analysis of how embolic events are related to CDAF burden and CHADS2 risk factors. From the studies by Singer et al20 and Friberg et al21 we have data on the annual rates of anticoagulation-related intracranial bleeding in large populations. Combining these data allows for an estimation of the net clinical benefit that CIED patients may derive from anticoagulation. Patients at low risk (i.e., CHADS2 ¼ 0) likely would not derive benefit, consistent with published data in AF. Conversely, high-risk patients (i.e., CHADS2 42) likely will derive benefit from anticoagulation. In the study by Botto et al,8 the authors observed an annual thromboembolic event rate of 17.6% in patients with CHADS2 42, although the sample size was small (n ¼ 17). In the larger ASSERT study, early CDAF in any patient with CHADS2 42 (n ¼ 848) yielded an annual embolic rate of 3.78%. In the report by Friberg et al., the average annual rate of ICH for patients with CHADS2 42 ranged from 0.7% to 1.1%. Patients at the highest bleeding risk (HAS-BLED ¼ 5) did experience rates of 2.0% to 2.3%, but these sample sizes also were smaller. For patients at moderate risk (CHADS2 ¼ 1–2), the data are less clear. In the report by Botto et al,8 the combination of CDAF 45 minutes and CHADS2 ¼ 2, or CDAF 424 hours and CHADS2 ¼ 1, yielded an annual thromboembolic rate of 4.0%. However, in ASSERT, the trend toward increased

723 embolic risk in patients with early CDAF and CHADS2 score of 1 or 2 did not reach statistical significance. Although the authors had previously documented that CDAF 417.72 hours predicted embolic events, there was no analysis of such longer episodes stratified by CHADS2 score. In the report by Friberg et al,21 ICH events are low in this group (average 0.5%–0.6%).

Conclusion and recommendations Patients with CIEDs are a unique population, characterized by the presence of multiple comorbidities known to predispose to AF. A diagnosis of CDAF is more likely in this group, and continuous monitoring increases the chances of early detection. Several prospective trials have shown CDAF to be an independent predictor of thromboembolism, including ischemic stroke. The optimal management of this risk is currently not known. In the interim, these patients remain at risk. Although the overall stroke rate in CDAF appears to be less than that in clinically recognized AF, current data suggest that certain high-risk patients can be identified based on CDAF duration and burden, as well as the presence of individual risk factors. Provided that presumptive embolic risk exceeds the risk of serious bleeding and ICH, we would strongly favor the use of anticoagulation therapy. Further studies are necessary to determine the safest and most effective options to these complex questions. Until clearer answers are available, we offer our opinions for consideration. In patients with a CHADS2 score of 0, we would not consider anticoagulation in most cases regardless of the burden of CDAF. In patients with a CHADS2 score of 1–2, we would consider anticoagulation if a single episode of CDAF exceeds 24 hours. In patients with a CHADS2 score 42, we would consider the use of anticoagulation for CDAF episodes 46 minutes. We encourage a dedicated section in future guidelines to address AF in this unique patient population, and we continue to look forward to the results of prospective, randomized trials examining this issue.

References 1. Healey JS, Connolly SJ, Gold MR, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120–129. 2. Faroogi FM, Talsania S, Hamid S, Rinaldi CA. Extraction of cardiac rhythm devices: indications, techniques, and outcomes for the removal of pacemaker and defibrillator leads. Int J Clin Pract 2010;64:1140–114-7. 3. Glotzer TV, Hellkamp AS, Zimmerman J, et al. Atrial high rate episodes detected by pacemaker diagnostics predict death and stroke. report of the Atrial Diagnostics Ancillary Study of the Mode Selection Trial (MOST). Circulation 2003;107:1614–1619. 4. Mittal S, Stein K, Gilliam FR, Kraus SM, Meyer TE, Christman SA. Frequency, duration, and predictors of newly-diagnosed atrial fibrillation following dualchamber pacemaker implantation in patients without a previous history of atrial fibrillation. Am J Cardiol 2008;102:450–453. 5. Jons C, Jacobsen UG, Joergensen RM, et al. The incidence and prognostic significance of new-onset atrial fibrillation in patients with acute myocardial infarction and left ventricular systolic dysfunction: a CARISMA substudy. Heart Rhythm 2011;8:342–348. 6. Borleffs CJW, Ypenburg C, van Bommel RJ, et al. Clinical importance of newonset atrial fibrillation after cardiac resynchronization therapy. Heart Rhythm 2009;6:305–310.

724 7. Cheung JW, Keating RJ, Stein KM, et al. Newly detected atrial fibrillation following dual chamber pacemaker implantation. J Cardiovasc Electrophysiol 2006;17:1323–1328. 8. Botto GL, Padeletti L, Santini M, et al. Presence and duration of atrial fibrillation detected by continuous monitoring: crucial implications for the risk of thromboembolic events. J Cardiovasc Electrophysiol 2009;20:241–248. 9. Glotzer TV, Daoud EG, Wyse DG, et al. The relationship between daily atrial tachyarrhythmia burden from implantable device diagnostics and stroke risk: the TRENDS study. Circ Arrhythm Electrophysiol 2009;2:474–480. 10. Capucci A, Santini M, Padeletti L, et al. Monitored atrial fibrillation duration predicts arterial embolism events in patients suffering from bradycardia and atrial fibrillation implanted with antitachycardia pacemaker. J Am Coll Cardiol 2005;46:1913–1920. 11. Ziegler PD, Glotzer TV, Daoud EG, et al. Detection of previously undiagnosed atrial fibrillation in patients with stroke risk factors and usefulness of continuous monitoring in primary stroke prevention. Am J Cardiol 2012;110:1309–1314. 12. Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for practice guidelines (Writing Committee to revise the 2001 guidelines for the management of patients with atrial fibrillation). Circulation 2006;114:e257–e354. 13. Healey JS, Toff WD, Lamas GA, et al. Cardiovascular outcomes with atrial-based pacing compared with ventricular pacing: meta-analysis of randomized trials, using individual patient data. Circulation 2006;114:11–17. 14. Hoppe UC, Casares JM, Eiskjaer H, et al. Effect of cardiac resynchronization on the incidence of atrial fibrillation in patients with severe heart failure. Circulation 2006;114:18–25. 15. Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA 2009;301: 2571–2577. 16. Kaufman ES, Israel CW, Nair GM, et al. Positive predictive value of devicedetected atrial high-rate episodes at different rates and durations: an analysis from ASSERT. Heart Rhythm 2012;9:1241–1246.

Heart Rhythm, Vol 11, No 4, April 2014 17. Glotzer TV. To the editor—is manual adjudication of AF episodes detected by implanted devices required? Heart Rhythm 2012;9:e17–e18. 18. Purerfellner H, Gillis AM, Holbrook R, Hettrick DA. Accuracy of atrial tachyarrhythmia detection in implantable devices with arrhythmia therapies. Pacing Clin Electrophysiol 2004;27:983–992. 19. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001;285:2864–2870. 20. Singer DE, Chang Y, Fang MC, et al. The net clinical benefit of warfarin anticoagulation in atrial fibrillation. Ann Intern Med 2009;151:297–305. 21. Friberg L, Rosenqvist M, Lip GYH. Net clinical benefit of warfarin in patients with atrial fibrillation: a report from the Swedish Atrial Fibrillation Cohort Study. Circulation 2012;125:2298–2307. 22. Ip J, Waldo AL, Lip GYH, et al. for the IMPACT Investigators. Multicenter randomized study of anticoagulation guided by remote rhythm monitoring in patients with implantable cardioverter-defibrillator and CRT-D devices: rationale, design and clinical characteristics of the initially enrolled cohort: the IMPACT study. Am Heart J 2009;158:364–370. 23. Camm AJ, Lip GY, Caterina De, et al. for the ESC Committee for Practice Guidelines-CPG. 2012 Focused update of the ESC guidelines for the management of atrial fibrillation: an update of the 2010 ESC guidelines for the management of atrial fibrillation—developed with the special contribution of the European Heart Rhythm Association. Europace 2012;14:1385–1413. 24. Fuster V, Chinitz JS. Net clinical benefit of warfarin: extending the reach of antithrombotic therapy for atrial fibrillation. Circulation 2012;125:2285–2287. 25. Lim HS, Willoughby SR, Schultz C, et al. Effect of atrial fibrillation on atrial thrombogenesis in humans: impact of rate and rhythm. J Am Coll Cardiol 2013;61:852–860. 26. Akar JG, Jeske W, Wilber DJ. Acute onset human atrial fibrillation is associated with local cardiac platelet activation and endothelial dysfunction. J Am Coll Cardiol 2008;51:1790–1793. 27. Daoud EG, Glotzer TV, Wyse DG, et al. Temporal relationship of atrial tachyarrhythmias, cerebrovascular events, and systemic emboli based on stored device data: a subgroup analysis of TRENDS. Heart Rhythm 2011;8:1416–1423.

Clinical significance of atrial fibrillation detected by cardiac implantable electronic devices.

The detection of atrial fibrillation (AF) by a cardiac implantable electronic device (CIED) in patients without a prior history of AF is increasing. T...
140KB Sizes 0 Downloads 0 Views