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Europace Advance Access originally published online on June 29, 2007
Europace 2007 9(8):621-626; doi:10.1093/europace/eum125
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

ATRIAL FIBRILLATION

Atrial fibrillatory rate and risk of left atrial thrombus in atrial fibrillation

Andreas Bollmann1,3,*, Daniela Husser1,3, Martin Stridh2, Fredrik Holmqvist1, Anders Roijer1, Carl J. Meurling1, Leif Sörnmo2 and S. Bertil Olsson1

1 Department of Cardiology, Lund University Hospital, Lund, Sweden; 2 Department of Electroscience, Lund University, Lund, Sweden; 3 Department of Cardiology, University Hospital, Leipziger Str., 39120 Magdeburg, Germany

Manuscript submitted 20 January 2007. Revision received 28 May 2007. * Corresponding author. Tel: +49 391 67 13203.E-mail address: andreas.bollmann{at}kard.lu.se


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgement
 References
 
Aims In atrial fibrillation (AF), a relation between electrocardiogram (ECG) fibrillatory wave amplitude and thrombus formation has been sought for long with conflicting results. In contrast, the possible relation between atrial fibrillatory rate obtained from the surface ECG and left atrial thrombus formation in patients with AF is unknown and was consequently evaluated in this study.

Methods and results One-hundred and twenty-five patients (mean age 64 ± 12 years, 72% male) with persistent non-valvular AF (mean duration 28 ± 80 days) undergoing transesophageal echocardiography were studied. In all patients, standard 12-lead ECG recordings were acquired before the examination. Atrial fibrillatory rate was determined using spatiotemporal QRST cancellation and time–frequency analysis of lead V1. Atrial fibrillatory rate measured 401 ± 63 fibrillations per minute (fpm, range 235–566 fpm) and was related with age (R = –0.326, P < 0.001), ventricular rate (R = –0.202, P = 0.024), gender (407 ± 62 in males vs. 387 ± 64 fpm in females, P = 0.038) but not AF duration (R = 0.088, P = 0.374), presence of lone AF (408 ± 66 vs. 394 ± 58 fpm, P = 0.228), or beta-blocker or calcium channel blocker treatment (398 ± 63 vs. 405 ± 62 fpm, P = 0.556). Age was the only independent predictor of fibrillatory rate (B = –1.714, P < 0.001).

In patients with left atrial thrombus (n = 10), spontaneous echo contrast (SEC) was more frequently present (70 vs. 29 %, p = 0.007) and left atrial appendage (LAA) outflow velocity was lower (26 ± 20 vs. 37 ± 15 cm/s, P = 0.012) than in patients without thrombus (n = 115). In contrast, mean fibrillatory rate, which showed a weak inverse correlation with LAA velocity (R = –0.118, P = 0.048) was not different between both groups (380 ± 56 vs. 403 ± 63 fpm, P = 0.226). Similarly, presence of thrombus and SEC combined was not related with fibrillatory rate.

Conclusion Atrial fibrillatory rate obtained from surface ECG lead V1 is not a risk marker for left atrial thrombus formation in AF.

Key Words: Atrial fibrillation, Electrocardiography, Echocardiography, Thrombus


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 Acknowledgement
 References
 
Atrial fibrillation (AF) is associated with contractile dysfunction of the atrial myocardium and subsequent increased risk of thromboembolism.1Go It is known since long, that reduced left atrial appendage (LAA) flow velocity, and the occurrence of spontaneous echocardiographic contrast (SEC) are strong predictors for left atrial thrombus formation.2Go Since both factors can only be assessed by transesophageal echocardiography (TEE), a semi-invasive technique, previous studies have attempted to stratify risk for reduced LAA flow velocity, SEC as well as thrombus formation and embolism by the amplitude of fibrillatory waves on standard electrocardiograms (ECG).3Go–5Go

Results of these studies are conflicting. Patients with coarse AF defined as fibrillatory wave amplitudes ≥1 mm have been reported to have a lower LAA flow velocity and subsequently higher rates of SEC, thrombus formation3Go and thromboembolic events.4Go This finding could, however, not be confirmed in the SPAF-III trial,5Go in which no correlation between fibrillatory wave size and LAA flow velocity and subsequent thromboembolic risk was found.

Differences in ECG lead selection6Go and recording techniques7Go as well as the influence of the body surface area or chest wall attenuation and finally the rather arbitrary division of AF into coarse and fine8Go may contribute to these conflicting results. Consequently, fibrillatory wave amplitude could not be established as a clinically useful indicator for LAA dysfunction, thrombus development and thromboembolic risk.

More recently, several studies have shown that fibrillatory rate can reliably be obtained from the ECG.9Go,10Go This measurement shows large inter-individual variability11Go and is a measure of atrial refractoriness12Go and AF complexity.13Go Previous studies have shown that fibrillatory wave characteristics of the resting ECG are reproducible under stable conditions.14Go

So far, a single study15Go in 49 patients has found a moderate negative correlation between fibrillatory rate and LAA flow velocity. Since thrombus and SEC formation is influenced by LAA flow, this study sought to investigate the possible relation between fibrillatory rate obtained from standard ECG recordings and echocardiographic variables with a focus on left atrial thrombus formation and presence of SEC in a large AF population.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 Acknowledgement
 References
 
Study population
The study group comprised 125 consecutive patients with persistent, non-valvular AF who underwent transthoracic (TTE) and TEE examination at our institution for TEE-guided cardioversion.16Go Non-valvular AF was defined as AF in the absence of mitral stenosis, severe mitral regurgitation, or valve prosthesis. The duration of AF was calculated from the onset of symptoms or first electrocardiographic documentation to the performance of the echocardiographic examination. A detailed patient history was taken to identify associated cardiovascular morbidity. None of the patients was taking any antiarrhythmic drugs or sufficient oral anticoagulation for > 4 weeks at the time of the study.

This study was approved by the local Ethical Board (111/2005).

Transthoracic and transesophageal echocardiography
All patients were studied by TTE and TEE using a Hewlett-Packard Sonos 5500 imaging system (Palo Alto, CA, USA). Two-dimensional and Doppler transthoracic echocardiography was performed immediately prior to the transesophageal study, with a 2.5 or 3.5-MHz imaging transducer. Transthoracic measurements were obtained according to the standards of the American Society of Echocardiography.17Go Mitral regurgitation was graded depending on the width and depth of the regurgitation jets on colour Doppler imaging.18Go

TEE was performed using a 5 MHz multiplane phased array transducer. Patients were studied in the fasting state after intravenous sedation with 2 mg midazolam.

The LAA was visualized from a transverse view and flow profiles were obtained by pulsed Doppler interrogation at the orifice of the appendage with the lowest possible filter settings (5–10 cm/s). The maximal LAA area was determined by tracing a line from the top of the limbus of the left upper pulmonary vein along the whole appendage border.2Go The flow profile was used to assess the LAA emptying velocity. In each patient, 3–5 consecutive cardiac cycles with stable flow signals obtained during end-tidal volume apnoea were selected for analysis and obtained values were averaged.

Specific attention was paid for the existence of SEC and thrombus formation which was verified by two independent observers. Spontaneous echo contrast was ascertained by the presence of dynamic swirling smoke-like echos within the left atrium (LA) and the LAA using normal gain settings.15Go,16Go LA thrombus was diagnosed in the presence of a well-defined intracavitary echogenic mass, distinct from endocardium and pectinate muscles.

Electrocardiogram acquisition and analysis
Standard 10-s, 12-lead surface ECG recordings were acquired in all patients ≤24 h prior to the echocardiographic examination. All recordings were done with the subject relaxed in a supine position. Digital ECG recordings (500 Hz sampling rate) were retrieved from the hospital ECG database (Siemens Elema AB, Solna, Sweden) for further signal processing.

After high-pass filtering to remove baseline wander, atrial fibrillatory activity was extracted in lead V1 using spatiotemporal QRST cancellation.19Go Since the dominant frequency component of interest is within the 4–9 Hz range, the resulting fibrillatory baseline signal was downsampled to 50 Hz and subjected to spectral analysis. The time–frequency distribution of the atrial signal (obtained by short-term Fourier transform) was decomposed such that each spectrum can be modelled as a frequency-shifted and amplitude-scaled version of the spectral profile. This procedure is based on a spectral profile, dynamically updated from previous spectra, which was matched to each new spectrum using weighted least squares estimation. The frequency shift needed to achieve optimal matching then yields a measure of instantaneous fibrillatory rate of a 2.5-s ECG segment (overlapping with one segment each second) and was trended as a function of time.20Go

It should be noted that the time–frequency analysis includes techniques for rejecting segments with poor signal quality.21Go Thus, frequencies were computed from segments with reliable estimates only, as opposed to conventional power spectral analysis where all segments are included.

Frequencies were converted to fibrillatory rates with its unit fibrillations per minute (fpm) as advocated previously (rate = frequency x 60).11Go Mean fibrillatory rate (in fpm) defined as average of instantaneous fibrillatory rates over the 10-s ECG segment was determined (Figure 1).


Figure 1
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  		Figure 1 Time-frequency analysis of AF. ECG recording of lead V1 from a patient with AF (upper panel), and the same interval after spatiotemporal QRST cancellation (middle panel). Please note the overlapping 2.5-s ECG windows, which are then subjected to short-term Fourier transform resulting in a power frequency spectrum (bottom left), and a frequency trend (bottom right).

 
Statistical analysis
Continuous variables are expressed as mean ± one standard deviation. Bivariate correlation between fibrillatory rate and clinical as well as echocardiographic variables was performed using Pearson correlation coefficients or linear regression. Clinical and echocardiographic parameters were compared in (i) patients with and without left atrial thrombus and (ii) with and without thrombus and SEC combined. Differences between groups were assessed using Mann–Whitney U-test for continuous and {chi}2 test for categoric variables. Multivariate analysis including variables with a P-value < 0.1 found in univariate analysis was used to identify independent predictors for (i) thrombus formation and (ii) thrombus formation and presence of SEC combined.

With a sample size of 125 patients and a predicted prevalence of thrombus of 10% or thrombus and SEC combined of 30%, differences in fibrillatory rate of ± 50 and ± 31 fpm, respectively, would have been detectable with a power of 80%. A P-value <0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 Acknowledgement
 References
 
Patient characteristics
Clinical and echocardiographic characteristics are summarized in Table 1. Atrial fibrillatory rate measured 401 ± 63 fpm (range 235–566 fpm).


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  		Table 1 Clinical and echocardiographic patient characteristics

 
There was an inverse correlation between fibrillatory rate and age (R = –0.326, P < 0.001) as well as with ventricular rate (R = –0.202, P = 0.024). Male patients had a higher fibrillatory rate than female patients (407 ± 62 vs. 387 ± 64 fpm, P = 0.038). In contrast, AF duration (R = 0.088, P = 0.374), presence of lone AF (408 ± 66 vs. 394 ± 58 fpm, P = 0.228), beta-blocker or calcium channel blocker treatment (398 ± 63 vs. 405 ± 62 fpm, P = 0.556) were not related with fibrillatory rate.

Fibrillatory rate exhibited a weak negative correlation with LAA velocity (R = –0.118, P = 0.048). In contrast, there was no association with left ventricular ejection fraction, left ventricular volumes, left atrial diameter, or LAA area.

Among clinical and echocardiographic variables, age was the only independent predictor of fibrillatory rate (B = –1.714, P < 0.001).

Predictors of left atrial thrombus and SEC
LA and LAA SEC was present in 40 patients (32%), and thrombus formation was detected in the LAA of 10 patients (8%). Spontaneous echo contrast or thrombus combined was observed in 43 patients (34%).

Patients with left atrial thrombus formation as well as thrombus and SEC combined are compared with those without thrombus/SEC in Table 2 and Figure 2. Patients with thrombus had a lower LAA outflow velocity, and more frequently SEC. In contrast, mean fibrillatory rate was comparable in both groups. Similarly, patients with thrombus or SEC combined, had a lower LAA outflow velocity but also larger left atrial and ventricular dimensions. Risk of thrombus and SEC was similar among all fibrillatory rate quartiles.


Figure 2
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  		Figure 2 Individual LAA outflow velocities and fibrillatory rates stratified by the presence (open circle) or absence (filled circle) of LAA thrombus.

 


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  		Table 2 Comparison of patients with and without left atrial thrombus formation and SEC

 
LAA outflow velocity was lower in patients with SEC (26 ± 11 vs. 41 ± 16 cm/s, P < 0.001), which in turn was the only independent predictor for LAA thrombus (B = 1.757, P = 0.015). LAA outflow velocity was the only independent predictor for LAA thrombus and SEC combined (B = –0.083, P < 0.001).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 Acknowledgement
 References
 
While previous studies3Go–5Go have attempted to predict reduced LAA flow, SEC, and thrombus formation in AF patients by ECG fibrillatory wave amplitude, to the best of our knowledge, this is the first study that analyses the relation between fibrillatory rate and thromboembolic risk factors such as left atrial thrombus and SEC as evidenced by TEE.

Atrial fibrillatory rate and clinical characteristics
Recent atrial mapping studies suggest that—depending on the patient population investigated—various frequency gradients within the atria/PV can be found.22Go–24Go Of special note and importance for this study, Larzar et al.23Go observed frequency gradients in patients with paroxysmal AF with the highest fibrillatory rates in the left atrium/pulmonary veins, intermediate in the coronary sinus and lowest in the right atrium. However, fibrillatory rates were similar among different sites in patients with persistent AF. Consequently, it is not surprising that ECG lead V1 closely reflects right atrial,9Go,10Go but is also related to pulmonary venous/left atrial rates,25Go especially as in our population when AF is persistent and the importance of thoracic veins as AF driver diminish. Moreover, the frequency of LAA contractions as mechanical correlate of electrical fibrillatory activity has been shown to be closely related with fibrillatory rates of ECG chest leads.7Go

Among the clinical characteristics, we found an inverse correlation between fibrillatory rate and patients' age which has already been reported in new-onset26Go and permanent AF.27Go This finding can be explained by longer refractory periods and slower conduction—both resulting in slower fibrillatory rates—which are present in aging atria.28Go Interestingly, no relation between fibrillatory rate and AF duration was observed. On the one hand, large inter-individual differences independent of AF duration may exist due to individual genotype (e.g. connexin 4029) or ion-channel gene expression30Go as previoulsy discussed for new-onset AF.26Go On the other hand, AF duration in our patients did not cover AF of very short duration (e.g <24 h) with limited or long-standing AF (e.g. > 6 months) with completed electrical remodelling.

Atrial fibrillatory rate and risk factors for thrombogenesis
Previous smaller studies have already investigated the association between fibrillatory rate measurements and LAA flow velocity7Go,15Go and SEC.31Go In the earlier studies, frequency of LAA contractions was not related with LAA flow velocity or SEC. In contrast, in the other study15Go which was restricted to lone AF and AF associated with hypertension of short duration, a moderate negative correlation between fibrillatory rate of lead V1 and LAA flow velocity was found. However, the variability was too great to allow sole use of atrial fibrillatory rate to predict LAA flow accurately, which can also be concluded from analysis of our larger population including also patients with underlying heart disease and AF of longer duration.

In agreement with previous studies,2Go LAA flow velocity and SEC were the strongest predictors for LAA thrombus formation. Since we found only a weak correlation between fibrillatory rate and LAA flow velocity and no relation between fibrillatory rate and SEC, it is not surprising that fibrillatory rate was not associated with LAA thrombus.

It may be speculated that, tachycardia-induced atrial myopathy is contributing to contractile dysfunction associated with the high rate of atrial activation during AF.32Go From ventricular myocardium it is known that the contractile function declines at persistently increased rates as low as 100/min.33Go The threshold at which damage including loss of contractile myofilaments34Go,35Go to human atrial myocytes occurs is not known. However, in atrial flutter, the LAA function seems to be preserved expressed by higher LAA velocities and lower rates of SEC and thrombus.36Go In this arrhythmia, atrial rates range between 180 and 300 per minute,37Go which is much lower then in patients with AF. In our study, only 5.6% had a fibrillatory rate ≤300 fpm, but interestingly in none of them a thrombus was present (Figure 2). A deterioration of LAA function with increased thrombus risk may consequently be observed above this threshold independently of actual fibrillatory rate.

Conversely, advancing patients' age being a risk factor for thrombus formation and subsequent thromboembolic complications38Go seems to be associated with lower fibrillatory rates. In other words, while a lower fibrillatory rate may be protective from a haemodynamic point of view, it is also found with higher age when other thrombogenic factors may dominate. Taken together, this provides further explanation for fibrillatory rate not being predictive for thrombus formation and presence of SEC.

Finally, although there was no relation between fibrillatory rate and thrombus formation, that does not preclude an association with embolization, whose mechanisms have not been explored in detail and are currently under investigation.

Limitations
Even though this study was one of the largest on electrical and echocardiographic parameters for AF risk stratification, only a small number of patients had left atrial thrombus. However, there was a large, overlapping variability of fibrillatory rates in patients with and without thrombus. This together with the results of the additional analysis on thrombus and SEC combined justifies the conclusion that V1 fibrillatory rate cannot be used for predicting thromboembolic risk factors such as thrombus and SEC.

This study was limited to the analysis of ECG lead V1. While this lead directly reflects right atrial rates, which in patients with persistent AF is similar to left atrial rates, other, so far undefined leads39Go may even better correspond with left atrial and LAA activity, and may consequently be related with LAA dysfunction and thrombus formation. Moreover, ECG analysis was restricted to a standard resting ECG as screening tool, and did not include longer recordings such as Holter ECG that may contain more information on circadian fibrillatory rate variability.40Go

Clearly, and after considering the results of this study probably most importantly, the presence of thrombus and SEC is not only related to electrophysiological but also humoral and endothelial factors that were, however, not the focus of this study.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
Acknowledgement
 References
 
Atrial fibrillatory rate obtained from surface ECG lead V1 correlates only poorly with LAA outflow velocity and SEC, the strongest predictor for left atrial thrombus formation. Consequently, fibrillatory rate in right precordial leads is not a risk marker for LAA thrombus formation in AF.


   Acknowledgement
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgement
References
 
This study has been performed in and supported in part by the NordForsk network ‘Electrocardiology in Atrial Fibrillation’. D.H. has been supported by the German Cardiac Society. D.H. and M.S. are supported by the Volkswagen Foundation, Germany.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgement
 References
 
[1] Allessie MA, Ausma J, Schotten U. Electrical, contractile and structural remodeling during atrial fibrillation. Cardiovasc Res (2002) 54:230–46.[Abstract/Free Full Text]

[2] Mugge A, Kuhn H, Nikutta P, Grote J, Lopez JA, Daniel WG. Assessment of left atrial appendage function by biplane transesophageal echocardiography in patients with nonrheumatic atrial fibrillation: identification of a subgroup of patients at increased embolic risk. J Am Coll Cardiol (1994) 23:599–607.[Abstract]

[3] Li YH, Hwang JJ, Tseng YZ, Kuan P, Lien WP. Clinical significance of fibrillatory wave amplitude—a clue to left atrial appendage function in nonrheumatic atrial fibrillation. Chest (1995) 108:359–63.[CrossRef][Web of Science][Medline]

[4] Yamamoto S, Suwa M, Ito T, Murakami S, Umeda T, Tokaji Y, et al. Comparison of frequency of thromboembolic events and echocardiographic findings in patients with chronic nonvalvular atrial fibrillation and coarse versus fine electrocardiographic fibrillatory waves. Am J Cardiol (2005) 96:408–11.[CrossRef][Web of Science][Medline]

[5] Blackshear JL, Safford RE, Pearce LA. F-amplitude, left atrial appendage velocity, and thromboembolic risk in nonrheumatic atrial fibrillation. Stroke Prevention in Atrial Fibrillation Investigators. Clin Cardiol (1996) 19:309–13.[Web of Science][Medline]

[6] Waktare JE, Gallagher MM, Murtagh AM, Camm AJ, Malik M. Optimum lead positioning for recording bipolar atrial electrocardiograms during sinus rhythm and atrial fibrillation. Clin Cardiol (1998) 21:825–30.[Web of Science][Medline]

[7] Bollmann A, Binias KH, Sonne K, Grothues F, Esperer HD, Nikutta P, et al. Electrocardiographic characteristics in patients with nonrheumatic atrial fibrillation and their relation to echocardiographic parameters. Pacing Clin Electrophysiol (2001) 24:1507–13.[CrossRef][Medline]

[8] Gallagher MM, Camm J. Classification of atrial fibrillation. Am J Cardiol (1998) 82:18N–28N.[CrossRef][Web of Science][Medline]

[9] Bollmann A, Kanuru NK, McTeague KK, Walter PF, DeLurgio DB, Langberg JJ. Frequency analysis of human atrial fibrillation using the surface electrocardiogram and its response to ibutilide. Am J Cardiol (1998) 81:1439–45.[CrossRef][Web of Science][Medline]

[10] Holm M, Pehrson S, Ingemansson M, Sörnmo L, Jahansson R, Sandhall L, et al. Non-invasive assessment of the atrial cycle length during atrial fibrillation in man: introducing, validating and illustrating a new ECG method. Cardiovasc Res (1998) 38:69–81.[Abstract/Free Full Text]

[11] Bollmann A, Husser D, Stridh M, Sörnmo L, Majic M, Klein HU, et al. Frequency measures obtained from the surface electrocardiogram in atrial fibrillation research and clinical decision-making. J Cardiovasc Electrophysiol (2003) 14:S154–61.[CrossRef][Web of Science][Medline]

[12] Capucci A, Biffi M, Boriani G, Ravelli F, Nollo G, Sabbatani P, et al. Dynamic electrophysiological behavior of human atria during paroxysmal atrial fibrillation. Circulation (1995) 92:1193–202.[Abstract/Free Full Text]

[13] Konings KT, Kirchhof CJ, Smeets JR, Wellens HJ, Penn OC, Allessie MA. High-density mapping of electrically induced atrial fibrillation in humans. Circulation (1994) 89:1665–80.[Abstract/Free Full Text]

[14] Xi Q, Sahakian AV, Ng J, Swiryn S. Atrial fibrillatory wave characteristics on surface electrogram: ECG to ECG repeatability over twenty-four hours in clinically stable patients. J Cardiovasc Electrophysiol (2004) 15:911–17.[Web of Science][Medline]

[15] Holmqvist F, Stridh M, Waktare JE, Sörnmo L, Roijer A, Meurling CJ. Indices of electrical and contractile remodeling during atrial fibrillation in man. Pacing Clin Electrophysiol (2006) 29:512–9.[CrossRef][Medline]

[16] Roijer A, Eskilsson J, Olsson B. Transoesophageal echocardiography-guided cardioversion of atrial fibrillation or flutter. Selection of a low-risk group for immediate cardioversion. Eur Heart J (2000) 21:837–47.[Abstract/Free Full Text]

[17] Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation (1978) 58:1072–83.[Abstract/Free Full Text]

[18] Grayburn PA, Fehske W, Omran H, Brickner ME, Luderitz B. Multiplane transesophageal echocardiographic assessment of mitral regurgitation by Doppler color flow mapping of the vena contracta. Am J Cardiol (1994) 74:912–7.[CrossRef][Web of Science][Medline]

[19] Stridh M, Sörnmo L. Spatiotemporal QRST cancellation techniques for analysis of atrial fibrillation. IEEE Trans Biomed Eng (2001) 48:105–11.[CrossRef][Web of Science][Medline]

[20] Stridh M, Sörnmo L, Meurling CJ, Olsson SB. Characterization of atrial fibrillation using the surface ECG: time-dependent spectral properties. IEEE Trans Biomed Eng (2001) 48:19–27.[CrossRef][Web of Science][Medline]

[21] Stridh M, Bollmann A, Olsson SB, Sörnmo L. Time-frequency analysis of atrial tachyarrhythmias: detection and feature extraction. IEEE Eng Med Biol Mag (2006) 25:31–9.[CrossRef][Web of Science][Medline]

[22] Lin YJ, Tai CT, Kao T, Tso HW, Higa S, Tsao HM, et al. Frequency analysis in different types of paroxysmal atrial fibrillation. J Am Coll Cardiol (2006) 47:1401–7.[Abstract/Free Full Text]

[23] Lazar S, Dixit S, Marchlinski FE, Callans DJ, Gerstenfeld EP. Presence of left-to-right atrial frequency gradient in paroxysmal but not persistent atrial fibrillation in humans. Circulation (2004) 110:3181–6.[Abstract/Free Full Text]

[24] Atienza F, Almendral J, Moreno J, Vaidyanathan R, Talkachou A, Kalifa J, et al. Activation of inward rectifier potassium channels accelerates atrial fibrillation in humans: evidence for a reentrant mechanism. Circulation (2006) 114:2434–42.[Abstract/Free Full Text]

[25] Husser D, Stridh M, Cannom DS, Bhandari AK, Girsky MJ, Kang S, et al. Validation and clinical application of time-frequency analysis of atrial fibrillation electrocardiograms. J Cardiovasc Electrophysiol (2007) 18:41–6.[CrossRef][Web of Science][Medline]

[26] Husser D, Cannom DS, Bhandari AK, Stridh M, Sörnmo L, Olsson SB, et al. Electrocardiographic characteristics of new-onset atrial fibrillation. Europace (2007) doi:10.1093/europace/eum074.

[27] Xi Q, Sahakian AV, Frohlich TG, Ng J, Swiryn S. Relationship between pattern of occurrence of atrial fibrillation and surface electrocardiographic fibrillatory wave characteristics. Heart Rhythm (2004) 1:656–63.[CrossRef][Web of Science][Medline]

[28] Sakabe K, Fukuda N, Soeki T, Shinohara H, Tamura Y, Wakatsuki T, et al. Relation of age and sex to atrial electrophysiological properties in patients with no history of atrial fibrillation. Pacing Clin Electrophysiol (2003) 26:1238–44.[CrossRef][Medline]

[29] Firouzi M, Ramanna H, Kok B, Jongsma HJ, Koeleman BP, Doevendans PA, et al. Association of human connexin40 gene polymorphisms with atrial vulnerability as a risk factor for idiopathic atrial fibrillation. Circ Res (2004) 95:e29–33.[Abstract/Free Full Text]

[30] Brundel BJJM, van Gelder IC, Henning RH, Tieleman RG, Tuinenburg AE, Wietses M, et al. Ion channel remodeling is related to intraoperative atrial effective refractory periods in patients with paroxysmal and persistent atrial fibrillation. Circulation (2001) 103:684–90.[Abstract/Free Full Text]

[31] Bollmann A, Binias KH, Grothues F, Schwerdtfeger A, Klein HU. Left atrial appendage function and pulmonary venous flow in patients with nonrheumatic atrial fibrillation and their relation to spontaneous echo contrast. Echocardiography (2002) 19:37–43.[CrossRef][Web of Science][Medline]

[32] Gallagher MM, Obel OA, Camm JA. Tachycardia-induced atrial myopathy: an important mechanism in the pathophysiology of atrial fibrillation? J Cardiovasc Electrophysiol (1997) 8:1065–74.[Web of Science][Medline]

[33] Van Gelder IC, Crijns HJ, Blanksma PK, Landsman ML, Posma JL, Van Den Berg MP, et al. Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease. Am J Cardiol (1993) 72:560–6.[CrossRef][Web of Science][Medline]

[34] Mary-Rabine L, Albert A, Pham TD, Hordof A, Fenoglio JJ Jr, Malm JR, et al. The relationship of human atrial cellular electrophysiology to clinical function and ultrastructure. Circ Res (1983) 52:188–99.[Abstract/Free Full Text]

[35] Ausma J, Wijffels M, Thone F, Wouters L, Allessie M, Borgers M. Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat. Circulation (1997) 96:3157–63.[Abstract/Free Full Text]

[36] Omran H, Jung W, Rabahieh R, MacCarter D, Illien S, Rang B, et al. Left atrial appendage function in patients with atrial flutter. Heart (1997) 78:250–4.[Abstract/Free Full Text]

[37] Saoudi N, Cosio F, Waldo A, Chen SA, Iesaka Y, Lesh M, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. Eur Heart J (2001) 22:1162–82.[Free Full Text]

[38] Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study. Arch Intern Med (1987) 147:1561–4.[Abstract/Free Full Text]

[39] Husser D, Stridh M, Sörnmo L, Toepffer I, Klein HU, Olsson SB, et al. Electroatriography—Time-frequency analysis of atrial fibrillation from modified 12-lead ECG configurations for improved diagnosis and therapy. Med Hypotheses (2007) 68:568–73.[CrossRef][Web of Science][Medline]

[40] Bollmann A, Sonne K, Esperer HD, Toepffer I, Klein HU. Circadian variations in atrial fibrillatory frequency in persistent human atrial fibrillation. Pacing Clin Electrophysiol (2000) 23:1867–71.[Medline]


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A. Bollmann, D. Husser, A. Lindgren, M. Stridh, B. M. Hardig, C. Piorkowski, A. Arya, L. Sornmo, and S. B. Olsson
Atrial fibrillatory rate and risk of stroke in atrial fibrillation
Europace, May 1, 2009; 11(5): 582 - 586.
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A. Bollmann, A. Tveit, D. Husser, M. Stridh, L. Sornmo, P. Smith, and S. B. Olsson
Fibrillatory rate response to candesartan in persistent atrial fibrillation
Europace, October 1, 2008; 10(10): 1138 - 1144.
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