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Objectives: This study sought to investigate whether left atrial (LA) functional measures predict atrial fibrillation (AF) in the general population., Background: Increasing evidence suggests LA functional measures are predictors of AF in several patient groups., Methods: In a community-based cohort study, approximately 2,000 individuals underwent a transthoracic echocardiogram. Conventional echocardiographic measures and extended LA measures, including the minimal and maximal LA volumes (LAV min and LAV max , respectively) and left atrial emptying fraction (LAEF), were performed. The endpoint was incident AF, and participants with known AF were excluded, which left 1,951 for inclusion., Results: Over 11.0 years of follow-up, 184 (9.4%) developed AF. Those who developed AF had significantly larger LA volumes and lower LAEF than participants free of AF. These LA measures were univariable predictors of AF (LAV max hazard ratio [HR]: 1.10 [95% confidence interval (CI): 1.08 to 1.12] per 1-ml increase, p < 0.001; LAV min HR: 1.14 [95% CI: 1.12 to 1.16] per 1-ml increase, p < 0.001; LAEF HR: 1.03 [95% CI: 1.02 to 1.04] per percent decrease, p < 0.001). All LA measures remained predictors independent of clinical risk scores, with LAV min providing the highest C-statistics when added to these risk scores (C-statistic for CHADS 2 0.728 vs. CHADS 2  + LAV min 0.778; C-statistic for CHARGE-AF 0.815 vs. CHARGE-AF + LAV min 0.830). However, hypertension modified the relationship between the measures of LA function (both LAV min and LAEF) and risk of AF (p for interaction < 0.001), which was not the case for LAV max (p = 0.22). The measures of LA function mainly provided prognostic information regarding risk of AF in participants without hypertension. Even when we restricted our analysis to individuals without hypertension and nondilated LA (LAV max <34 ml/m 2 ), the LAV min and LAEF remained significantly independent predictors of AF after multivariable adjustments (LAV min HR: 1.12 [95% CI: 1.01 to 1.24], p = 0.028, and LAEF HR: 1.03 [95% CI: 1.00 to 1.06], p = 0.021, respectively)., Conclusions: LA functional measures predict AF in the general population and provide prognostic information incremental to clinical risk scores. In individuals without hypertension and nondilated LA, these measures indicate an increased risk of AF., (Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Previous findings regarding physical activity and risk of incident atrial fibrillation (AF) are controversial, focusing on leisure-time physical activity (LTPA) and without distinguishing it from occupational physical activity (OPA). Our aim was to study the association between physical activity and risk of AF, with special attention to the possible divergent effects of OPA and LTPA., Methods and Results: In a prospective, observational cohort study, 17,196 subjects were included from the Copenhagen Population Register. All participants had a physical examination, a 12-lead electrocardiogram (ECG), and answered a questionnaire regarding health and physical activity. Participants without previously diagnosed AF who answered adequately regarding OPA and LTPA were included. LTPA and OPA were each graded into four levels. Follow-up were carried out between 1981-1983, 1991-1994, and 2001-2003. Information regarding hospitalization and mortality was drawn from the National Patient Registry and the Registry of Causes of Death. Outcome was incident AF as determined by follow-up ECG or register diagnosis. In univariable Cox regression analysis all sub-groups of OPA had a significant higher risk of AF compared to moderate OPA. When adjusting for confounders, the risk remained significantly increased for high OPA (hazard ratio (HR) 1.21 (95% confidence interval (CI) 1.02-1.43), p = 0.028), and very high OPA (HR 1.39 (95% CI 1.03-1.88), p = 0.034). We found no significant association between LTPA and incident AF., Conclusions: High and very high OPA were associated with a significantly increased risk of incident AF. LTPA was not associated with risk of incident AF., (© The European Society of Cardiology 2016.)

Aims: Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with substantial morbidity and mortality. AF is associated with enlargement of the left atrium (LA), and the LA volume has important prognostic implications for the disease. The objective of the study was to determine how measurements of LA volume and function obtained by transthoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and 320-slice multi-detector computed tomography (MDCT) correlate in patients with permanent AF., Methods and Results: Thirty-four patients with permanent AF participated in the study. TTE, CMR, and 320-slice MDCT imaging procedures were performed within 7 ± 4 days. 320-slice MDCT overestimated maximal LA volume (LAmax) and minimal LA volume (LAmin) compared with CMR (LAmax: 80 vs. 73 mL/m(2), P = 0.0017; LAmin: 69 vs. 64 mL/m(2), P = 0.0217), whereas TTE underestimated these parameters compared with CMR (LAmax: 60 vs. 73 mL/m(2), P < 0.0001; LAmin: 50 vs. 64 mL/m(2), P < 0.0001), and also compared with MDCT (LAmax: 60 vs. 80 mL/m(2), P < 0.0001; LAmin: 50 vs. 69 mL/m(2), P < 0.0001). Measurements of LA volumes by MDCT and CMR closely correlated, and both MDCT and CMR had excellent intra- and inter-observer agreement with correlation coefficients of >0.90. The correlation between TTE-derived measurements and CMR/MDCT was fair to moderate. Intra- and inter-observer agreement for LA volume measurements by TTE were inferior to CMR and MDCT., Conclusion: Measurements of LA volumes by CMR and 320-slice MDCT correlate closely in patients with permanent AF, and both modalities improve the reproducibility of measurements of LA volumes and function compared with 2D TTE.

Background: Atrial fibrillation is associated with inflammation. In contrast to inflammatory markers like C-reactive protein (CRP) and fibrinogen produced in the liver, YKL-40 is produced at the site of inflammation including in the myocardium. We hypothesized that elevated plasma YKL-40 levels associate with increased risk of atrial fibrillation., Method and Results: We measured plasma YKL-40 in 8731 participants from the prospective Copenhagen City Heart Study including 896 individuals who developed atrial fibrillation during up to 18 years of follow-up. Additionally, we measured YKL-40 in 6621 individuals from the cross-sectional Copenhagen General Population Study including 337 cases with atrial fibrillation. A YKL-40 level >95% percentile (>204 μg/L) versus <25% percentile (<36 μg/L) associated prospectively with a 2.10-fold (95%CI:1.43-3.09) increased risk of atrial fibrillation. Hazard ratios attenuated slightly after multifactorial adjustment to 2.01 (1.35-2.98), and further after additional adjustment for heart failure to 1.89 (1.27-2.80), for plasma CRP to 1.79 (1.20-2.67), and for fibrinogen levels to 1.89 (1.27-2.81). Adjusting multifactorially including both heart failure, CRP, and fibrinogen attenuated the risk of atrial fibrillation to 1.79 (1.20-2.67). These findings were supported in the cross-sectional study with an odds ratio of 2.73 (1.46-5.11) for a YKL-40 level >95% percentile versus <25% percentile, attenuating to an odds ratio of 2.13 (1.09-4.18) when adjusting multifactorially including heart failure, CRP, and fibrinogen., Conclusions: Elevated plasma YKL-40 levels robustly associated with increased risk of atrial fibrillation originating from hospital admissions or visits to the emergency department, independent of heart failure, and CRP and fibrinogen levels. These findings need to be confirmed in other independent studies., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Aims: Activation of the angiotensin II type 1 (AT1 ) receptor has been shown to mediate the structural and electrical remodelling of the atrial myocardium associated with atrial fibrillation. We hypothesized that AT1 genotypic variation is associated with atrial fibrillation or diseases predisposing to atrial fibrillation, such as hypertension, heart failure, ischaemic heart disease and myocardial infarction, in the general population., Methods: We resequenced the AT1 gene in 760 individuals with atrial fibrillation and identified two nonsynonymous variants (I103T and A244S), which were subsequently genotyped in the prospective Copenhagen City Heart Study (n = 10 603) and the prospective Copenhagen General Population Study (n = 60 647)., Results: Risk of atrial fibrillation for heterozygotes for AT1 genetic variants A244S and I103T/A244S vs. noncarriers was increased by 2.7-fold (95% confidence interval 1.5- to 5.1-fold) and 2.6-fold (95% confidence interval 1.6- to 4.2-fold), respectively, for men., Conclusions: Heterozygosity for the nonsynonymous AT1 genetic variants A244S and I103T/A244S was associated with increased risk of atrial fibrillation in men. The AT1 recptor might be a target for the pharmaceutical industry. This finding needs to be validated in independent studies., (© 2012 The Authors. British Journal of Clinical Pharmacology © 2012 The British Pharmacological Society.)

Background: Atrial fibrillation (AF) is associated with significant morbidity and mortality. To test the effect of interventions, knowledge of cardiac output (CO) is important. However, the irregular heart rate might cause some methods for determination of CO to have inherent weaknesses. Objective. To assess the validity of these methods in AF, a new inert gas rebreathing device and impedance cardiography was tested with echocardiography as reference., Methods: Using a cross-sectional design, 127 patients with AF and 24 in SR were consecutively recruited. Resting CO was measured using inert gas rebreathing (n = 62) or impedance measurement of intrathoracic blood flow (n = 89) in separate studies with echocardiographic measurement as reference., Results: CO determined with impedance cardiography was mean 4.77 L/min ± 2.24(SD) compared to 4.93 L/min ± 1.17 by echocardiography (n = 89, n.s.) in patients with AF. CO by inert gas rebreathing was 4.98 L/min ± 2.49(SD) compared to 5.70 L/min ± 2.49 by echocardiography (n = 62, n.s.) in patients with AF and SR (AF 5.42 ± 2.9 vs. 6.27, n.s. and SR 4.09 ± 1.08 vs. 4.35 ± 0.86, n.s.). Mean bias between impedance cardiography and echocardiography was 0.14 ± 0.95 L/min and -0.13 ± 0.98 L/min between inert gas rebreathing and echocardiography. Inert gas rebreathing showed larger intra-patient variation than impedance cardiography (0.11 vs. 0.054). Correlation between inert gas rebreathing and echocardiography was r = -0.060 and between impedance cardiography and echocardiography was r = 0.128. Impedance cardiography and inert gas rebreathing both underestimated CO compared to echocardiography., Conclusion: Variation between the inert gas rebreathing and the reference method for AF patients was less than desired. Impedance cardiography was superior to inert gas rebreathing and showed acceptable agreement with echocardiography and variability similar to echocardiography.

Objectives: The purpose of this study was to test whether the association of C-reactive protein (CRP) with increased risk of atrial fibrillation is a robust and perhaps even causal association., Background: Elevated levels of CRP previously have been associated with increased risk of atrial fibrillation., Methods: We studied 10,276 individuals from the prospective Copenhagen City Heart Study, including 771 individuals who had atrial fibrillation during follow-up, and another 36,600 persons from the cross-sectional Copenhagen General Population Study, including 1,340 cases with atrial fibrillation. Individuals were genotyped for 4 CRP gene polymorphisms and had high-sensitivity CRP levels measured., Results: A CRP level in the upper versus lower quintile associated with a 2.19-fold (95% confidence interval [CI]: 1.54- to 3.10-fold) increased risk of atrial fibrillation. Risk estimates attenuated slightly after multifactorial adjustment to 1.77 (95% CI: 1.22 to 2.55), and after additional adjustment for heart failure and plasma fibrinogen level to 1.47 (95% CI: 1.02 to 2.13) and 1.63 (95% CI: 1.21 to 2.20), respectively. Genotype combinations of the 4 CRP polymorphisms associated with up to a 63% increase in plasma CRP levels (p < 0.001), but not with increased risk of atrial fibrillation. The estimated causal odds ratio for atrial fibrillation by instrumental variable analysis for a doubling in genetically elevated CRP levels was lower than the odds ratio for atrial fibrillation observed for a doubling in plasma CRP on logistic regression (0.94 [95% CI: 0.70 to 1.27] vs. 1.36 [95% CI: 1.30 to 1.44]; p < 0.001)., Conclusions: Elevated plasma CRP robustly associated with increased risk of atrial fibrillation; however, genetically elevated CRP levels did not. This suggests that elevated plasma CRP per se does not increase atrial fibrillation risk., (Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: The renin-angiotensin system may play a role in the pathogenesis of atrial fibrillation, and renin-angiotensin system blockers reduce the risk of atrial fibrillation. We hypothesized that polymorphisms in the angiotensinogen and angiotensin-converting enzyme (ACE) genes encoding proteins in this system predict risk of atrial fibrillation., Methods and Results: We genotyped 9235 individuals from the Danish general population, The Copenhagen City Heart Study, for the a-20c, g-6a, T174M, and M235T polymorphisms in the angiotensinogen gene and the insertion/deletion (I/D) polymorphism in the ACE gene; rare allele frequencies were 0.16, 0.40, 0.12, 0.41, and 0.49, respectively. Participants had sinus rhythm at inclusion. During 26 years of follow-up, 968 individuals developed atrial fibrillation. Multifactorially adjusted hazard ratios for atrial fibrillation for a-20c ac and cc versus aa genotype were 1.1(95% confidence interval: 1.0-1.3; P=0.05) and 1.5(1.1-2.1; P=0.01). Compared with double noncarriers (angiotensinogen -20aa and ACE II), double heterozygotes (ac-I/D genotype), and double homozygotes (cc-DD) had hazard ratios for atrial fibrillation of 1.2(0.9-1.6; P=0.06) and 2.4(1.4-4.1; P=0.001). a-20c cc homozygotes above 70 years of age who were overweight, severely hypertensive, and had heart failure, had an absolute 10-year risk of atrial fibrillation of 61%., Conclusion: Angiotensinogen a-20c genotype alone and in combination with ACE I/D genotype predicts an increased risk of atrial fibrillation. Therefore, genetic variation in the renin-angiotensin system may influence effect of renin-angiotensin system blockers on atrial fibrillation.

Objective: To assess the long-term risk of developing permanent AF in relation to the signal-averaged P wave duration (SAPWD) and clinical and echocardiographic characteristics., Design: In an observational study design we studied 131 patients with earlier ECG-documented AF and successfully restored sinus rhythm attending a long-term, follow-up visit at hospital or at home. Established permanent AF was examined in relation to primary clinical, echocardiographic, and electrophysiological parameters., Results: Only prolonged SAPWD (p=0.006) was associated with an increased risk of development of permanent AF. The risk of permanent AF after 3 years follow-up was 0.72 with an SAPWD equal to 180 ms versus 0.39 with a normal SAPWD (130 ms). We found no prognostic effect of age, gender, dilated left atrium, long duration of AF history, or long duration of the most recent episode of AF. Co-existing hypertension reduced the risk of permanent AF; this could be explained by concomitant treatment with angiotensin-converting-enzyme-inhibitors., Conclusion: Prolonged SAPWD (a marker of atrial remodelling) appears to be a risk factor for long-term development of permanent AF.

Background and Aims: During atrial fibrillation (AF), the renin-angiotensin-aldosterone system (RAAS) may be activated. In this study, our aim was to evaluate at a long-term follow-up visit the levels of plasma aldosterone and natriuretic peptides as markers of neurohormonal remodeling in patients with earlier, documented AF in relation to present heart rhythm, clinical data, and the left ventricular ejection fraction (LVEF). We hypothesized that increased levels of aldosterone and natriuretic peptides were significantly associated with present AF as markers of RAAS activation during the arrhythmia., Methods: We studied 158 patients with earlier ECG-documented AF followed by restored sinus rhythm (SR) attending a follow-up visit 2.6 years (mean) after primary inclusion., Results: At follow-up, 93 patients had SR. Heart rhythm at follow-up visit (SR/AF), plasma aldosterone, plasma N-terminal pro Brain Natriuretic Peptide (Nt-proBNP), plasma N-terminal pro Atrial Natriuretic Peptide (Nt-proANP), LVEF, medication, and clinical characteristics were recorded. Standard linear multiple regression analysis including age, sex, weight, hypertension, congestive heart failure, ischemic heart disease, present AF at follow-up, total duration of AF disease, ongoing medication, and the LVEF as explanatory variables showed that only ongoing treatment with diuretics was significantly associated (likelihood ratio test, p = 0.0057) with a raised log-transformed plasma aldosterone, although present AF at follow-up was related to a high aldosterone level (p = 0.09). For the natriuretic peptides, present AF at follow-up (p < 0.0001), age (p < 0.0001), female gender (p = 0.0047), ischemic heart disease (p = 0.0154), and ongoing treatment with sotalol (p = 0.0003) were all independently associated with high log-transformed plasma Nt-proANP. Likewise, present AF at follow-up (p = 0.0008) as well as age (p < 0.0001) were associated with high log-transformed plasma Nt-proBNP., Conclusions: In patients with earlier AF, AF at long-term follow-up visit was independently associated with raised levels of Nt-proANP and Nt-proBNP and to some extent with plasma aldosterone indicating neurohormonal activation during arrhythmia., (Copyright 2007 S. Karger AG, Basel.)

The Copenhagen City Heart Study is a population-based cohort study. Using baseline data from 3 cohort examinations (1976 to 1978, 1981 to 1983, and 1991 to 1994), we analyzed the gender-specific effect of atrial fibrillation (AF) on the risk of stroke and cardiovascular death during 5 years of follow-up. Baseline data from 29,310 subjects were included. AF was documented in 276 subjects (110 women and 166 men). During a mean follow-up of 4.7 years, 635 strokes were identified, 35 of which occurred in subjects who had AF (22 women and 13 men). After adjustment for age and co-morbidity, the effect of AF on the risk of stroke was 4.6-fold greater in women (hazard ratio 7.8, 95% confidence interval 5.8 to 14.3) than in men (hazard ratio 1.7, 95% confidence interval 1.0 to 3.0). Cardiovascular death occurred in 1,122 subjects, 63 of whom had AF (28 in women and 35 in men). The independent effect of AF on cardiovascular mortality rate was 2.5-fold greater in women (hazard ratio 4.4, 95% confidence interval 2.9 to 6.5) than in men (hazard ratio 2.2, 95% confidence interval 1.6 to 3.1). Our results indicate that AF is a much more pronounced risk factor for stroke and cardiovascular death in women than in men.

Atrial fibrillation (AF) is the most frequently encountered cardiac arrhythmia. It is a risk factor for stroke and premature death. We studied the temporal changes in the prevalence of AF from 1976 to 1994 in a random population aged 50 to 89 years. The prevalence of AF, diagnosed from electrocardiograms (ECGs), was determined in 8,606 patients examined in 1976 to 1978, in 8,943 patients examined in 1981 to 1983, and in 6,733 subjects examined in 1991 to 1994. Changes in prevalence of AF were estimated by logistic regression analysis. In men, the age-standardized prevalence of AF increased from 1.4% in 1976 to 1978 (odds ratio [OR] 1.0, reference) to 1.9% in 1981 to 1983 (OR 1.6, 95% confidence interval [CI] 1.1 to 2.1), and to 3.3% in 1991 to 1994 (OR 2.3, 95% CI 1.6 to 3.4, p<0.001, adjusted for age). In women, the prevalence of AF decreased from 1.5% in 1976 to 1978 (OR 1.0, reference) to 1.0% in 1981 to 1983 (OR 0.7, 95% CI 0.5 to 1.0), and to 1.1% in 1991 to 1994 (OR 0.7, 95% CI 0.5 to 1.0), although the overall decrease was not significant (p=0.11, adjusted for age). After adjusting for changes in comorbidity, body weight, and height, the increase in the prevalence of AF in men from 1976 to 1978 and from 1991 to 1994 remained significant (OR 1.9, 95% CI 1.3 to 2.8, p=0.002). Although unchanged in women, the prevalence of AF in men more than doubled from the 1970s to the 1990s. The factors responsible for this gender-specific increase in the prevalence of this common arrhythmia have yet to be identified.

Background: Atrial fibrillation is a common arrhythmia associated with excess morbidity and mortality. We studied temporal changes in hospital admission rates for atrial fibrillation using data from a prospective population-based cohort study spanning 2 decades (the Copenhagen City Heart Study)., Methods: The study included baseline data collected in 1981 through 1983 on 10,955 persons age 40 to 79 years and baseline data collected in 1991 through 1994 on 7212 persons age 40 to 79 years. We used hospital diagnosis data from the Danish National Hospital Discharge Register to determine the rate of first hospital admission for atrial fibrillation during 7 years following each of the 2 baseline data collecting periods. Changes in admission rates were analyzed using Cox proportional hazard models., Results: During the 2 7-year periods, 379 subjects were admitted with a hospital diagnosis of atrial fibrillation. The rate of hospital admissions for atrial fibrillation increased among both men and women from the first to the second period (relative risk = 1.6; 95% confidence interval = 1.3-1.9 [adjusted for age, sex, prior myocardial infarction, arterial hypertension, diabetes mellitus, electrocardiographic left ventricular hypertrophy, decreased lung function, smoking, height, and weight])., Conclusion: During the latest 10 to 20 years, there has been a 60% increase in hospital admissions for atrial fibrillation independent of changes in known risk factors. This increase could result from changes in admission threshold or coding practices, or it could reflect a genuine increase in the population incidence of atrial fibrillation.

Aims Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with substantial morbidity and mortality. AF is associated with enlargement of the left atrium (LA), and the LA volume has important prognostic implications for the disease. The objective of the study was to determine how measurements of LA volume and function obtained by transthoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and 320-slice multi-detector computed tomography (MDCT) correlate in patients with permanent AF. Methods and results Thirty-four patients with permanent AF participated in the study. TTE, CMR, and 320-slice MDCT imaging procedures were performed within 7 ± 4 days. 320-slice MDCT overestimated maximal LA volume (LAmax) and minimal LA volume (LAmin) compared with CMR (LAmax: 80 vs. 73 mL/m2, P = 0.0017; LAmin: 69 vs. 64 mL/m2, P = 0.0217), whereas TTE underestimated these parameters compared with CMR (LAmax: 60 vs. 73 mL/m2, P < 0.0001; LAmin: 50 vs. 64 mL/m2, P < 0.0001), and also compared with MDCT (LAmax: 60 vs. 80 mL/m2, P < 0.0001; LAmin: 50 vs. 69 mL/m2, P < 0.0001). Measurements of LA volumes by MDCT and CMR closely correlated, and both MDCT and CMR had excellent intra- and inter-observer agreement with correlation coefficients of >0.90. The correlation between TTE-derived measurements and CMR/MDCT was fair to moderate. Intra- and inter-observer agreement for LA volume measurements by TTE were inferior to CMR and MDCT. Conclusion Measurements of LA volumes by CMR and 320-slice MDCT correlate closely in patients with permanent AF, and both modalities improve the reproducibility of measurements of LA volumes and function compared with 2D TTE. [ABSTRACT FROM PUBLISHER]

Aims Activation of the angiotensin II type 1 (AT1) receptor has been shown to mediate the structural and electrical remodelling of the atrial myocardium associated with atrial fibrillation. We hypothesized that AT1 genotypic variation is associated with atrial fibrillation or diseases predisposing to atrial fibrillation, such as hypertension, heart failure, ischaemic heart disease and myocardial infarction, in the general population. Methods We resequenced the AT1 gene in 760 individuals with atrial fibrillation and identified two nonsynonymous variants ( I103 T and A244 S), which were subsequently genotyped in the prospective Copenhagen City Heart Study ( n = 10 603) and the prospective Copenhagen General Population Study ( n = 60 647). Results Risk of atrial fibrillation for heterozygotes for AT1 genetic variants A244 S and I103 T/ A244 S vs. noncarriers was increased by 2.7-fold (95% confidence interval 1.5- to 5.1-fold) and 2.6-fold (95% confidence interval 1.6- to 4.2-fold), respectively, for men. Conclusions Heterozygosity for the nonsynonymous AT1 genetic variants A244 S and I103 T/ A244 S was associated with increased risk of atrial fibrillation in men. The AT1 recptor might be a target for the pharmaceutical industry. This finding needs to be validated in independent studies. [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation (AF) is the most common aberrant cardiac arrhythmia. Many AF patients present with symptoms of dyspnea and fatigue, but have normal left ventricular ejection fraction (LVEF). Purpose: To determine the reproducibility of measurements of global longitudinal strain (GLS) and strain rate in patients with AF and examine if the arrhythmia is associated with abnormal LV strain and strain rate independent of age, sex, heart rate, LVEF and LV mass. We hypothesized that AF independently reduces ventricular systolic performance. Methods: The study was conducted as a retrospective analysis of images from 150 randomly selected patients with AF compared to an equal number of subjects with sinus rhythm (SR) matched for age, sex, heart rate, LVEF and LV mass. Half of the patients had normal LVEF (LVEF > 50%) and half had reduced LVEF (LVEF < 50%). GLS and strain rate were measured in each group, as were quantitative LV volumes and standard systolic and diastolic parameters. Results: GLS was significantly impaired in patients with AF compared to subjects with SR, both in the overall population (-12.25 ± 4.1% vs. –16.13 ± 4.7%, p<0.0001), in patients with normal LVEF (-14.41 ± 3.9% vs. –19.42 ± 3.1%, p<0.0001) and in patients with reduced LVEF (-10.10 ± 3.1% vs. –12.85 ± 3.5%, p<0.0001). Linear regression and Bland Altman analyses demonstrated good intraobserver and interobserver agreement for measurements of GLS and strain rate parameters even in patients with AF. Conclusions: Measurements of GLS and strain rate parameters are reproducible in patients with AF. Patients with AF have significantly impaired values of GLS when compared to similar patients with SR independent of age, sex, heart rate, LVEF and LV mass. [ABSTRACT FROM AUTHOR]