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Novel association patterns of cardiac remodeling markers in patients with essential hypertension and atrial fibrillation
Andreas S Kalogeropoulos, Sotirios Tsiodras, Angelos G Rigopoulos, Eleftherios A Sakadakis, Andreas Triantafyllis, Dimitrios TH Kremastinos, Ioannis Rizos
BMC Cardiovascular Disorders , 2011, DOI: 10.1186/1471-2261-11-77
Abstract: Serum levels of MMP-2, MMP-3, MMP-9 and TIMP-1 were measured in 86 patients: 27 on SR without any AF history, 33 with paroxysmal and 26 with permanent AF. All subjects had essential hypertension, normal systolic function and no coronary artery disease.Patients with AF had higher MMP-2, MMP-3 and MMP-9 and lower TIMP-1 compared to SR subjects (all p < 0.001). Paroxysmal AF was associated with higher MMP-2 levels compared to permanent AF (p < 0.001). Matrix metalloproteinase-9 but not MMP-3 was higher in permanent compared to paroxysmal AF group (p < 0.001). Patients with AF had lower levels of TIMP-1 compared to those with SR while permanent AF subjects had lower TIMP-1 levels than those with paroxysmal AF (p < 0.001 for both comparisons). Lower TIMP-1 was the only independent factor associated with AF (OR: 0.259, 95%CI: 0.104-0.645, p = 0.004).In hypertensives, paroxysmal AF and permanent AF differ with respect to serum MMPs. Increased MMP-2 is associated with paroxysmal, whereas increased MMP-9 with permanent AF. Additionally, lower levels of TIMP-1 had a strong association with AF incidence.Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice, with the highest prevalence observed among elderly people. Atrial fibrillation is responsible for markedly increased cardiovascular morbidity, and mortality and has been associated with various cardiovascular disorders, predominantly with hypertension, coronary artery disease, heart failure and valvular heart disease [1]. Various factors, including atrial remodeling and inflammation, have been implicated in the pathogenesis and perpetuation of AF; nevertheless the exact mechanism still remains uncertain [2-6]. Electrical remodeling is the possible substrate for persistence of AF after the initial event [7,8]. On the other hand, an underlying structural remodeling might occur before, during and after electrical remodeling, that is only in part reversible and can additionally contri
Effects of Electrical and Structural Remodeling on Atrial Fibrillation Maintenance: A Simulation Study  [PDF]
Trine Krogh-Madsen,Geoffrey W. Abbott,David J. Christini
PLOS Computational Biology , 2012, DOI: 10.1371/journal.pcbi.1002390
Abstract: Atrial fibrillation, a common cardiac arrhythmia, often progresses unfavourably: in patients with long-term atrial fibrillation, fibrillatory episodes are typically of increased duration and frequency of occurrence relative to healthy controls. This is due to electrical, structural, and contractile remodeling processes. We investigated mechanisms of how electrical and structural remodeling contribute to perpetuation of simulated atrial fibrillation, using a mathematical model of the human atrial action potential incorporated into an anatomically realistic three-dimensional structural model of the human atria. Electrical and structural remodeling both shortened the atrial wavelength - electrical remodeling primarily through a decrease in action potential duration, while structural remodeling primarily slowed conduction. The decrease in wavelength correlates with an increase in the average duration of atrial fibrillation/flutter episodes. The dependence of reentry duration on wavelength was the same for electrical vs. structural remodeling. However, the dynamics during atrial reentry varied between electrical, structural, and combined electrical and structural remodeling in several ways, including: (i) with structural remodeling there were more occurrences of fragmented wavefronts and hence more filaments than during electrical remodeling; (ii) dominant waves anchored around different anatomical obstacles in electrical vs. structural remodeling; (iii) dominant waves were often not anchored in combined electrical and structural remodeling. We conclude that, in simulated atrial fibrillation, the wavelength dependence of reentry duration is similar for electrical and structural remodeling, despite major differences in overall dynamics, including maximal number of filaments, wave fragmentation, restitution properties, and whether dominant waves are anchored to anatomical obstacles or spiralling freely.
Atrial Remodeling And Atrial Fibrillation: Mechanistic Interactions And Clinical Implications
Bandar Al Ghamdi,Walid Hassan
Journal of Atrial Fibrillation , 2009, DOI: 10.4022/jafib.v1.i7.537
Abstract: Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. The prevalence of AF increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. Although the pathophysiological mechanism underlying the genesis of AF has been the focus of many studies, it remains only partially understood. Conventional theories focused on the presence of multiple re-entrant circuits originating in the atria that are asynchronous and conducted at various velocities through tissues with various refractory periods. Recently, rapidly firing atrial activity in the muscular sleeves at the pulmonary veins ostia or inside the pulmonary veins have been described as potential mechanism,. AF results from a complex interaction between various initiating triggers and development of abnormal atrial tissue substrate. The development of AF leads to structural and electrical changes in the atria, a process known as remodeling. To have effective surgical or catheter ablation of AF good understanding of the possible mechanism(s) is crucial. Once initiated, AF alters atrial electrical and structural properties that promote its maintenance and recurrence. The role of atrial remodeling (AR) in the development and maintenance of AF has been the subject of many animal and human studies over the past 10-15 years. This review will discuss the mechanisms of AR, the structural, electrophysiologic, and neurohormonal changes associated with AR and it is role in initiating and maintaining AF. We will also discuss briefly the role of inflammation in AR and AF initiation and maintenance, as well as, the possible therapeutic interventions to prevent AR, and hence AF, based on the current understanding of the interaction between AF and AR.
In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation  [PDF]
Jussi T. Koivum?ki,Gunnar Seemann,Mary M. Maleckar,Pasi Tavi
PLOS Computational Biology , 2014, DOI: doi/10.1371/journal.pcbi.1003620
Abstract: Chronic atrial fibrillation (AF) is a complex disease with underlying changes in electrophysiology, calcium signaling and the structure of atrial myocytes. How these individual remodeling targets and their emergent interactions contribute to cell physiology in chronic AF is not well understood. To approach this problem, we performed in silico experiments in a computational model of the human atrial myocyte. The remodeled function of cellular components was based on a broad literature review of in vitro findings in chronic AF, and these were integrated into the model to define a cohort of virtual cells. Simulation results indicate that while the altered function of calcium and potassium ion channels alone causes a pronounced decrease in action potential duration, remodeling of intracellular calcium handling also has a substantial impact on the chronic AF phenotype. We additionally found that the reduction in amplitude of the calcium transient in chronic AF as compared to normal sinus rhythm is primarily due to the remodeling of calcium channel function, calcium handling and cellular geometry. Finally, we found that decreased electrical resistance of the membrane together with remodeled calcium handling synergistically decreased cellular excitability and the subsequent inducibility of repolarization abnormalities in the human atrial myocyte in chronic AF. We conclude that the presented results highlight the complexity of both intrinsic cellular interactions and emergent properties of human atrial myocytes in chronic AF. Therefore, reversing remodeling for a single remodeled component does little to restore the normal sinus rhythm phenotype. These findings may have important implications for developing novel therapeutic approaches for chronic AF.
Association of inflammation with atrial fibrillation in hyperthyroidism
Mehmet Ozaydin,Ali Kutlucan,Yasin Turker,Banu Koroglu
老年心脏病学杂志(英文版) , 2012,
Abstract: Objectives The aim of this study was to evaluate the relationship between inflammation and development of atrial fibrillation (AF) in patients with hyperthyroidism. Methods A total of 65 patients with newly diagnosed hyperthyroidism, 35 of whom were in sinus rhythm and 30 of whom in AF. Thirty five age- and gender-matched patients in a control group were included in the study. Factors associated with the development of AF were evaluated by multivariate regression analysis. Results Factors associated with AF in multivariate analysis included high sensitivity C reactive protein [(HsCRP); odds ratio (OR): 11.19; 95% confidence interval (95% CI): 1.80-69.53; P = 0.003], free T4 (OR: 8.76; 95% CI: 2.09–36.7; P = 0.003), and left atrial diameter (OR: 1.25; 95% CI: 1.06–1.47; P = 0.008). Conclusions The results of the present study suggest that high sensitivity C reactive protein, an indicator of inflammation, free T4 and left atrial diameter are associated with the development AF in patients with hyperthyroidism.
Aortic Stiffness in Lone Atrial Fibrillation: A Novel Risk Factor for Arrhythmia Recurrence  [PDF]
Dennis H. Lau, Melissa E. Middeldorp, Anthony G. Brooks, Anand N. Ganesan, Kurt C. Roberts-Thomson, Martin K. Stiles, Darryl P. Leong, Hany S. Abed, Han S. Lim, Christopher X. Wong, Scott R. Willoughby, Glenn D. Young, Jonathan M. Kalman, Walter P. Abhayaratna, Prashanthan Sanders
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076776
Abstract: Background Recent community-based research has linked aortic stiffness to the development of atrial fibrillation. We posit that aortic stiffness contributes to adverse atrial remodeling leading to the persistence of atrial fibrillation following catheter ablation in lone atrial fibrillation patients, despite the absence of apparent structural heart disease. Here, we aim to evaluate aortic stiffness in lone atrial fibrillation patients and determine its association with arrhythmia recurrence following radio-frequency catheter ablation. Methods We studied 68 consecutive lone atrial fibrillation patients who underwent catheter ablation procedure for atrial fibrillation and 50 healthy age- and sex-matched community controls. We performed radial artery applanation tonometry to obtain central measures of aortic stiffness: pulse pressure, augmentation pressure and augmentation index. Following ablation, arrhythmia recurrence was monitored at months 3, 6, 9, 12 and 6 monthly thereafter. Results Compared to healthy controls, lone atrial fibrillation patients had significantly elevated peripheral pulse pressure, central pulse pressure, augmentation pressure and larger left atrial dimensions (all P<0.05). During a mean follow-up of 2.9±1.4 years, 38 of the 68 lone atrial fibrillation patients had atrial fibrillation recurrence after initial catheter ablation procedure. Neither blood pressure nor aortic stiffness indices differed between patients with and without atrial fibrillation recurrence. However, patients with highest levels (≥75th percentile) of peripheral pulse pressure, central pulse pressure and augmentation pressure had higher atrial fibrillation recurrence rates (all P<0.05). Only central aortic stiffness indices were associated with lower survival free from atrial fibrillation using Kaplan-Meier analysis. Conclusion Aortic stiffness is an important risk factor in patients with lone atrial fibrillation and contributes to higher atrial fibrillation recurrence following catheter ablation procedure.
Could successful cryoballoon ablation of paroxysmal atrial fibrillation prevent progressive left atrial remodeling?
Tamás Erdei, Mónika Dénes, Attila Kardos, Attila Mihálcz, Csaba F?ldesi, András Temesvári, Mária Lengyel
Cardiovascular Ultrasound , 2012, DOI: 10.1186/1476-7120-10-11
Abstract: 36 patients selected for their first CCA because of nonvalvular paroxysmal AF had echocardiography before and 3, 6 and 12 months after CCA. LA diameters, volumes (LAV) and LA volume index (LAVI) were evaluated. LA function was assessed by: early diastolic velocities of the mitral annulus (Aasept, Aalat), LA filling fraction (LAFF), LA emptying fraction (LAEF) and the systolic fraction of pulmonary venous flow (PVSF). Detailed left ventricular diastolic function assessment was also performed.Excluding recurrences in the first 3-month blanking period, the clinical success rate was 64%. During one-year of follow-up, recurrent atrial arrhythmia was found in 21 patients (58%). In the recurrent group at 12 months after ablation, minimal LAV (38 ± 19 to 44 ± 20 ml; p < 0.05), maximal LAV (73 ± 23 to 81 ± 24 ml; p < 0.05), LAVI (35 ± 10 to 39 ± 11 ml/m2; p = 0.01) and the maximal LA longitudinal diameter (55 ± 5 to 59 ± 6 mm; p < 0.01) had all increased. PVSF (58 ± 9 to 50 ± 10%; p = 0.01) and LAFF (36 ± 7 to 33 ± 8%; p = 0.03) had decreased. In contrast, after successful cryoballoon ablation LA size had not increased and LA function had not declined. In the recurrent group LAEF was significantly lower at baseline and at follow-up visits.In patients whose paroxysmal atrial fibrillation recurred within one year after cryoballoon catheter ablation left atrial size had increased and left atrial function had declined. In contrast, successful cryoballoon catheter ablation prevented progressive left atrial remodeling.The relationship between left atrial (LA) dilatation and atrial fibrillation (AF) has been widely accepted for a long time [1]. Electrophysiological, structural and functional atrial remodeling have been observed in patients with AF, and it has been shown that normal myocardial tissue is often replaced with fibrosis [2]. Dilated left atrium predict later cardiovascular events [3]. Catheter ablation of atrial fibrillation has been established as a therapeutic option f
Hyperglycemia aggravates atrial interstitial fibrosis, ionic remodeling and vulnerability to atrial fibrillation in diabetic rabbits  [cached]
Changle Liu,Huaying Fu,Jian Li,Wansong Yang
Anadolu Kardiyoloji Dergisi , 2012,
Abstract: Objective: The purpose of this study was to investigate the effects of hyperglycemia on atrial interstitial fibrosis, ionic remodeling and vulnerability to atrial fibrillation (AF) in alloxan-induced diabetic rabbits.Methods: Sixty Japanese rabbits were randomly assigned to alloxan-induced diabetic group (n=30) and control group (n=30). Ten rabbits in each group were respectively used to electrophysiological and histological study, patch-clamp study and Western blotting analysis. Langendorff perfusion was used to record inter-atrial conduction time (IACT), atrial effective refractory period (AERP) and dispersion (AERPD) and vulnerability to AF. Histological study was measured by Sirius-red stain. Patch-clamp technique was used to measure action potential duration (APD) and atrial ionic currents (INa and ICaL). Western blotting was applied to assess atrial protein expression of transforming growth factor beta 1 (TGFβ1).Results: Compared with control group, electrophysiological studies showed IACT was prolonged (37.91±6.81 vs. 27.43±1.63ms, p<0.01), AERPD was increased (30.37±8.33 vs. 14.70±5.16ms, p<0.01) in diabetic group. Inducibility of AF in diabetic group was significantly higher than in controls (8/10 vs. 1/10 of animals, p<0.01). Collagen volume fraction was increased (6.20±0.64% vs. 2.15±0.21%, p<0.01) in diabetic group. Patch-clamp studies demonstrated APD90 and APD50 were prolonged in diabetic rabbits (p<0.05 vs. control). The densities of INa were reduced and the densities of ICaL were increased (p<0.01 vs. control). Protein expression of TGFβ1 was increased in diabetic group (p<0.001 vs. control).Conclusion: Our study suggests that hyperglycemia contributes to atrial interstitial fibrosis, ionic remodeling and vulnerability to AF in diabetic rabbits, resulting in atrial structural remodeling and electrical remodeling for the development and perpetuation of AF.
Relationship of CHA2DS2-VASc and CHADS2 Score to Left Atrial Remodeling Detected by Velocity Vector Imaging in Patients with Atrial Fibrillation  [PDF]
Yihui Li, Wenyuan Ding, Hua Wang, Nianpeng Song, Leyu Lin, Zhihao Wang, Ming Zhong, Yun Zhang, Wei Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0077653
Abstract: Background The CHADS2/CHA2DS2-VASc scores are used to predict thrombo-embolic/stroke in patients with nonvalvular atrial fibrillation (AF). Nevertheless, limited data are available regarding the association between these risk stratification for stroke and left atrial (LA) remodeling status of AF patients. The purpose of this study was to explore the association between these scores and LA remodeling status assessed quantificationally by echocardiography in AF patients. Methods One hundred AF patients were divided into 3 groups based on the CHA2DS2-VASc/CHADS2 score: the score of 0 (low stroke risk), the score of 1 (moderate stroke risk) and the score of ≥2 (high stroke risk). All patients were performed through conventional and velocity vector imaging echocardiography. Echocardiographic parameters: maximum LA volume index (LAVImax), LA total emptying fraction (LAEFt) and LA mean strain were obtained to assess quantificationally LA remodeling status. Results On categorizing with CHA2DS2-VASc, the score of 1 group showed augment in LAVImax and attenuation in LA mean strain derived from VVI, compared with the score of 0 group (LAVImax: 40.27±21.91 vs. 26.79±7.87, p=0.002; LA mean strain: 15.18±6.36 vs. 22±8.54, p=0.001). On categorizing with the CHADS2 score, similar trends were seen between the score of ≥2 and 1 groups (LAVImax: 43.72±13.77 vs. 31.41±9.50, p<0.001; LA mean strain: 11.01±5.31 vs. 18.63±7.00, p<0.001). With multivariate logistic regression, LAVImax (odds ratio: 0.92 , 95% C=I: 0.85 to 0.98, p= 0.01) and LA mean strain reflecting LA remodeling (odds ratio: 1.10, 95% CI: 1.02 to 1.19, p=0.01) were strongly predictive of the CHA2DS2-VASc score of 0. Conclusions The superiority of the CHADS2 score may lay in identifying LA remodeling of AF patients with high stroke risk. Whereas, the CHA2DS2-VASc score was better than the CHADS2 score at identifying LA remodeling of AF patients presenting low stroke risk.
Preliminary study of circulating microRNA expression profiles in patients with atrial fibrillation  [cached]
Yu ZHANG,Yue-xiang ZHAO,Hong-yang GUO,Jian-ping GUO
Medical Journal of Chinese People's Liberation Army , 2012,
Abstract: Objective To investigate the expression profiles of the circulating microRNA (miRNA) of patients suffering from persistent or paroxysmal atrial fibrillation (AF) by using miRNA chips to provide the basis for further investigation of the regulatory mechanisms of miRNAs in AF. Methods A total of 10 patients with persistent AF in 5 and paroxysmal AF in 5 and 5 healthy volunteers were enrolled in the study from Cardiology Department of General Hospital of PLA. Their whole blood specimens were taken to extract the total serum RNA. MiRNA chips were used for hybridization, and then miRNA expression profiles were obtained. The volcano plot method was adopted to search for differentially expressed miRNAs, and MEV software was used to conduct cluster analyses. Results Compared with the healthy control group, 13 miRNA models exhibited significant differential expressions in the serum from persistent or paroxysmal AF patients. Among the 13 models, 8 were up-regulated of expression, namely, miR-316, miR-3612, miR-634, miR-376a, miR-517b, miR-377*, miR-590-3p, and miR-664, and 5 were downregulated, namely, miR-1, kshv-miR-K12-5, miR-378c, miR-204, and miR-27a. A difference in miRNA expression profiles between patients with persistent and paroxysmal AF was discovered. Conclusion The circulating miRNA expression profiles may present significant changes in persistent or paroxysmal AF patients, showing that circulating miRNA could be used to study the regulatory mechanisms in the occurrence and development of AF.
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