Atrial fibrosis and the mechanisms of atrial fibrillation

Everett, Thomas H.; Olgin, Jeffrey E.

doi:10.1016/j.hrthm.2006.12.040

Cited by 296 publications

(200 citation statements)

References 58 publications

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“…3,4 Correlative data in biopsy and autopsy specimens from AF patients have demonstrated the presence of atrial fibrosis. 8 -10 Increased amounts of fibrosis were seen in the atria of patients with AF as opposed to those patients in sinus rhythm.…”

Section: Discussionmentioning

confidence: 99%

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

Xiao

Shu

et al. 2010

Clinical Cardiology

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Background:Atrial fibrosis was considered a structural basis for the development and sustaining of atrial fibrillation (AF). Transforming growth factor‐β1 (TGF‐β1) was one of the main factors for accelerating collagen production. The contribution of TGF‐β1 in the pathogenesis of AF needs further investigation.Hypothesis:The altered expression and distribution of TGF‐β1 will be associated with the changes in atrial fibrosis in different types of AF patients with rheumatic heart disease (RHD).Methods:Right atrial specimens obtained from 38 RHD patients undergoing mitral valve replacement surgery were divided into 3 groups: the sinus rhythm group (n = 8), the paroxysmal AF group (pAF; n = 10), and the chronic AF group (cAF; AF lasting ≥ 6 mo; n = 20). The degree of atrial fibrosis, collagen content, serum levels, messenger RNA (mRNA), and protein expression of TGF‐β1 were detected.Results:The collagen content, serum level, TGF‐β1 mRNA, and protein expression of the atrial tissue increased gradually in sinus rhythm, for both pAF and cAF groups, respectively. A positive correlation between TGF‐β1 and the degree of atrial fibrosis was also demonstrated (P < 0.05).Conclusion:The TGF‐β1 expression in atrial tissue increased gradually in proportion to the degree of atrial fibrosis in AF and was associated with the type of AF, which suggests that TGF‐β1 is possibly involved in the pathogenesis of AF in RHD patients. Copyright © 2010 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

Xiao

Shu

et al. 2010

Clinical Cardiology

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“…mechanism of insulin resistance that results in impaired atrial synchronicity and atrial electrical remodeling is still not well understood. It may be related to an altered myocardial protein degradation, 30 atrial myocardial fibrosis 31 or disruption of cardiocyte coupling at gap junctions, 32 which may finally cause electrophysiological instability in the atrial myocardium and lead to impaired atrial synchronicity and atrial electrical remodeling. Further studies are needed to identify in detail the exact mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Impaired atrial synchronicity in patients with metabolic syndrome associated with insulin resistance and independent of hypertension

Yang

Gong

et al. 2009

Hypertens Res

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The risk of developing atrial fibrillation is increased in patients with metabolic syndrome, but atrial conduction properties are uncharacterized in patients who have metabolic syndrome without atrial arrhythmia. We used tissue Doppler imaging to evaluate intra-and interatrial synchronicity in such patients. The imaging was performed in 145 patients with metabolic syndrome and 110 controls. Atrial synchronicity was determined from the intervals between the onset of the P-wave to the onset of the A-wave at the left atrial free wall (P-LA), interatrial septum (P-IAS) and right atrial free wall (P-RA). Intra-atrial synchronicity was defined as the differences between P-IAS and P-RA (RA synchronicity) and between P-LA and P-IAS (LA synchronicity). Interatrial synchronicity was defined as the difference between P-LA and P-RA. P-LA and P-IAS were significantly prolonged in the metabolic syndrome group relative to the control group (P-LA: 64.34 ± 13.99 vs. 55.35 ± 12.67, Po0.001; P-IAS: 36.49±12.39 vs. 31.55±11.61, P¼0.001), whereas P-RA showed no difference. As a result, this caused impaired intra-and interatrial synchronicity in patients with metabolic syndrome. Stepwise multivariate linear analysis revealed insulin resistance as an independent predictor of impaired intra-and interatrial synchronicity. Subgroup analysis indicated that there was no difference in atrial asynchrony between non-hypertensive and hypertensive subgroups in metabolic syndrome patients. In conclusion, patients with metabolic syndrome without atrial arrhythmia have impaired intra-and interatrial synchronicity. Insulin resistance has an important role in impaired atrial conduction in these patients.

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“…12 Although the precise signaling processes involved in the development of atrial fibrosis are unknown, the potentially important role of RAAS in AF is presented in a recent article. 13 Clinical trials showed a reduction in the development and recurrence of AF with ACEIs and ARBs. 1,2,14 -18 Surprisingly however, the association of aldosterone and AF, and aldosterone blockade for the prevention of AF have received little attention.…”

Section: Aldosterone Mineralocorticoid Receptor and Atrial Fibrillamentioning

confidence: 99%

Increased Expression of Mineralocorticoid Receptor and 11β‐Hydroxysteroid Dehydrogenase Type 2 in Human Atria During Atrial Fibrillation

Pei

Zhao

et al. 2010

Clinical Cardiology

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BackgroundAtrialfibrillation (AF) is associated with the activation of the renin‐angiotensin‐aldosterone system in the atria. It is not clear whether the expression of a mineralocorticoid receptor (MR), or 11β‐hydroxysteroid dehydrogenase type 2 (11βHSD2), conferring aldosterone specificity to the MR, in patients with AF is altered.HypothesisPatients with AF may be associated with increased expression of MR and 11βHSD2 in the atria.MethodsAtrial tissue samples of 25 patients with rheumatic heart valve disease undergoing a valve replacement operation were examined. A total of 13 patients had chronic persistent AF (>6 mo) and 12 patients had no history of AF. The MR and 11βHSD2 expression were analyzed at the mRNA and protein level. The localization of MR and 11βHSD2 in atrial tissue was performed using specific immunohistochemistry staining.ResultsThe results of real‐time quantitative polymerase chain reaction (PCR) showed that AF groups, in comparison with sinus rhythm, had a higher mRNA expression level of MR or 11βHSD2 (all P < 0.01). Both the MR and 11βHSD2 protein expression level in atrial tissue were also significantly increased in patients with AF compared with patients with sinus rhythm (P < 0.05 or P < 0.01). The immunohistochemical staining of MR or 11βHSD2 demonstrated that MR and 11βHSD2 predominately located in the cytoplasm of myocardial cells in the atrium and the intensity and density of immunostaining appeared to be increased in the atria of patients with AF compared to those without AF.ConclusionsIncreasing expression of MR and 11βHSD2 in the atria during AF is one of the molecular mechanisms for development of atrial interstitial fibrosis in patients with AF. These findings may have an important impact on the treatment of AF with aldosterone antagonists. Copyright © 2010 Wiley Periodicals, Inc.

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Atrial fibrosis and the mechanisms of atrial fibrillation

Cited by 296 publications

References 58 publications

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

TGF‐β1 Expression and Atrial Myocardium Fibrosis Increase in Atrial Fibrillation Secondary to Rheumatic Heart Disease

Impaired atrial synchronicity in patients with metabolic syndrome associated with insulin resistance and independent of hypertension

Increased Expression of Mineralocorticoid Receptor and 11β‐Hydroxysteroid Dehydrogenase Type 2 in Human Atria During Atrial Fibrillation

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