Histological Substrate of Atrial Biopsies in Patients With Lone Atrial Fibrillation

Frustaci, Andrea; Chimenti, Cristina; Bellocci, Fulvio; Morgante, Emanuela; Russo, Matteo Antonio; Maseri, Attilio

doi:10.1161/01.cir.96.4.1180

Cited by 1,256 publications

(916 citation statements)

References 13 publications

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“…It should be emphasized that previous studies did not compare the role of inflammation in valvular AF and nonvalvular AF. 3,4,6,8 This study is the first to report the correlation of nonvalvular AF with elevated expression of markers of systemic inflammation, such as TNF-α mRNA, IL-6 mRNA in peripheral blood monocytes, and serum IL-1.…”

Section: Discussionmentioning

confidence: 86%

“…3,4 Furthermore, Frustaci et al reported that inflammatory infiltrates and oxidative damage were uniformly found in multiple biopsy specimens in 12 patients with paroxysmal lone AF refractory to conventional antiarrhythmic treatment. 8 Inflammation may promote the persistence of AF and hypertension, but the mechanism is poorly understood and needs further investigation.…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Chen¹,

Bing²,

He³

et al. 2009

Clinical Cardiology

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Background: Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-γ (PPARγ) has been proved to have anti-inflammatory effects and is implicated as a molecular pathway involved in many cardiovascular diseases, such as hypertension. The correlation between PPARγ inflammation and AF is still unknown. Methods: Using a case-control study design, 57 patients with hypertensive AF (persistent AF: 32, paroxysmal AF: 25) were included into the study groups. A total of 32 age-matched patients with hypertension, but without AF were selected as the control group. The expressions of PPARγ, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA in monocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods. Results: The PPARγ mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 ± 0.0702 vs 0.564 ± 0.0436, P<0.01). TNF-α mRNA, IL-6 mRNA, and IL-1 were increased in patients with hypertensive AF compared to the non-AF group and it was even higher in persistent AF than in paroxysmal AF (0.721 ± 0.0541 vs 0.530 ± 0.0496, 0.567 ± 0.044 vs 0.457 ± 0. 0505, 325.61 ± 88.10 vs 190.65 ± 59.38, respectively, P<0.01). TNF-α, IL-6, and IL-1 were in negative correlation with PPARγ, the correlation coefficient was −0.854, −0.769, and −0.702, respectively (P<0.01). Conclusions: In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARγ may be involved in the pathogenesis of AF by regulation of inflammation.

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Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Chen¹,

Bing²,

He³

et al. 2009

Clinical Cardiology

View full text Add to dashboard Cite

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“…26 Inflammatory changes have been observed in atrial tissues obtained from patients with isolated persistent AF. 27 Serum CRP level has been found to be significantly higher in patients with paroxysmal and chronic AF than in normal controls. 9 In a retrospective analysis of the Cardiovascular Health Study, it was shown that higher inflammation status during sinus rhythm potentially increases the risk of occurrence of AF in a follow-up period.…”

Section: Discussionmentioning

confidence: 96%

Association Between Serum C‐reactive Protein Elevation and Atrial Fibrillation After First Anterior Myocardial Infarction

Gedikli¹,

Örem²,

Baykan³

et al. 2008

Clinical Cardiology

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Background: Elevated inflammatory markers have been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that C-reactive protein (CRP) may be involved in the initiation process of atrial fibrillation (AF). However, the role of CRP levels in the occurence of AF in patients with AMI has not been studied. This study investigated whether CRP is a risk factor for AF in patients with acute anterior MI. Methods: We prospectively evaluated 92 consecutive patients (25 women and 67 men; aged 58±11 y) with a first acute anterior wall MI. Blood samples were obtained at the time of admission to the hospital, and serum CRP levels were measured by an ultrasensitive immunonephelometry method. All patients were evaluated by echocardiography to measure the left ventricular (LV) diameter and functions. All patients were monitored continuously for the detection of AF in the coronary care unit. Results: Atrial fibrillation occured in 19 (20%) of 92 patients. Univariate analysis showed that patients with AF had an advanced age (63±9.9 versus 56.7±11.7 y, p = 0.034), higher serum CRP level (2.95±2.5 versus 1.71±2.12 mg/dL, p = 0.034), larger LV end-systolic volume (74±15 versus 63±19, mL p = 0.02), higher LV ejection fraction (31.1±6.2 versus 38.4±10%, p = 0.001), and larger left atrial (LA) diameter (37.1±4.2 versus 34.7±3.3 mm, p = 0.01). In multivariate analysis, only age (odds ratio [OR]: 1.05, 95% confidence interval [CI]: 1-1.11, p = 0.036) and CRP levels (OR: 1.27, 95% CI: 1-1.59, p = 0.039) were independent predictors of AF. Conclusion: These results suggest that CRP may be a risk factor for AF in patients with acute anterior wall MI.

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“…31,32 Frustaci et al first demonstrated a high prevalence of inflammatory infiltrates, myocyte necrosis and fibrosis in atrial biopsies from patients with lone AF, but not in atrial biopsies from control patients. 33 Other papers have reported that an increase in high-sensitivity C-reactive protein levels is an independent risk factor for future AF among patients with sinus rhythm. 34,35 Whether inflammation is a consequence or a cause of AF is still controversial.…”

Section: Discussionmentioning

confidence: 99%

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

et al. 2011

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Hypertension is well known to increase atrial fibrillation (AF) and the development of AF is associated with atrial chamber remodeling. Although mineralocorticoid receptor (MR) inhibition provides cardiovascular protection, the role of MR on atrial structural remodeling and inducibility of AF in hypertension remains unclear. Here, we investigated roles of the MR on atrial structural remodeling and inducibility of AF in hypertensive rats by using MR antagonist eplerenone (EPL). Dahl salt-sensitive (DS) rats were fed a normal-salt or a high-salt (HS) diet from 7 weeks, and a non-antihypertensive dose of EPL or vehicle was administrated from 13 weeks, at which time myocytes hypertrophy, interstitial fibrosis in the atrium and AF inducibility had increased, until 20 weeks. There was no significant difference in systolic blood pressure between DS+HS (186±4 mm Hg) and DS+HS+EPL (184±5 mm Hg) at 20 weeks. Burst atrial pacing demonstrated decreased AF inducibility in DS+HS+EPL (0 of 10) compared with DS+HS (7 of 10). Fibrosis and myocytes hypertrophy in the atrium were decreased in DS+HS+EPL with the reduction of atrial inflammatory cytokines. These beneficial effects of EPL were associated with less atrial oxidative stress, as assessed by 4-hydroxy-2-nonenal staining, and reduced activation of the Rho GTPase Rac1 in the atrium. Thus, MR has important roles in atrial structural remodeling and AF inducibility in Dahl rats. The effects of MR are associated, at least in part, with activation of Rac1-oxidative stress/inflammatory axis.

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Histological Substrate of Atrial Biopsies in Patients With Lone Atrial Fibrillation

Cited by 1,256 publications

References 13 publications

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

Association Between Serum C‐reactive Protein Elevation and Atrial Fibrillation After First Anterior Myocardial Infarction

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

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