Relation of elevated C-reactive protein and interleukin-6 levels to left atrial size and duration of episodes in patients with atrial fibrillation

Psychari, Stavroula N.; Αποστολου, Θωμασ; Sinos, Loukas; Hamodraka, E.; Liakos, G.; Kremastinos, Dimitrios Th.

doi:10.1016/j.amjcard.2004.11.032

Cited by 284 publications

(196 citation statements)

References 11 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: 81%

“…Thereafter, several studies found that plasma inflammatory cytokines such as high sensitivity C-reactive protein (hs-CRP), CRP, IL-6, and TNF-α were elevated in AF, especially in persistent AF. 3,4,6,7 The association between AF, CRP, IL-6 levels, and increased left atrial diameter (LAD) supports a link between the burden of AF, inflammation, and atrial structural remodeling. 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.…”

Section: Introductionmentioning

confidence: 97%

“…3,4,6,7 The association between AF, CRP, IL-6 levels, and increased left atrial diameter (LAD) supports a link between the burden of AF, inflammation, and atrial structural remodeling. 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: 97%

“…1,2 More recently, increasing data show that inflammation may be related to AF. 3,4 Bruins et al 3 has reported that frequency of AF was increased after cardiac surgery, and changes in levels of CRP, complement-CRP complexes after surgery, and cardiopulmonary bypass (CPB) were responsible for the occurrence of postoperative AF. Thereafter, several studies found that plasma inflammatory cytokines such as high sensitivity C-reactive protein (hs-CRP), CRP, IL-6, and TNF-α were elevated in AF, especially in persistent AF.…”

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: 81%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

show abstract

“…32 Elevated markers of inflammation such as C-reactive protein, interleukin-1 (IL-1), IL-6, tumor necrosis factor, and inflammatory changes in histopathologic examination of atrial tissues showed that chronic inflammation may play a role in AF initiation and perpetuation. [33][34][35][36] Polymorphisms of IL-1β have been associated with AF likely because of the inadequate limitation of inflammatory reactions. 37 Canakinumab is a human monoclonal antibody that selectively neutralizes the proinflammatory cytokine IL-1β.…”

Section: Maintenance Canakinumabmentioning

confidence: 99%