Plasma oxidative stress and inflammatory biomarkers are associated with the sizes of the left atrium and pulmonary vein in atrial fibrillation patients

Abstract

Background Oxidative stress and inflammatory processes are responsible for the pathogenesis of AF, but their relationship with the sizes of the LA and PVs in AF patients remains unclear. Hypothesis Oxidative stress and inflammatory processes are associated with the sizes of the LA and PVs in AF patients. Methods 82 AF patients were compared to 30 control patients by using a case‐control study design. Oxidative stress, inflammatory biomarkers and the sizes of the LA and PVs were detected. Results (1) Hs‐CRP, IL‐6, IL‐8, TNF‐α, MDA and ox‐LDL were higher, and SOD was lower in AF patients than in control patients. Hs‐CRP, MDA and ox‐LDL were higher in permanent AF patients than in paroxysmal and persistent AF patients. (2) CsA of LSPV, RSPV, RIPV, LAA and LAV were statistically higher in AF patients than in control patients. CsA of RSPV, LSPV, LIPV and LAV were higher in permanent AF patients than in paroxysmal and persistent AF patients. (3) In the AF group, hs‐CRP and TNF‐α were positively correlated with LAV; MDA was positively correlated with CsA of LAA, LSPV and LAV; SOD was passively correlated with CsA of LAA and LAV; ox‐LDL was positively correlated with CsA of LAA and LAV. Multivariate logistic regression analysis showed hs‐CRP, ox‐LDL, RSPV CsA, LIPV CsA and LAV were associated with AF. Conclusions Oxidative stress, inflammatory biomarkers and the sizes of the LA and PVs were significantly increased in AF patients. Hs‐CRP, ox‐LDL, RSPV CsA, LIPV CsA and LAV were associated with AF persistence.

Increased C-reactive protein plasma levels are not involved in the onset of post-operative atrial fibrillation

“…In this regard, several other proinflammatory cytokines have also been associated with the onset of AF. Recent evidence indicates that activated macrophages secrete other cytokines such as TNF-a and IL-1b, which can be involved in AF onset through the modifications of Ca 2+ currents and subsequent arrhythmia [43]. Moreover, increased levels of IL-1b, IL-2, IL-8, IL-9, IL-10, IL-15, IL-17A, IL-17F, IL-21, IL-22, interferong, and transforming growth factor-b1 [44][45][46][47][48] were also associated with AF onset.…”

Blood Plasma Resistin and Atrial Fibrillation in Patients With Cardiovascular Disease

“…The consequence of pathological necrosis is a remodeling of the atrium, which practically inactivates the contractile capacity of the atria and thus burdens the circulation in the heart cavities. On the other hand, resistin in the context of inflammatory response is produced by the monocytes that in turn activate the endothelium for the secretion of intercellular adhesion molecules-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) [34,35].…”

DNA methylation dysregulations in valvular atrial fibrillation

“…Zhang et al showed that global DNA methylation is related to inflammation in atherosclerosis. Evidence shows that cardiac fibrosis, endothelial dysfunction, oxidative stress, and inflammation contribute to the pathogenesis of AF . This means that global DNA hypermethylation–related fibrotic and inflammatory changes may have a tight relationship with AF.…”

“…Experimental and clinical studies of AF indicate that atrial remodeling, such as electrical remodeling and structural remodeling, is very important in arrhythmia maintenance . Previous studies also have shown that cardiac fibrosis, endothelial dysfunction, oxidative stress, and inflammation were associated with AF . Many research studies focused on unraveling the mechanisms of atrial remodeling have demonstrated that human AF often reflects multiple interacting causative factors; thus, the mechanisms underlying AF susceptibility are multiple and incompletely understood…”

“…3 Previous studies also have shown that cardiac fibrosis, endothelial dysfunction, oxidative stress, and inflammation were associated with AF. 4,5 Many research studies focused on unraveling the mechanisms of atrial remodeling have demonstrated that human AF often reflects multiple interacting causative factors; thus, the mechanisms underlying AF susceptibility are multiple and incompletely understood. 6 Epigenetic alterations could bring about heritable changes in gene expression without mutating the DNA sequence and regulate key events in cellular homeostasis.…”