Evaluation of New Potential Inflammatory Markers in Patients with Nonvalvular Atrial Fibrillation

Abstract

Atrial fibrillation (AF), the most common arrhythmia in clinical practice, is associated with an increase in mortality and morbidity due to its high potential to cause stroke and systemic thromboembolism. Inflammatory mechanisms may play a role in the pathogenesis of AF and its maintenance. We aimed to evaluate a range of inflammatory markers as potentially involved in the pathophysiology of individuals with nonvalvular AF (NVAF). A total of 105 subjects were enrolled and divided into two groups: patients with NVAF (n = 55, mean age 72 ± 8 years) and a control group of individuals in sinus rhythm (n = 50, mean age 71 ± 8 years). Inflammatory-related mediators were quantified in plasma samples by using Cytometric Bead Array and Multiplex immunoassay. Subjects with NVAF presented significantly elevated values of interleukin (IL)-2, IL-4, IL-6, IL-10, tumor necrosis factor (TNF), interferon-gamma, growth differentiation factor-15, myeloperoxidase, as well as IL-4, interferon-gamma-induced protein (IP-10), monokine induced by interferon-gamma, neutrophil gelatinase-associated lipocalin, and serum amyloid A in comparison with controls. However, after multivariate regression analysis adjusting for confounding factors, only IL-6, IL-10, TNF, and IP-10 remained significantly associated with AF. We provided a basis for the study of inflammatory markers whose association with AF has not been addressed before, such as IP-10, in addition to supporting evidence about molecules that had previously been associated with the disease. We expect to contribute to the discovery of markers that can be implemented in clinical practice hereafter.

New Trends in Pathology: From Cell Morphology to Molecular Medicine

“…Similarly, Reis and coworkers studied 105 patients with nonvalvular atrial fibrillation, looking for relevant inflammatory biomarkers [7]. Through cytometric bead array and multiplex immunoassay, they confirmed the correlation between atrial fibrillation and plasmatic levels of IL-6, IL-10 and TNF, while discovering a new potential inflammatory marker, i.e., interferon-gamma-induced protein (IP-10).…”

C-C,N,S treats atrial fibrillation through regulating inflammatory procession: a study of network pharmacology research and gene set enrichment analysis validation

“…The PPI network analysis indicated that TNF and IL6 were key genes, cellular response to chemical stress and response to oxidative stress were key biological processes. The relationship between IL6, TNF and AF had been validated [51][52] and that pointed that the mechanism of C-C,N,S treating AF maybe related to in ammation. Then the gene speci c expression analysis provided a possibilities that C-C,N,S can regulate the in ammation occurred in cardiac myocytes, adipocytes and endothelial which maybe generated by liver diseases and heart diseases [53][54][55] .…”

Pathophysiology of Atrial Fibrillation and Approach to Therapy in Subjects Less than 60 Years Old

“…These mechanisms prolong transient calcium refractoriness and promote arrhythmogenic and spatially discordant atrial alternans. The involvement of circulating autoantibodies against M2-muscarinic acetylcholine receptors (anti-M2-R) in AF has been studied in preclinical models [6] and in humans as The involvement of circulating autoantibodies against M2-muscarinic acetylcholine receptors (anti-M2-R) in AF has been studied in preclinical models [6] and in humans as well [7]. The increased expression of tumor growth factor (TGF)-β1 and connective tissue GF (CTGF) in left atrial appendage tissues correlates with the severity of atrial fibrosis [8].…”