Our results establish that soluble TNFα is required for exercise-induced increases in AF vulnerability, which is linked to fibrosis, inflammation, and enlargement of the atria, but largely independent of changes in vagal tone.
Decreases in TNF-α (8.5-42.9%), BNP (15.3-34.6%) and left ventricular mass (9.6-26.2%) were only observed in patients in SR, whereas increases in peak oxygen uptake were only observed in patients in AF (19.5-23.2%).
The aim of this study was to determine the associations of leptin, adiponectin (ADA), tumor necrosis factor α (TNF‑α), and irisin levels with the diagnosis of atrial fibrillation (AF) on admission to the hospital as well as parameters of transthoracic echocardiography among inpatients with cardiovascular diseases (CVDs).
Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in the serum and the left atrial (LA).
To evaluate the risk of AF and major adverse cardiovascular events (MACE) associated with use of ustekinumab vs tumor necrosis factor inhibitors (TNFi) in patients with psoriasis or psoriatic arthritis.
The increased mRNA expressions of classic inflammatory factors (i.e., interleukin-1 beta, interleukin 6, and tumor necrosis factor-alpha) in AF(+)thrombus(+) group further validated the correlation between inflammation and thrombi in atrial fibrillation.
Methyllycaconitine blunted the effects of MNS on the AERP, AERP dispersion, the AF vulnerability, and TNF-a and IL-6 levels in the atrium, but had no impact on the levels of Ach.
AF inducibility and duration were substantially increased in collagen-induced arthritis rats, and AF duration was significantly and positively correlated with the serum IL-6 and TNF-α levels.
This upregulated expression and activity were positively correlated with higher regulatory indicators of atrial structural remodeling as reflected by higher transcripts of tumor necrosis factor (TNF)-related apoptosis-inducing ligand, matrix metalloproteinase (MMP)-2 and MMP-9, pro-inflammatory factors TNF-α and interleukin-6, and higher ratios of MMP-9/tissue inhibitor of metalloproteinase (TIMP)-1 and MMP-2/TIMP-2 in AF.
History and clinical examination were done with the following investigations at first admission and followed up for 24 weeks: serum and AFtumour necrosis factor-alpha (TNF-alpha), AF polymorphonuclear leukocytes, AF cultivation and detection of blood and AF bacterial DNA.