RESUMEN
Numerous studies have reported that physical or emotional stress can provoke atrial fibrillation (AF) or vice versa, which suggests a potential link between exposure to external stressors and AF. This review article sought to describe in detail the relationship between major stress biomarkers and the pathogenesis of AF and presents up-to-date knowledge on the role of physiological and psychological stress in AF patients. For this purpose, this review article contends that plasma cortisol is linked to a greater risk of AF. A previous study has investigated the association between increased copeptin levels and paroxysmal AF (PAF) in rheumatic mitral stenosis and reported that copeptin concentration was not independently associated with AF duration. Reduced levels of chromogranin were measured in patients with AF. Furthermore, the dynamic activity of antioxidant enzymes, including catalase as well as superoxide dismutase, was examined in PAF patients during a period of <48 h. Malondialdehyde activity, serum high-sensitivity C-reactive protein, and high mobility group box 1 protein concentrations were significantly greater in patients with persistent AF or PAF compared to controls. Pooled data from 13 studies confirmed a significant reduction in the risk of AF related to the administration of vasopressin. Other studies have revealed the mechanism of action of heat shock proteins (HSPs) in preventing AF and also discussed the therapeutic potential of HSP-inducing compounds in clinical AF. More research is required to detect other biomarkers of stress, which have not been reported in the pathogenesis of AF. Further studies are required to identify their mechanism of action and drugs to manage these biomarkers of stress in AF patients, which might help to reduce the prevalence of AF globally.
RESUMEN
Many studies have reported a relationship between inflammation and atrial fibrillation (AF). According to the literature, inflammation is the key component in pathophysiological processes during the development of AF; the amplification of inflammatory pathways triggers AF, and, at the same time, AF increases the inflammatory state. The plasma levels of several inflammatory biomarkers are elevated in patients with AF; therefore, inflammation might contribute to both the maintenance and occurrence of AF and its thromboembolic complications. Numerous inflammatory markers have been linked to AF, including CD40 ligand, fibrinogen, matrix metalloproteinase (MMP)-9, monocyte chemoattractant protein-1, myeloperoxidase, plasminogen activator inhibitor-1, and serum amyloid A. There are many pathophysiological aspects of AF that are linked to these inflammatory biomarkers, including atrial structural remodeling and atrial dilatation, increased atrial myocyte expression, fluctuations in calcium cycling, cardiac remodeling promotion, increased cardiac myocyte proliferation and terminal differentiation, production of several MMPs, the pathogenesis of atherosclerosis and cardiomyocyte apoptosis, an increased degree of fibrosis in atrial myocardium, and the progression and development of atherogenesis and atherothrombosis. The present review article aims to provide an updated overview and focus on the basic role of different biomarkers of inflammation in the pathophysiological aspects of the pathogenesis of AF.
