Cardiac fibrosis and atrial fibrillation

Abstract

Abstract Cardiac fibrosis is characterized by the imbalance of production and degradation of the extracellular matrix. The result of this process is an accumulation of scar tissue, which is associated with many pathological processes such as excessive mechanical stress on the heart, inflammation, ischemia, oxidative stress, or excessive neurohormonal activation. Fibrotic response results in damaged heart architecture and dysfunction of the heart. Cardiac fibrosis leads to increased stiffness of the left ventricle and arteries, promotes disorders of contraction and relaxation of the heart, disrupts electrophysiology of heart cells, and induces arrhythmias. Atrial fibrillation is one of the most common arrhythmias. It is associated with a deterioration in the quality of life and more frequent use of medical assistance. It is also an instantaneous risk factor for many diseases, including stroke. The underlying cause of this arrhythmia is electrical and structural remodeling induced by cardiac fibrosis. Therefore, much attention is paid to the search for biochemical markers that would allow non-invasive determination of the degree of this fibrosis. The promising markers include galectin-3, human epididymis protein 4 (HE4), serum soluble ST2, and adipose triglyceride lipase (ATGL). Studies have shown that plasma concentrations of these substances reflect the degree of myocardial fibrosis and are indirectly associated with AF. There are high hopes for the use of these markers in patients undergoing arrhythmia ablation. More research is needed to confirm that these markers can be used to estimate the chance of maintaining sinus rhythm in patients after ablation.