The role of biomarkers of stress in heart failure

According to the literature, there are numerous stress biomarkers. However, for the first time, this review article summarizes the role of major physiological stress biomarkers in heart failure collectively which include chromogranin A, catecholamines, copeptin, cortisol, liver-type fatty acid-binding protein (L-FABP), superoxide dismutase (SOD) and catalase, fibrinogen, malondialdehyde, heat shock proteins. Chromogranin A (CgA) serum levels are increased in patients with chronic heart failure and are a predictive factor for mortality. A novel mechanistic insight for elevated catecholamine levels in plasma commonly seen in chronic heart failure (HF) conditions, suggests that increased trans-synaptic activation of the chromaffin cells within the adrenal medulla may increase catecholamines in the circulation and, in turn, contribute to the enhanced neurohumoral drive. Elevated copeptin plasma concentrations seen in HF patients were linked to an increased risk of all-cause death suggesting that copeptin may function as an HF outcome predictor. Since cortisol is a general stress indicator, serum cortisol levels in congestive heart failure (CHF) may reflect worse hemodynamic parameters and systemic sympathetic nerve activity. In individuals with acute heart failure, an elevated urine L-FABP level before therapy may indicate worsening renal function. Compared to children without heart failure, children with heart failure have decreased levels of SOD. In contrast to children without heart disease, children with heart failure had greater catalase (CAT) levels. In children with left-to-right shunt congenital heart disease (CHD), oxidative stress was the primary factor contributing to the development of heart failure. The individuals with acute aggravation of chronic heart failure who have high fibrinogen levels ( > 284 mg/dL) were independently predicted to die. Malondialdehyde is a sign of lipid peroxidation which was detected in the plasma of congestive heart failure patients with varied levels of clinical symptoms and in healthy individuals. HSPs can reduce heart dysfunction in HF and carry out a variety of additional functions, including regulating apoptosis and possessing anti-oxidant and anti-inflammatory properties