The Role of Suppression of Tumorigenicity-2 with Left Ventricular Global Strain and Aerobic Capacity in Systolic Heart Failure

Systolic heart failure is a pathophysiological state in which, an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. It is a final condition from all heart diseases that is associated with high mortality and morbidity rates. This situation leads to the remodeling process resulting in reduced cardiac contractility as well as impaired aerobic capacity. The remodeling process is associated with an inflammatory process involving release of many inflammatory mediators as well as biomarkers. Numerous biomarkers that are released in this process can be used as a risk stratification and prognosis in patients with heart failure. One of these biomarkers is suppression of Tumorigenicity-2 (ST2). Cardiomyocytes subjected to mechanical stress express ST2 in vitro, whereas the circulating levels of soluble ST2 (sST2) are associated with left heart failure. The increased concentration of ST2 that involves Interleukin-33 (IL-33) depends on the biomechanical stress of cardiomyocytes (biomechanical strain). IL-33, as a ligand of ST2, is known to be involved in reducing tissue fibrosis and myocyte hypertrophy in mechanically strained hearts, which leads to left ventricular global strain. Thus, the present review aims to clarify the role of ST2 in systolic heart failure as a diagnostic, prognostic, and monitoring therapy