The relation between inflammation and HF is complex and bidirectional, since HF-related hemodynamic stress induces a state of inflammation that triggers the release of proinflammatory cytokines by cardiomyocytes and cardiac fibroblasts, including tumor necrosis factor (TNF-α), interleukin (IL)-6, IL-1β, angiotensin II, and myostatin, which impair cardiac structure and function [16]. This evidence concerns the gene MSTN and hydrops fetalis.