This discrepancy may be due to significant ECM remodeling in HF patients, causing MFAP4 to preferentially bind to the ECM rather than being released into the bloodstream; increased activity of ECM-degrading enzymes (e.g., elastase) accelerates MFAP4 degradation; and HF-associated vascular remodeling, changes in vascular elastin structure, and vascular dysfunction may impair MFAP4 entry into the circulation. Here, ELN is linked to hydrops fetalis.