Yet, our observations of an increase in the abundance of several indicators of inflammation (discussed above), cardiac arteriopathy (↑APOA1, ↑FGA, ↑THBS1, ↑TKT, ↓TUBB1, p value 1.02E − 03), and hypertrophy (↑CPT1A, ↓GSN, ↑MYL9, ↑S100A6, ↓TPM1, p value 4.49E − 03), many of which (e.g., CPT1A, GRB2, HSPA1A/HSPA1B, and S100A6) were also increased in S-NO levels (p value 1.01E − 03) in HF subjects, suggested that fragmented THBS1 is potentially a signaling molecule in cardiac remodeling/inflammatory processes in heart failure, to be validated in future studies. This evidence concerns the gene CPT1A and hydrops fetalis.