Since inflammation signaling pathways play a crucial role in cardiac fibrosis [14], HF may induce various damage-associated molecular patterns (DAMPs) and activate nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome through pattern recognition receptors such as toll-like receptor (TLR), thereby triggering cardiac fibrosis [15,16,17]. This evidence concerns the gene NLRP3 and hydrops fetalis.