ACTA1 and hydrops fetalis: However, excessive PC will be metabolized to diglyceride, which is further converted to TAG.[36] High levels of TAG accumulation are considered to be a risk factor for HF, which manifests as myocardial lipid toxicity, leading to mitochondrial dysfunction, oxidative stress and inflammation, and ultimately damaging myocardial function.[37,38] PE is considered to be an early lipid marker of HF.[39] Researches have shown that PE significantly aggravates atrial fibrosis by increasing collagen deposition in atrial tissue and up-regulating the expression of fibrosis markers such as α-SMA.[40,41]