The condition’s cardiovascular impact becomes particularly evident by mid-gestation, when failed hemodynamic adaptation manifests as pathological cardiac remodeling including left ventricular concentric hypertrophy and diastolic dysfunction, accompanied by elevated biomarkers of myocardial strain such as NT-proBNP and troponin, even in the absence of overt heart failure [66,67]. This evidence concerns the gene NPPB and heart failure.