Patients whoexperienced HF or cardiac dysfunction (e.g., a high NT-proBNP, a low LVEF, or alarge left ventricular end-diastolic volume) at baseline, faced a higher rate ofthromboembolism, and it could be attributed to complex pathophysiologicalmechanisms such as neurohormonal activation or decreased myocardialcontractility, resulting in an increased vulnerability to thromboses [25]. Here, NPPB is linked to hydrops fetalis.