Peripartum Cardiomyopathy Associated With Gestational Transient Thyrotoxicosis and Severe Preeclampsia: A Case Report.

Human chorionic gonadotropin (hCG) exerts a thyrotropic effect and contributes to the pathophysiology of gestational transient thyrotoxicosis (GTT), a typically benign, self-limiting form of hyperthyroidism that usually resolves by the late first or early second trimester of pregnancy, which is generally considered to have minimal obstetric or fetal consequences. However, identifying hyperthyroidism in pregnancy remains essential, as maternal and fetal complications may occur depending on the etiology and the presence of overt hyperthyroidism. Thyroid hormones significantly influence cardiovascular function. Although the pathophysiology of preeclampsia (PE) is not fully understood, it is associated with cardiovascular dysfunction, and several studies have explored the relationship between thyroid dysfunction and PE with inconsistent findings. In this context, we report the case of a 30-year-old Angolan woman in the first trimester who was admitted for hyperemesis gravidarum. Laboratory tests revealed a markedly elevated hCG level (271,215 IU/L) for her gestational age. After exclusion of other causes, GTT was diagnosed, with normalization of hCG levels by 18 weeks of gestation. At 35 weeks, she developed gestational hypertension, managed with close monitoring. At 38 weeks, she presented with acute respiratory failure and hemodynamic pulmonary edema in the setting of PE and peripartum cardiomyopathy. This case highlights that GTT, though usually benign, can lead to severe maternal complications when associated with extreme hCG levels. It also illustrates the coexistence of PE and peripartum cardiomyopathy, a rare and diagnostically challenging situation, in which distinguishing hypertensive heart failure of pregnancy from primary cardiomyopathy proved particularly difficult. These findings underscore the importance of early recognition, close monitoring, and further research to clarify the cardiovascular impact of hCG-mediated thyroid dysfunction in pregnancy.