Ultrasound Obstet Gynecol 2018; 52: 297–301 Published online in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/uog.18987 Editorial Pre-eclampsia and heart failure: a close relationship R. ORABONA 1# , E. SCIATTI 2# , F. PREFUMO 1 , E. VIZZARDI 2 , I. BONADEI 2 , A. VALCAMONICO 1 , M. METRA 2 and T. FRUSCA 3 1 Department of Obstetrics and Gynecology, University of Brescia, Brescia, Italy; 2 Section of Cardiovascular Diseases, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy; 3 Department of Obstetrics and Gynecology, University of Parma, Parma, Italy *Correspondence. (e-mail: federico.prefumo@gmail.com) #R.O. and E.S. contributed equally to this article. Introduction Heart failure (HF) is a clinical syndrome characterized by signs (e.g. pulmonary crackles, peripheral edema, jugular turgor) and symptoms (e.g. breathlessness, fatigue, ankle swelling) caused by structural and/or functional cardiac abnormalities and leading to elevated intracardiac pressure and/or low cardiac output (CO) at rest or during stress 1 . According to the most recent European survey and guidelines 2,3 , HF represents one of the pandemics of the 21 st century, affecting about 2% of the adult population worldwide and at least 10% of people aged over 70 years, and reaching a 1-year all-cause mortality of 23.6% in the acute setting and of 6.4% in the chronic setting. Notably, HF is a still-growing burden on healthcare systems worldwide, because of a need for frequent rehospitalization and the introduction of new drugs and devices 2–4 . Acute HF is a life-threatening condition characterized by new onset or recurrence of symptoms and signs of HF, and requires urgent evaluation and treatment. It is the most frequent cause of hospitalization in people older than 65 years 1,3 . Pre-eclampsia (PE) is most commonly defined by new-onset hypertension (at least 140/90 mmHg confirmed on two occasions 4 – 6 h apart) after the 20 th week of gesta- tion, combined with at least one of the following: de-novo onset of proteinuria (≥ 300 mg/24 h), one (or more) sign(s) of maternal organ dysfunction or fetal growth restriction (FGR) 5 . Signs of maternal organ dysfunction include renal insufficiency, liver involvement and neurological or hema- tological complications. Severe maternal complications include eclampsia, cerebrovascular and cardiovascular (CV) accidents, liver rupture and acute renal failure 6 . PE remains a leading cause of maternal and perinatal morbidity and mortality worldwide, complicating 2–8% of all pregnancies 7 . Perinatal outcome depends primarily on the incidence of preterm delivery, FGR or fetal death 8 . According to the timing of onset of PE, the disorder is frequently dichotomized into early-onset PE (EOPE) and late-onset PE (LOPE), considering 34 weeks’ gesta- tion as cut-off 9 , although gestational age at onset might be related to different pathophysiological mechanisms involving different patterns of cardiac output and periph- eral resistance as well as trophoblastic infiltration. EOPE seems to be associated with higher perinatal risks and maternal mortality than does LOPE 10 , although the risk of complications in LOPE cannot be underestimated 11 . Pathophysiologic relationship between pre-eclampsia and heart failure The etiology of HF is heterogeneous and varies worldwide, depending principally on myocardial ischemia/infarction, idiopathic cardiomyopathies, valvular heart disease, hypertensive cardiopathy, congenital defects and car- diac toxicity 3 . In about 50% of cases, all etiologies lead to a common pathway characterized by myocyte loss and fibrosis replacement, leading to increased myocar- dial stretch and left ventricular (LV) remodeling and dilatation, reduced pump efficiency and impaired periph- eral perfusion 1 . Consequently, the sympathetic and renin – angiotensin – aldosterone systems react with persis- tent neurohormonal activation causing sodium retention, fluid overload (i.e. edema) and renal dysfunction in a vicious cycle. Gut congestion with cachexia, and acti- vated systemic inflammatory pathways with endothelial dysfunction, contribute to the syndrome, defined as HF with reduced LV ejection fraction 1 . In the remaining 50% of cases, despite having the same etiologies, global pump function is preserved at the expense of increased car- diopulmonary filling pressure, namely HF with preserved LV ejection fraction (HFpEF). This syndrome principally affects women, particularly hypertensive or elderly indi- viduals, and those who suffer from atrial fibrillation, diabetes mellitus, renal failure or chronic pulmonary lung disease. Although the pathophysiology of HFpEF is still debated, it seems to be related to a proinflammatory state enhanced by the cited comorbidities, which leads to endothelial dysfunction, myocyte hypertrophy and col- lagen deposition together with fibrosis and reduced LV compliance 12 . PE results from a mismatch between uteroplacental supply (with impaired placenta due to ischemic and/or oxidative stress damage) and fetal demands, leading to sys- temic inflammatory maternal and fetal manifestations 6,9 . The presence of a fetus is not a requirement for the development of PE, since PE can also complicate molar pregnancies in which only the placenta is present 13 . These factors act in a proinflammatory and prothrombotic way, determining maternal endothelial dysfunction and Copyright  2017 ISUOG. Published by John Wiley & Sons Ltd. EDITORIAL