Congestion in Acute Heart Failure with Reduced vs. Preserved Left Ventricular Ejection Fraction: Differences, Similarities and Remaining Gaps

This article refers to 'Acutely decompensated heart failure with preserved and reduced ejection fraction present with comparable haemodynamic congestion' by L.N.L. Van Aelst et al., published in this issue on pages 738-747.Acute heart failure (AHF) is defined as the rapid onset or worsening of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment.1 It imposes a significant burden on both patients and health care systems, due to the high mortality rate (30% one year post-discharge) and need for repeated hospitalizations (20% within 30 days and 50% 6 months post-discharge). 2 Under the general definition of AHF is encompassed a wide spectrum of clinical presentations, with varying precipitating factors, underlying aetiology, pathophysiologic mechanisms and clinical outcomes.In several large AHF registries, patients with AHF and reduced (HFrEF) vs. preserved ejection fraction (HFpEF) constitute approximately equal 50% fractions of hospitalized patients.These populations differ in their demographic and clinical characteristics and outcomes.2 Patients with HFrEF are more frequently younger males, with history of chronic heart failure and coronary artery disease.They usually present with normal or low blood pressure, weight gain and signs of systemic venous congestion.On the other hand, HFpEF patients are usually older women with new-onset heart failure and several cardiometabolic co-morbidities, presenting with increased blood pressure, less systemic venous congestion and usually no significant weight gain.Although in-hospital mortality is higher in HFrEF, both groups are equally affected by high rates of post-discharge mortality, unplanned outpatient visits and rehospitalizations.3 Venous congestion is the cardinal manifestation in AHF.Two main pathophysiologic mechanisms have been implicated in the development of congestion: first, rapid redistribution of blood volume from the systemic to the pulmonary venous circulation and, second, intravascular volume accumulation in the setting of chronic cardiorenal dysfunction and impaired sodium and waterThe opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.