Acute Heart Failure and Valvular Heart Disease: A Scientific Statement of the Heart Failure Association, the Association for Acute CardioVascular Care and the European Association of Percutaneous Cardiovascular Interventions of the European Society of Cardiology
Ovidiu Chioncel, Marianna Adamo, Maria Nikolaou, John Parissis, Alexandre Mebazaa, Mehmet Birhan Yılmaz, Christian Hassager, Brenda Moura, Johann Bauersachs, Veli‐Pekka Harjola, Elena‐Laura Antohi, Tuvia Ben‐Gal, Sean P. Collins, Vlad Anton Iliescu, Magdy Abdelhamid, Jelena Čelutkienė, Stamatis Adamopoulos, Lars H. Lund, Mariantonietta Cicoira, Josep Masip, Hadi Skouri, Finn Gustafsson, Amina Rakisheva, Ingo Ahrens, Andrea Mortara, E Janowska, Abdallah Almaghraby, Kevin Damman, Òscar Miró, Kurt Huber, Arsen Ristić, Loreena Hill, Wilfried Müllens, Alaide Chieffo, Jozef Bartúnek, Pasquale Paolisso, Antoni Bayés‐Genís, Stefan D. Anker, Susanna Price, Gerasimos Filippatos, Frank Ruschitzka, Petar Seferović, Rafael Vidal-Pérez, Alec Vahanian, Marco Metra, Theresa A. McDonagh, Emanuele Barbato, Andrew J.S. Coats, Giuseppe Rosano
Abstract
Acute heart failure (AHF) represents a broad spectrum of disease states, resulting from the interaction between an acute precipitant and a patient's underlying cardiac substrate and comorbidities. Valvular heart disease (VHD) is frequently associated with AHF. AHF may result from several precipitants that add an acute haemodynamic stress superimposed on a chronic valvular lesion or may occur as a consequence of a new significant valvular lesion. Regardless of the mechanism, clinical presentation may vary from acute decompensated heart failure to cardiogenic shock. Assessing the severity of VHD as well as the correlation between VHD severity and symptoms may be difficult in patients with AHF because of the rapid variation in loading conditions, concomitant destabilization of the associated comorbidities and the presence of combined valvular lesions. Evidence-based interventions targeting VHD in settings of AHF have yet to be identified, as patients with severe VHD are often excluded from randomized trials in AHF, so results from these trials do not generalize to those with VHD. Furthermore, there are not rigorously conducted randomized controlled trials in the setting of VHD and AHF, most of the data coming from observational studies. Thus, distinct to chronic settings, current guidelines are very elusive when patients with severe VHD present with AHF, and a clear-cut strategy could not be yet defined. Given the paucity of evidence in this subset of AHF patients, the aim of this scientific statement is to describe the epidemiology, pathophysiology, and overall treatment approach for patients with VHD who present with AHF.