title: Myocardial reverse remodeling: how far can we rewind?
abstract: Heart failure (HF) is a systemic disease that can be divided into HF with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF). HFpEF accounts for over 50% of all HF patients and is typically associated with high prevalence of several comorbidities, including hypertension, diabetes mellitus, pulmonary hypertension, obesity, and atrial fibrillation. Myocardial remodeling occurs both in HFrEF and HFpEF and it involves changes in cardiac structure, myocardial composition, and myocyte deformation and multiple biochemical and molecular alterations that impact heart function and its reserve capacity. Understanding the features of myocardial remodeling has become a major objective for limiting or reversing its progression, the latter known as reverse remodeling (RR). Research on HFrEF RR process is broader and has delivered effective therapeutic strategies, which have been employed for some decades. However, the RR process in HFpEF is less clear partly due to the lack of information on HFpEF pathophysiology and to the long list of failed standard HF therapeutics strategies in these patient's outcomes. Nevertheless, new proteins, protein-protein interactions, and signaling pathways are being explored as potential new targets for HFpEF remodeling and RR. Here, we review recent translational and clinical research in HFpEF myocardial remodeling to provide an overview on the most important features of RR, comparing HFpEF with HFrEF conditions.
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal.
authors.forename: Patrícia G
authors.initials: PG
authors.lastname: Rodrigues
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal.
authors.forename: Adelino F
authors.initials: AF
authors.lastname: Leite-Moreira
authors.affiliation: Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, Universidade do Porto, Porto, Portugal ipires@med.up.pt.
authors.forename: Inês
authors.identifier: 0000-0003-1937-3782
authors.initials: I
authors.lastname: Falcão-Pires
mesh_terms: D000818:Animals; D002317:Cardiovascular Agents / Q000627:therapeutic use; D015195:Drug Design; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D058990:Molecular Targeted Therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D020127:Recovery of Function; D015398:Signal Transduction; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D002317:Cardiovascular Agents
keywords: diastolic dysfunction; heart failure with preserved ejection fraction; heart failure with reduced ejection fraction; left ventricle hypertrophy; myocardial reverse remodeling