title: The Role of Inflammation in Cardiovascular Outcome.
abstract: OBJECTIVE
  The aim of this review is to update the pathophysiological role of innate immune response in the cardiovascular (CV) disease outcomes, particularly focusing on coronary atherosclerosis and heart failure.
  
  
  RESULTS
  Inflammatory processes comprised with the innate immunity reaction are believed to actively trigger CV disease development and final clinical events. For instance, by releasing proteases and neutrophil extracellular traps, neutrophil recruitment and activation might strongly influence atherosclerotic plaque stability. Similarly, neutrophils drive the early inflammatory response following a myocardial infarction. However, these cells contribute themselves to infarct healing by orchestrating monocyte/macrophage recruitment and polarization within the ischemic myocardium. Given their heterogeneity and plasticity, the balance between recruitment, proliferation, and polarization of monocyte/macrophage is a further leading determinant of advanced plaque maturation. Moreover, timely shift from a pro-inflammatory to a resolving macrophage phenotype may influence cardiac remodeling as well as development of heart failure (HF). Alongside macrophage recruitment and activation into the remote, non-ischemic myocardium also contributes to cardiac remodeling and HF development. Innate immune response is a tightly regulated process where a timely modulation of the balance between damaging and resolving properties critically impacts on CV outcome. Further progress may improve the determination of the prognostic relevance of inflammatory biomarkers on clinical CV outcome.
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy.|IRCCS AOU San Martino-IST, Genova, 10 Largo Benzi, 16132, Genoa, Italy.|Centre of Excellence for Biomedical Research (CEBR), University of Genoa, 9 viale Benedetto XV, 16132, Genoa, Italy.
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Montecucco
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy.
authors.forename: Luca
authors.initials: L
authors.lastname: Liberale
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy.
authors.forename: Aldo
authors.initials: A
authors.lastname: Bonaventura
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Vecchiè
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy.|IRCCS AOU San Martino-IST, Genova, 10 Largo Benzi, 16132, Genoa, Italy.
authors.forename: Franco
authors.initials: F
authors.lastname: Dallegri
authors.affiliation: First Clinic of Internal Medicine, Department of Internal Medicine and Medical Specialties, University of Genoa, 6 viale Benedetto XV, 16132, Genoa, Italy. federico.carbone@edu.unige.it.
authors.forename: Federico
authors.initials: F
authors.lastname: Carbone
mesh_terms: D000818:Animals; D003324:Coronary Artery Disease / Q000276:immunology / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000276:immunology / Q000503:physiopathology; D058226:Plaque, Atherosclerotic / Q000276:immunology / Q000503:physiopathology
keywords: Atherosclerosis; Heart failure; Inflammation; Macrophage; Myocardial infarction; Neutrophil