title: Remodeling in the ischemic heart: the stepwise progression for heart failure.
abstract: Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.
authors.affiliation: Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.
authors.forename: J G
authors.initials: JG
authors.lastname: Mill
authors.forename: I
authors.initials: I
authors.lastname: Stefanon
authors.forename: L
authors.initials: L
authors.lastname: dos Santos
authors.forename: M P
authors.initials: MP
authors.lastname: Baldo
mesh_terms: D059331:Adrenergic Neurons / Q000502:physiology; D000450:Aldosterone / Q000502:physiology; D000809:Angiotensins / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology; D001145:Arrhythmias, Cardiac / Q000209:etiology; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications*; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D013997:Time Factors
chemical_list: D000809:Angiotensins; D018836:Inflammation Mediators; D000450:Aldosterone