title: Post-infarct remodelling: contribution of wound healing and inflammation.
abstract: In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and function. MI and the consequent loss of myocardium are the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains poor in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to improve healing of the cardiac wound to maintain structure and function of the heart. Healing in the heart occurs in overlapping phases. Herein, we review the inflammatory phase as a trigger of tissue formation.
authors.affiliation: Medizinische Klinik und Poliklinik I, Universitätsklinikum Würzburg, Josef-Schneider-Str. 2, 97080 Würzburg, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
authors.forename: Johann
authors.initials: J
authors.lastname: Bauersachs
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
mesh_terms: D000818:Animals; D000917:Antibody Formation; D006801:Humans; D007111:Immunity, Cellular; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; D009203:Myocardial Infarction / Q000276:immunology / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D009206:Myocardium / Q000276:immunology / Q000473:pathology*; D011379:Prognosis; D020257:Ventricular Remodeling; D014945:Wound Healing
chemical_list: D018836:Inflammation Mediators