title: Does FXIII deficiency impair wound healing after myocardial infarction?
abstract: Inadequate healing of myocardial infarction may contribute to local expansion of the infarct, frequently leading to chamber dilation, heart failure, or myocardial rupture. Experimental evidence in mouse models suggests that Factor XIII might play a key role in wound healing, and low persistent values lead to increased incidence of cardiac rupture following myocardial infarction. Here we would like to share our initial clinical experiences with strikingly similar observations in patients with this grave disease, and compare these observations to experimental findings.
authors.affiliation: Medizinische Klinik und Poliklinik I, Universität Würzburg, Germany; Center for Molecular Imaging Research, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, United States of America.
authors.forename: Matthias
authors.initials: M
authors.lastname: Nahrendorf
authors.forename: Ralph
authors.initials: R
authors.lastname: Weissleder
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005177:Factor XIII Deficiency / Q000150:complications* / Q000235:genetics / Q000503:physiopathology*; D006342:Heart Rupture, Post-Infarction / Q000209:etiology / Q000473:pathology; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000097:blood* / Q000150:complications* / Q000473:pathology; D014945:Wound Healing / Q000235:genetics / Q000502:physiology*