Areas of Cartilaginous and Osseous Metaplasia After Experimental Myocardial Infarction in Rats

• Published in: Anatomical record (Hoboken, N.J. : 2007) Vol. 302; no. 6; pp. 947 - 953
• Main Authors: Manole, Catalin Gabriel, Marinescu, Bogdan Gabriel, Marta, Daciana, Nicolescu, Mihnea Ioan
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01.06.2019; Wiley Subscription Services, Inc
• Subjects: Aging; Cartilage; Chondrogenesis; Congestive heart failure; Coronary artery; Extracellular matrix; Heart attacks; hyaline cartilage; Inflammation; Metaplasia; Muscles; Myocardial infarction; Myocardium; Rodents; transmission electron microscopy; Ventricle; Wistar rats; Wistar rats; transmission electron microscopy; myocardial infarction; hyaline cartilage
• ISSN: 1932-8486; 1932-8494
• DOI: 10.1002/ar.24010

ABSTRACT The presence of hyaline cartilage has been previously documented in heart tissue of different vertebrates, ranging from birds to superior mammals. However, there is scarce published data regarding the appearance of focal deposits of hyaline‐like cartilage within the hearts of laboratory rats. Few mechanisms that could trigger the appearance of this type of cartilage in heart were hypothesized (e.g., mechanical stress, ageing). Using different microscopy techniques this report confirms the presence of hyaline cartilage and bone in Wistar rats, which underwent left anterior coronary artery ligation for experimental myocardial infarction. The presented (ultra)structural evidence of focal chondroid metaplasia in the papillary muscles and close to the insertion point in the ventricular mass of the infarcted heart suggests a structural adaptation of cardiac myocardium to the newly acquired kinetics of left ventricular wall, after experimental myocardial infarction. Specific cartilaginous matrix proteins are known to mediate cardiac extracellular matrix remodeling, and this study provides evidence of a complete transition to a cartilaginous pattern in postinfarcted heart, which may nonetheless constitute a supplemental risk factor of a further heart failure condition. Moreover, for heart focal chondrogenesis, we also presume the involvement of the cellular and molecular inflammatory milieu that dominates the first 24 hr border zone landscape of the experimental myocardial infarction lesion. Anat Rec, 302:947–953, 2019. © 2018 Wiley Periodicals, Inc.