Author/Authors :
Aljinovic، Jure نويسنده Department of Physical Medicine and Rehabilitation, University Hospital Center Split, Croatia , , Vukojevic، Katarina نويسنده Department of Anatomy, Histology and Embryology, School of Medicine in Split, Croatia , , Saraga-Babic، Mirna نويسنده Department of Anatomy, Histology and Embryology, School of Medicine in Split, Croatia , , Marinovic Guic، Maja نويسنده Department of Radiology, University Hospital Center Split, Croatia , , Kosta، Vana نويسنده Department of Neurology, University Hospital Center Split, Croatia , , Poljicanin، Ana نويسنده Department of Physical Medicine and Rehabilitation, University Hospital Center Split, Croatia , , Grkovic، Ivica نويسنده Department of Anatomy, Histology and Embryology, School of Medicine in Split, Croatia ,
Abstract :
We report the first finding a left ventricular aneurysm from bone metaplasia following myocardial infarction in a young Sprague-Dawley rat. Areas of cartilagineous and osseous metaplasia were found in the papillary muscle, chordae tendineae, and subendocardial tissue seven weeks after experimental ligation of the left coronary artery. In this experiment, a breed of normotensive, two-month-old rats was used, meaning that all potential genetic and age-related factors for the development of metaplasia can be ruled out. Trichrome Mallory and hematoxylin-eosin staining showed an aneurysmatically changed heart wall with central parts of several trabeculae occupied by cartilaginous tissue, that in which some areas displayed signs of endochondral ossification: characteristic chondrocyte hypertrophy with small areas of calcified matrix and osteoid bone formation. The metaplastic areas expressed strong immunoreactivity with bone morphogenetic proteins 4 and 7. Cartilage tissue formation in the rat’s heart was the result of oxygen diffusion from the oxygen-enriched blood inside the left ventricle and the local slowing of blood current inside the aneurysm, because the coronary artery supply in that area was cut off from ligation. Cartilage is known to be the only tissue that can survive in ischemic environments because it can obtain oxygen by diffusion from nearby blood. The presence of bone morphogenetic protein in the ischemic area directs myofibroblasts in the scar area to differentiate into chondrocytes and osteocytes, presenting as ossifying cartilage in the papillary muscle and subendocardial zone.