Cellular changes and damage in mechanically overloaded hearts.
The electron microscopic aspects of myocardial cells in several types of mechanically overloaded heart are reviewed. Alterations which may be interpreted as degenerative changes are all the more frequent as the load is more severe. They seem to be the cause of the interstitial fibrosis which often accompanies hypertrophy. Their mechanism is dubious: swelling of mitochondria and intracellular lipidosis, which could signify cellular hypoxia, are rarely present. Other changes are characteristic of an increase of proteosynthesis and of the active growth of the main structures of the cell: myofibrils, mitochondria, T- and L-tubules. Some pictures of myofibrillar growth are not always easily distinguished from those of myofibrillar lesions. The mitochondria/myofibril ratio may be modified or not. The apparent volume of the mitochondria may remain normal while their density increases, which implies a decrease of their average size. In severe and long-lasting overloads, hypertrophy and hyperplasia of the Golgi apparatus and multiplication of granules of the auricular type evoke a regression of the cell toward its fetal type.
D000818:Animals; D006332:Cardiomegaly / Q000473:pathology*; D006056:Golgi Apparatus / Q000473:pathology; D008931:Mitochondria, Muscle / Q000473:pathology; D009206:Myocardium / Q000648:ultrastructure; D009210:Myofibrils / Q000473:pathology; D011817:Rabbits; D051381:Rats