A decrease in the mass of mitochondria relative to the mass of myofibrils occurs in experimental hypertrophy. There may be defects in mitochondrial oxidative phosphoryla-tion and in mitochondrial calcium metabolism that could later lead to myocardial muscle failure.
E. Other Factors
1. Myosin and Myofibrillar ATPase
During hypertrophic processes there is decreased activity of myofibrillar and myosin adenosine triphosphatase which may explain alterations in contractile velocity.
2. Connective Tissue
The loss of cardiac myocytes stimulates hypertrophy of existing myocytes, but it is always accompanied by a variable replacement with collagen and other connective tissue elements. Connective tissue is good supporting tissue, but its tensile strength is poor compared to that of myocardial muscle. It also has no contractile properties. Marked replacement with collagen is seen in hypertro-phic as well as in other cardiomyopathies. Patchy and exten¬sive replacement of contractile myocardium with collagen causes weakening of the ventricular muscle. Ventricular systolic and diastolic dysfunction results in and leads to heart failure, which is a common feature of dilated car-diomyopathies (see the chapter Cardiomyopathy). Follow¬ing a myocardial infarction or myocarditis some patchy replacement of necrotic myocytes by collagen and fibrous tissue occurs.

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