Myocardial connective tissue alterations

• Published in: Toxicologic pathology Vol. 18; no. 4 Pt 1; p. 488
• Main Authors: Caulfield, J B, Wolkowicz, P E
• Format: Journal Article
• Language: English
• Published: United States 1990
• Subjects: Animals; Cardiomyopathies - etiology; Cardiomyopathies - pathology; Collagen - ultrastructure; Coronary Disease - pathology; Disulfides; Doxorubicin; Extracellular Matrix - pathology; Humans
• ISSN: 0192-6233
• DOI: 10.1177/0192623390004part_107

There is a complex network of collagen throughout the heart. It is composed of a hierarchy of fibrils and fibers ranging from 10 nm to 2-3 microns in diameter. This network can be broken down by ischemia, adriamycin administration, or disulfide administration in laboratory animals. Following loss due to coronary artery ligation, the ischemic area begins bulging within 3 h. General loss of portions of the collagen matrix is induced by intravenous oxidizing glutathione, and results in marked diffuse ventricular dilatation. Generalized collagen loss in the ventricles, as induced by disulfide administration or adriamycin infusion, persists for 6 months at which time evidence of some replacement is visible, and evidence of diffuse fibrosis is present. In humans, cardiac dilatation occurs in a variety of disease states without overstretch of sarcomeres. This presumes rearrangement of the muscle bundles, which can only occur with marked alterations of the collagen matrix. Ventricular dilatation, associated with viral myocarditis or puerperal cardiomyopathy, may persist for months, suggesting the collagen loss, as with the experimental animals, takes many months to repair. The cardiac dilatation may ameliorate, or, in some patients, deteriorate into heart failure. The animal experiments with loss of the collagen matrix, ventricular dilatation, and failure to replace the matrix for many months provide an explanation for persistent cardiac dilatation in various human diseases.