A substantial increase in
fibrillar collagen has been observed in the left cardiac ventricle of animals and humans with arterial
hypertension. Hypertensive myocardial
fibrosis is the result of both increased
collagen types I and III due to the fact that its synthesis by fibroblasts and myofibroblasts is stimulated and its extracellular
collagen degradation unchanged or decreased extracellular
collagen degradation. Hemodynamic and non-hemodynamic factors may be involved in the disequilibrium between
collagen synthesis and degradation that occurs in
hypertension. As shown experimentally and clinically, an exaggerated rise in
fibrillar collagen content promotes abnormalities of cardiac function, contributes to the decrease in coronary reserve and facilitates alterations in the electrical activity of the left ventricle. Although microscopic examination of cardiac biopsies is the most reliable method for documenting and measuring myocardial
fibrosis, the development of non-invasive methods to indicate the presence of myocardial
fibrosis in hypertensive patients would be useful. We have therefore applied a biochemical method based on the measurement of serum
peptides derived from the tissue formation when synthesized and degradation of
fibrillar collagens to monitor the turnover of these molecules in rats with spontaneous
hypertension and patients with
essential hypertension.