Diez J, Laviades C, Varo N, Querejeta R, Lopez B. Biochemical diagnosis of hypertensive myocardial fibrosis. Rev Esp Cardiol 2000;53(Suppl. 1):8-13.
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 fibrilar 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