[Altered fibrillar collagen metabolism in hypertensive heart failure. Current understanding and future prospects].

Arterial hypertension induces numerous alterations in the composition of cardiac tissue, which, in turn, result in structural remodeling of the myocardium. This remodeling is due to a range of pathologic mechanisms associated with mechanical, neurohormonal and cytokine processes that affect both cardiomyocyte and non-cardiomyocyte compartments of the myocardium. One of these processes involves disruption of the equilibrium between the synthesis and degradation of type-I and type-III collagen molecules. The result is excess accumulation of type-I and type-III collagen fibers in interstitial and perivascular spaces in the myocardium. The clinical significance of myocardial fibrosis lies in its contribution to the development of cardiac complications in hypertensive patients. This brief review focuses on the mechanisms of myocardial fibrosis and their clinical consequences. In addition, the techniques used for diagnosing myocardial fibrosis and the main therapeutic strategies for reducing fibrosis are also discussed.