Mechanisms of disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease

Nat Clin Pract Cardiovasc Med. 2005 Apr;2(4):209-16. doi: 10.1038/ncpcardio0158.

Abstract

Changes in the composition of cardiac tissue develop in arterial hypertension and lead to structural remodeling of the myocardium. Structural remodeling is the consequence of a number of pathologic processes, mediated by mechanical, neurohormonal and cytokine routes, occurring in the cardiomyocyte and the noncardiomyocyte compartments of the heart. One of these processes is related to the disruption of the equilibrium between the synthesis and degradation of collagen type I and III molecules, which results in an excessive accumulation of collagen type I and III fibers in the interstitium and the perivascular regions of the myocardium. The clinical relevance of ventricular fibrosis is that it might contribute to the increased cardiac risk of patients with hypertensive heart disease. This review focuses on the mechanisms of hypertensive ventricular fibrosis and its clinical consequences. In addition, we discuss the noninvasive methods for the diagnosis of cardiac fibrosis and the therapeutic strategies aimed to promote its reduction.

Publication types

  • Review

MeSH terms

  • Collagen Type I / biosynthesis
  • Collagen Type III / biosynthesis
  • Fibrosis / etiology*
  • Humans
  • Hypertension / physiopathology*
  • Hypertrophy, Left Ventricular / physiopathology*
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Remodeling*

Substances

  • Collagen Type I
  • Collagen Type III