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

Nature Clinical Practice Cardiovascular Medicine volume 2, pages 209–216 (2005)Cite this article

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.

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Figure 1: Comparison of collagen fibers in endomyocardial tissue.
Figure 2: Mechanisms and consequences of myocardial fibrosis in hypertensive heart disease.

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Author information

Author notes

  1. Javier Díez, Arantxa González and Begoña López: J Díez is Professor of Vascular Medicine and Director of Research, and A González and B López are Junior Investigators

Authors and Affiliations

  1. Division of Cardiovascular Pathophysiology, Center for Applied Medical Research, University of Navarra, Pamplona, Spain

    Javier Díez, Arantxa González & Begoña López

  2. Consultant in the Division of Cardiology, Donostia University Hospital, San Sebastián, Spain

    Ramón Querejeta

Authors
  1. Javier Díez
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  2. Arantxa González
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  3. Begoña López
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  4. Ramón Querejeta
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Corresponding author

Correspondence to Javier Díez.

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The authors declare no competing financial interests.

Glossary

EXTRACELLULAR MATRIX

A complex network of polysaccharides and proteins secreted by cells that serves as a structural element in tissues and influences cell physiology

COLLAGEN TYPE I

A major component of the extracellular matrix, rich in glycine and proline; the most abundant collagen type present in the heart

PROTEIN KINASE B

A member of the protein kinase family, that transfers one terminal phosphate group of ATP to a specific amino acid of a target protein

EXTRACELLULAR-SIGNAL-REGULATED KINASES

Serine or threonine kinases activated by various extracellular signals that induce proliferation and differentiation; also called mitogen-activated kinases

TISSUE-INTEGRATED BACKSCATTER

Measurement of changes in ultrasonic attenuation with an index of backscatter to distinguish normal from abnormal (i.e. fibrotic) myocardium

PROCOLLAGEN TYPE I

Molecule secreted by fibroblasts into the extracellular space, where it is converted to collagen type I by specific endoproteinases

UBIQUITIN-PROTEASOME SYSTEM

Type of large-protein complex in the cytosol that is responsible for degrading proteins that have been marked for destruction by ubiquitination

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Díez, J., González, A., López, B. et al. Mechanisms of Disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease. Nat Rev Cardiol 2, 209–216 (2005). https://doi.org/10.1038/ncpcardio0158

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