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Fibrosis and hypertensive heart disease

K T Weber1

  • 1Department of Medicine, University of Tennessee Health Science Center, Memphis 38163, USA. ktweber@utmem.edu

Current Opinion in Cardiology
|January 4, 2001
PubMed

Insights

Hypertensive heart disease alters heart muscle quality, not just size, leading to dysfunction and increased cardiovascular risk. Fibrous tissue growth in coronary arteries contributes to this adverse remodeling.

Area of Science:

  • Cardiovascular Biology
  • Cardiac Pathology
  • Vascular Remodeling

Background:

  • The normal myocardium comprises cardiac myocytes and non-cardiomyocytes like endothelial cells, smooth muscle cells, and fibroblasts.
  • Hypertensive heart disease is characterized by structural remodeling affecting both muscular and non-muscular myocardial compartments.
  • Pathologic hypertrophy and subsequent ventricular dysfunction are linked to myocardial quality, not solely quantity, increasing adverse cardiovascular event risk.

Purpose of the Study:

  • To review factors regulating myocardial compartment growth.
  • To examine signals promoting adverse remodeling of intramyocardial coronary arteries and arterioles via fibrous tissue deposition.

Main Methods:

  • Literature review of factors regulating myocardial growth.
  • Analysis of signaling pathways involved in hypertensive heart disease remodeling.

Main Results:

  • Myocardial quality, rather than quantity, is critical in pathologic hypertrophy and ventricular dysfunction.
  • Adverse remodeling of intramyocardial vessels by fibrous tissue is a key feature.

Conclusions:

  • Understanding the quality of myocardial tissue is crucial for addressing hypertensive heart disease.
  • Targeting signals that promote fibrous tissue deposition in coronary arteries may mitigate adverse cardiovascular events.

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