Pathogenesis of ventricular hypertrophy

Academic Article

Abstract

  • Growth of the vertebrate heart during embryonic and fetal life is characterized by hyperplasia of myocardial cells. Shortly after birth, myocardial cells lose the capability of dividing, and further growth of the heart is due to myocardial cell hypertrophy and nonmuscle cell hyperplasia. This process results in a 30- to 40-fold increase in volume of individual myocardial cells during normal postnatal growth and maturation. The transition from hyperplastic to hypertrophic growth is related to formation of binucleated myocardial cells as a result of karyokinesis without cytokinesis. The molecular mechanism of this transition is uncertain. The response of the heart to increased metabolic demands or an increased work load depends on the age of the animal at the time when the stress is imposed. Increased myocardial work loads in fetal or early neonatal life lead to cardiac enlargement by causing an increased rate of hyperplasia of myocardial cells or continuation of hyperplasia beyond the normal period of hyperplastic growth. In contrast, imposition of increased loads on the hearts of older animals results in cardiac hypertrophy due to enlargement of myocardial cells and hyperplasia of nonmuscular components. In addition to cellular enlargement, structural remodeling of the myocardial cells and of the chambers of the heart occurs during the development of hypertrophy. Important stimuli of cardiac hypertrophy include increased systolic force or tension generated by the myocardial fibers (pressure overload), increased end-dia-stolic wall stress (volume overload) and neurohumoral factors such as increased circulating catecholamines or discharge of cardiac sympathetic nerves, or both, activation of the renin-angiotensin system and increased levels of thyroxine and growth hormone. Myocardial growth factors may provide a biochemical basis for genetically based myocardial hypertrophy. © 1985, American College of Cardiology Foundation. All rights reserved.
  • Authors

    Digital Object Identifier (doi)

    Author List

  • Oparil S
  • Start Page

  • 57B
  • End Page

  • 65B
  • Volume

  • 5
  • Issue

  • 6