title: Myocyte nuclear and possible cellular hyperplasia contribute to ventricular remodeling in the hypertrophic senescent heart in humans.
abstract: OBJECTIVE
  The present investigation was designed to evaluate the growth reserve capacity of the aged and senescent myocardium.
  
  
  BACKGROUND
  Aging affects the ability of the heart to sustain alterations in ventricular loading, and this phenomenon may be coupled with attenuation of the hypertrophic reaction of the myocardium. However, because myocyte cellular hyperplasia has been documented experimentally in the old heart, a similar adaptation may also occur in humans and play a role in this process.
  
  
  METHODS
  The changes in number and size of ventricular myocytes were measured quantitatively in pathologic hearts of elderly subjects. Morphometric methodologies were applied to the analysis of 13 hypertrophic hearts obtained at autopsy from patients 80 +/- 4 (mean +/- SD) years old. An identical number of nonhypertrophic hearts collected from subjects 76 +/- 7 years old were used as control hearts.
  
  
  RESULTS
  A 71% increase in left ventricular weight was associated with a 33% increase in average myocyte cell volume per nucleus and a 36% augmentation in the total number of myocyte nuclei in the ventricular myocardium. However, a 55% increase in right ventricular weight was the result of a 59% increase in the aggregate number of myocyte nuclei, with no change in myocyte cell volume. These cellular processes were associated with a 95% and 83% enlargement of the myocardial interstitium in the left and right ventricle, respectively.
  
  
  CONCLUSIONS
  Myocyte nuclear and possibly cellular hyperplasia appear to be the prevailing growth mechanism of the overloaded aging myocardium. Proliferation of myocyte nuclei and connective tissue accumulation are the major determinants of ventricular remodeling in the hypertrophic senescent heart.
authors.affiliation: Department of Pathology, University of Parma, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Olivetti
authors.forename: M
authors.initials: M
authors.lastname: Melissari
authors.forename: T
authors.initials: T
authors.lastname: Balbi
authors.forename: F
authors.initials: F
authors.lastname: Quaini
authors.forename: E H
authors.initials: EH
authors.lastname: Sonnenblick
authors.forename: P
authors.initials: P
authors.lastname: Anversa
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000473:pathology*; D002467:Cell Nucleus / Q000473:pathology*; D006352:Heart Ventricles / Q000648:ultrastructure; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology*; D017380:Hypertrophy, Right Ventricular / Q000209:etiology / Q000473:pathology*; D007620:Karyometry / Q000379:methods / Q000706:statistics & numerical data; D009206:Myocardium / Q000648:ultrastructure*; D009929:Organ Size