Literature DB >> 8432290

Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study.

S Grajek1, M Lesiak, M Pyda, M Zajac, S Paradowski, E Kaczmarek.   

Abstract

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, and density of myocyte nuclei. The values of all histometric parameters correlated well with left ventricular (LV) weight up to 350 g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g. The influence on LV weight of age, coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue was also evaluated. On the basis of a linear discriminant function, hearts were divided into three classes: (1) LV weight < or = 250 g (absence of hyperplasia, hypertrophy only); (2) LV weight 251-350 g (hypertrophy+signs of hyperplasia); (3) LV weight > 350 g (marked signs of hyperplasia). The percent of fibrosis increased proportionally to LV weight. Where LV weight was above 250 g there was a subsequent increase in the mean percent of fibrosis (approx. 26%). This phenomenon (plateau of percent fibrosis) is the result of an increased number of myocytes (myocyte hyperplasia). We suggest that, independent of aetiology, in all hearts above 350 g (patients with congestive heart failure) hyperplasia phenomenon exists.

Entities:  

Mesh:

Year:  1993        PMID: 8432290     DOI: 10.1093/eurheartj/14.1.40

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


  9 in total

1.  The human heart: a self-renewing organ.

Authors:  Jan Kajstura; Toru Hosoda; Claudia Bearzi; Marcello Rota; Silvia Maestroni; Konrad Urbanek; Annarosa Leri; Piero Anversa
Journal:  Clin Transl Sci       Date:  2008-05       Impact factor: 4.689

2.  Differences between outward currents of human atrial and subepicardial ventricular myocytes.

Authors:  G J Amos; E Wettwer; F Metzger; Q Li; H M Himmel; U Ravens
Journal:  J Physiol       Date:  1996-02-15       Impact factor: 5.182

Review 3.  Cellular mechanisms of cardiac hypertrophy.

Authors:  P E Glennon; P H Sugden; P A Poole-Wilson
Journal:  Br Heart J       Date:  1995-06

4.  Temporal evaluation of cardiac myocyte hypertrophy and hyperplasia in male rats secondary to chronic volume overload.

Authors:  Yan Du; Eric Plante; Joseph S Janicki; Gregory L Brower
Journal:  Am J Pathol       Date:  2010-07-22       Impact factor: 4.307

Review 5.  Heart regeneration.

Authors:  Michael A Laflamme; Charles E Murry
Journal:  Nature       Date:  2011-05-19       Impact factor: 49.962

6.  Chronic right ventricular pressure overload results in a hyperplastic rather than a hypertrophic myocardial response.

Authors:  Boudewijn P J Leeuwenburgh; Willem A Helbing; Arnold C G Wenink; Paul Steendijk; Roos de Jong; Enno J Dreef; Adriana C Gittenberger-de Groot; Jan Baan; Arnoud van der Laarse
Journal:  J Anat       Date:  2008-02-01       Impact factor: 2.610

7.  Myocyte proliferation in end-stage cardiac failure in humans.

Authors:  J Kajstura; A Leri; N Finato; C Di Loreto; C A Beltrami; P Anversa
Journal:  Proc Natl Acad Sci U S A       Date:  1998-07-21       Impact factor: 11.205

Review 8.  Metabolic modulation and cellular therapy of cardiac dysfunction and failure.

Authors:  Diana Revenco; James P Morgan
Journal:  J Cell Mol Med       Date:  2009-04-20       Impact factor: 5.310

9.  Automatic Quantification of Cardiomyocyte Dimensions and Connexin 43 Lateralization in Fluorescence Images.

Authors:  Antoni Oliver-Gelabert; Laura García-Mendívil; José María Vallejo-Gil; Pedro Carlos Fresneda-Roldán; Katarína Andelová; Javier Fañanás-Mastral; Manuel Vázquez-Sancho; Marta Matamala-Adell; Fernando Sorribas-Berjón; Carlos Ballester-Cuenca; Narcisa Tribulova; Laura Ordovás; Emiliano Raúl Diez; Esther Pueyo
Journal:  Biomolecules       Date:  2020-09-17
  9 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.