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European Heart Journal 1993 14(1):40-47;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The European Society of Cardiology

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

S. GRAJEK, M. LESIAK, M. PYDA, M. ZAJAC, ST. PARADOWSKI and E. KACZMAREK

1st Department of Cardiology, Medical Academy Poznan, Poland

Received 27 January 1992; revised 8 June 1992; .

Correspondence: Stefan Grajek MD, 1st Department of Cardiology, ul. Dluga 1 2, 61–848 Poznan, Poland

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 350g. In heavier hearts these parameters remained approximately of the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250g. 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 ≤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) the hyperplasia phenomenon exists.

Key Words: Myocyte hypertrophy • myocyte hyperplasia • cardiac hypertrophy


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