Left ventricular cellular hypertrophy in pressure- and volume-overload valvular heart disease

Frederick J. Schoen, Gerald M. Lawrie, Jack L. Titus

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

To determine the dependence of myocyte hypertrophy in chronic valvular heart disease on the site and type of lesion, the myocardium was studied from 11 patients with either pressure-overload hypertrophy (PO; four patients with aortic stenosis and two with mixed aortic stenosis/insufficiency) or pure volume-overload hypertrophy (VO; two patients with mitral regurgitation and three with aortic insufficiency). These patients, all without coronary artery disease, died zero to 34 days after valve replacement surgery. Diameters of 25 longitudinally oriented myocytes in the circular midwall myocardium were measured with a calibrated light microscope eyepiece reticle on each of five transmural, transverse, histologic sections from the apical, anterolateral, posterolateral, anteroseptal, and posteroseptal left ventricle. Statistical analysis by modified two-way analysis of variance (ANOVA) demonstrated that mean myocyte size (based on 125 measurements) varied widely among cases but was not statistically different among sites. The myocyte diameter for PO lesions (25.9 ±1.1 μm, mean±SEM) was significantly greater (P<0.05) than that for pure VO lesions (20.4±0.7 μm), despite equal relative heart weights (measured/predicted from body weight: 2.5 ±0.2 [mean±SD] versus 2.5±0.5). This study suggests that 1) cellular hypertrophy in valvular heart disease occurs uniformly throughout the left ventricular myocardium; and 2) mean myocyte diameters are greater in PO than in VO hypertrophy for equivalent cardiac enlargement.

Original languageEnglish (US)
Pages (from-to)860-865
Number of pages6
JournalHuman Pathology
Volume15
Issue number9
DOIs
StatePublished - Jan 1 1984

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Fingerprint Dive into the research topics of 'Left ventricular cellular hypertrophy in pressure- and volume-overload valvular heart disease'. Together they form a unique fingerprint.

Cite this