Critical analysis of endomyocardial biopsies from patients suspected of having cardiomyopathy. I: Morphological and morphometric aspects.

Baandrup, Ulrik; Olsen, E. G. J.

doi:10.1136/hrt.45.5.475

Cited by 147 publications

(34 citation statements)

References 25 publications

(8 reference statements)

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“…A light microscopy study showed that one or two biopsies are not always representative of the state of the rest of the myocardium and that at least five biopsies are necessary. 25 We have shown that the same condition applies to ultrastructural changes. It may be that the observed differences are fortuitous, as the studies cited were all based on fewer than five biopsies per patient, usually varying between one and three.…”

Section: Reproducibility Of Electron Microscopic Evaluationmentioning

confidence: 81%

Electron microscopic investigation of endomyocardial biopsy samples in hypertrophy and cardiomyopathy. A semiquantitative study in 48 patients.

Baandrup¹,

Florio²,

Roters³

et al. 1981

Circulation

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SUMMARY Electron microscopic and statistical analyses of 66 right ventricular biopsies from 48 patients were undertaken to investigate whether quantitative differences exist between those patients with "ordinary" myocardial hypertrophy and those suffering from a form of cardiomyopathy.The electron microscopic changes were scored and correlated with hemodynamic variables such as ejection fraction (EF), left ventricular end-diastolic pressure (LVEDP) and length of history. The patients were followed for an average of 22.5 months, permitting an assessment of prognosis.The results show that the three diagnostic groups "ordinary" hypertrophy, hypertrophic cardiomyopathy (HOCM) and congestive cardiomyopathy (COCM) overlap, but crossover of sarcomeres is more frequent in patients in whom HOCM is diagnosed. Except for a tenuous relationship between EF, and the electron microscopy (EM) (r = -0.46,p < 0.1) and between LVEDP and EM score (r = 0.61,p < 0.01), in the COCM group, no correlation could be established between EF, LVEDP and length of history when the patients were grouped according to histologic or clinical diagnosis.This study shows that the various claims regarding relationships between morphologic changes and the functional status of patients or prognosis cannot be confirmed.

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Section: Reproducibility Of Electron Microscopic Evaluationmentioning

confidence: 81%

Electron microscopic investigation of endomyocardial biopsy samples in hypertrophy and cardiomyopathy. A semiquantitative study in 48 patients.

Baandrup¹,

Florio²,

Roters³

et al. 1981

Circulation

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“…It has been suggested for some time that the failing human heart is a transition from normal, to compensated left ventricular hypertrophy, to decompensated failure with LV dilation (4,6). We combined this fundamental concept with that of energy starvation and hypothesized that human DCM is a cardiac phenotype of defective LV mtDNA replication and ETC with OXPHOS dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Thymidine kinase and mtDNA depletion in human cardiomyopathy: epigenetic and translational evidence for energy starvation

Koczor

Torres

Fields

et al. 2013

Physiological Genomics

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Koczor CA, Torres RA, Fields EJ, Boyd A, He S, Patel N, Lee EK, Samarel AM, Lewis W. Thymidine kinase and mtDNA depletion in human cardiomyopathy: epigenetic and translational evidence for energy starvation. Physiol Genomics 45: 590 -596, 2013. First published May 21, 2013 doi:10.1152/physiolgenomics.00014.2013.-This study addresses how depletion of human cardiac left ventricle (LV) mitochondrial DNA (mtDNA) and epigenetic nuclear DNA methylation promote cardiac dysfunction in human dilated cardiomyopathy (DCM) through regulation of pyrimidine nucleotide kinases. Samples of DCM LV and right ventricle (n ϭ 18) were obtained fresh at heart transplant surgery. Parallel samples from nonfailing (NF) controls (n ϭ 12) were from donor hearts found unsuitable for clinical use. We analyzed abundance of mtDNA and nuclear DNA (nDNA) using qPCR. LV mtDNA was depleted in DCM (50%, P Ͻ 0.05 each) compared with NF. No detectable change in RV mtDNA abundance occurred. DNA methylation and gene expression were determined using microarray analysis (GEO accession number: GSE43435). Fifty-seven gene promoters exhibited DNA hypermethylation or hypomethylation in DCM LVs. Among those, cytosolic thymidine kinase 1 (TK1) was hypermethylated. Expression arrays revealed decreased abundance of the TK1 mRNA transcript with no change in transcripts for other relevant thymidine metabolism enzymes. Quantitative immunoblots confirmed decreased TK1 polypeptide steady state abundance. TK1 activity remained unchanged in DCM samples while mitochondrial thymidine kinase (TK2) activity was significantly reduced. Compensatory TK activity was found in cardiac myocytes in the DCM LV. Diminished TK2 activity is mechanistically important to reduced mtDNA abundance and identified in DCM LV samples here. Epigenetic and genetic changes result in changes in mtDNA and in nucleotide substrates for mtDNA replication and underpin energy starvation in DCM.

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“…Fixed tissues were routinely processed for paraffin embedding, sectioned, and stained with hematoxylin and eosin for morphometric evaluation. Using a video image-analyzing system (Mitani-Shoji Co., Chiba, Japan), the diameters of myocardial fibers of the left and right ventricles as well as the septum were measured by the 'least diameter method' (Baandrup and Olsen, 1981).…”

Section: Pathologymentioning

confidence: 99%

Peroxisome proliferator-activated receptor .ALPHA. (PPAR.ALPHA.) agonist, WY-14,643, increased transcription of myosin light chain-2 in cardiomyocytes.

et al. 2001

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Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that can be activated by xenobiotics and natural fatty acids. To assess the potential physiological activity of PPAR ligands on cardiac muscular cells, the effects of PPAR agonist, WY-14,643, on both rat hearts and a rat cardiomyocyte cell line (H9c2 cells) were investigated. Male F344 rats were fed a diet containing WY-14,643 at a concentration of 100 ppm for 26 weeks. Cardiac muscular hypertrophy was revealed by morphometric analysis in which the diameter of the muscular fibers in WY-14,643-treated rats was larger than those of control rats. Using H9c2 cells in vitro, the protein content per cell was increased in a dosedependent manner with the treatment of WY-14,643. The transcription of myosin light chain-2 (MLC-2), a parameter of myocardial hypertrophy, was increased in H9c2 cells transfected with the rat MLC-2/luciferase fusion gene by WY-14,643 as well as other peroxisome proliferators, clofibrate and di(2-ethylhexyl) phthalate. In addition, accumulation of myosin light chain protein was confirmed in H9c2 cells treated with WY-14,643 at 10 g/ml for 7 days or more by immunohistochemistry. These results suggest that PPAR ligands have a potential to regulate MLC-2, which is a contractile protein in cardiomyocytes and may play a part of role in the pathogenesis of cardiac hypertrophy.

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Critical analysis of endomyocardial biopsies from patients suspected of having cardiomyopathy. I: Morphological and morphometric aspects.

Abstract: SUMMARY Three hundred and sixty-one biopsies obtained by bioptome from 201

Cited by 147 publications

References 25 publications

Electron microscopic investigation of endomyocardial biopsy samples in hypertrophy and cardiomyopathy. A semiquantitative study in 48 patients.

Electron microscopic investigation of endomyocardial biopsy samples in hypertrophy and cardiomyopathy. A semiquantitative study in 48 patients.

Thymidine kinase and mtDNA depletion in human cardiomyopathy: epigenetic and translational evidence for energy starvation

Peroxisome proliferator-activated receptor .ALPHA. (PPAR.ALPHA.) agonist, WY-14,643, increased transcription of myosin light chain-2 in cardiomyocytes.

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