# Histopathological Analysis of Myocardial Remodeling Following Heart Failure: A Cadaveric Case Report

**Authors:** Anthony DeSomma, Jeung Woon Lee

PMC · DOI: 10.7759/cureus.87889 · 2025-07-14

## TL;DR

This case report describes heart tissue changes in a cadaver with heart failure, showing increased fibrosis and larger heart cells compared to healthy controls.

## Contribution

The study provides a detailed histopathological analysis of myocardial remodeling in a single heart failure cadaver case.

## Key findings

- Heart failure tissue showed increased collagen deposition and fibrosis compared to controls.
- Cardiomyocyte hypertrophy was observed in heart failure samples using Cresyl Violet staining.
- Findings support the role of structural remodeling in heart failure pathophysiology.

## Abstract

Cardiovascular disease and aging are key contributors to myocardial remodeling, often leading to fibrosis, cellular hypertrophy, and impaired cardiac function. Understanding these structural changes is essential for explaining the pathophysiology of heart failure.

This study examined histopathological changes in myocardial tissue from a post-mortem cadaver with heart failure. Two age-matched cadavers without cardiac disease were used as controls. Ventricular tissue samples were thin-sectioned and stained for collagen deposition and cellular morphology using Masson’s Trichrome and Cresyl Violet dyes.

Histopathological findings showed the presence of increased collagen deposition and fibrosis in the myocardial tissue with heart failure, consistent with a stiffened myocardium. Additionally, Cresyl Violet staining showed cardiomyocyte hypertrophy compared to control samples, suggesting cellular remodeling, which is well characterized following heart failure.

These findings provide further histological evidence of myocardial remodeling in heart failure, characterized by fibrosis and cardiomyocyte hypertrophy. Further quantitative analysis is needed to deepen our understanding of these pathological changes and their implications for cardiac function.

## Linked entities

- **Chemicals:** Cresyl Violet (PubChem CID 29092)
- **Diseases:** heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}
- **Diseases:** hypertrophic cardiomyopathy (MESH:D002312), CHF (MESH:D006333), cardiomyocyte hypertrophy (MESH:D006984), HIV-associated cardiomyopathy (MESH:D016263), ischemia (MESH:D007511), COVID-19 (MESH:D000086382), pneumonia (MESH:D011014), hypertension (MESH:D006973), myocardial alterations (MESH:D004408), cancer (MESH:D009369), cardiac hypertrophy (MESH:D006332), diastolic dysfunction (MESH:D018487), Fibrosis (MESH:D005355), coronary artery disease (MESH:D003324), inflammation (MESH:D007249), death (MESH:D003643), hypertrophic remodeling (MESH:D020257), cardiac disease (MESH:D006331), necrosis (MESH:D009336), Cardiovascular disease (MESH:D002318), arrhythmias (MESH:D001145), myocardial infarction (MESH:D009203), Myocardial Remodeling (MESH:D064752)
- **Chemicals:** paraformaldehyde (MESH:C003043), oxygen (MESH:D010100), Cresyl (-), Cresyl Violet (MESH:C028911)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12345069/full.md

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Source: https://tomesphere.com/paper/PMC12345069