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Updated: Jan 20, 2026

Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
Myofibrillolysis and fibrosis predicts myocardial insufficiency
Jerzy Pacholewicz1, Michał Zakliczyński1, Jerzy Nożyński1
1Department of Cardiac, Vascular and Endovascular Surgery and Transplantology in Zabrze, Medical University of Silesia in Katowice, Silesian Center for Heart Diseases in Zabrze, Poland.
Insights
Cardiomyopathy progression, including fibrosis, is driven by the loss of heart muscle cells (cardiomyocytes), not their degeneration. This impacts left ventricular assist device (LVAD) patient outcomes.
Area of Science:
- Cardiovascular Pathology
- Cardiac Surgery
- Histopathology
Background:
- Cardiomyopathies involve histopathological changes like cardiocyte myofibrillolysis and interstitial fibrosis, contributing to heart failure.
- These changes are critical in understanding disease progression and treatment efficacy.
Purpose of the Study:
- To evaluate histopathological changes, specifically fibrosis and myofibrillolysis, in myocardial tissue resected during left ventricular assist device (LVAD) implantation.
- To compare these changes in patients with cardiomyopathy (CM/VAD group) against a control group of healthy heart donors.
Main Methods:
- Analysis of apical myocardial samples from 40 patients with cardiomyopathy undergoing LVAD implantation (CM/VAD group) and 6 healthy heart donors (control group).
- Quantification of area fraction (AF) for fibrosis, cardiocytes with myofibrillolysis (MFL), and non-myofibrillolytic cardiocytes (non-MFL).
- Semiquantitative evaluation of cardiomyopathy grade and correlation analysis between fibrosis and cardiomyocyte types.
Main Results:
- The CM/VAD group exhibited significantly higher fibrosis (nearly 10x) and MFL cell area (nearly 5x) compared to the control group.
- A strong negative correlation was observed between fibrosis progression and the presence of normal cardiomyocytes, indicating cardiomyocyte loss.
- Cardiomyopathy was graded as slight, moderate, or advanced, with lymphocyte presence noted in 45% of CM/VAD cases.
Conclusions:
- Cardiomyopathy and fibrosis progression are primarily associated with the depletion of cardiomyocytes.
- The findings suggest that the loss of functional heart muscle cells, rather than cellular degeneration, is the key driver in advanced cardiomyopathy.
- Understanding these mechanisms is crucial for managing heart failure and optimizing LVAD therapy.
Introduction:
Cardiocyte myofibrillolysis and interstitial fibrosis belong to histopathological changes in cardiomyopathies, leading to heart failure.
Aim:
To evaluate these changes in apical resection during left ventricular assist device (LVAD) implantation.
Material And Methods:
The studied group consisted of 40 patients with cardiomyopathy, and apical samples excised during left ventricular assist device implantation were studied (CM/VAD group, mean: 48.1 ±10 y/o). A control group consisted of 6 apical samples from healthy heart graft donors (mean: 29 ±2.3 years old). Area fraction (AF) was calculated for: fibrosis, cardiocytes with myofibrillolysis (MFL), non-myofibrillolytic cardiocytes (non-MFL).
Results:
Single lymphocytes were seen in 18 (45%) cases in the CM/VAD group. Cardiomyopathy grade evaluated semiquantitatively in CM/VAD was: slight (25% of a group), moderate (35.5%), advanced (35.5%). CM/VAD cases showed nearly ten times higher fibrosis than the control group. The MFL cells occupied nearly a five times larger area in CM/VAD than in the control group, whereas non-MFL cells were found in the control group, as a predominant pattern. The linear regression calculated between fibrosis AF and types of cardiocytes indicated the depletion of cardiomyocytes with fibrosis increase. The control group presented insignificant dependency between fibrosis and MFL cells, suggesting the lack of replacement fibrosis. Significant negative dependence between fibrosis and non-MFL cardiocytes suggested remodeling in controls. Correlation analysis showed a strong relation between depletion of normal cardiocytes and progression of fibrosis.
Conclusions:
Progression of cardiomyopathy and fibrosis depends on the loss of cardiocytes rather than degeneration of these cells.
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