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Extent of myocardial fibrosis and cellular hypertrophy in dilated cardiomyopathy
Insights
Dilated cardiomyopathy (DC) hearts show increased fibrosis and larger myocardial cells compared to healthy hearts. Fibrosis patterns vary across the left ventricle and septum in DC patients, aiding in disease characterization.
Area of Science:
- Cardiovascular Pathology
- Cardiac Histology
Background:
- Dilated cardiomyopathy (DC) is a significant cause of heart failure.
- Understanding the structural changes in DC is crucial for diagnosis and treatment.
Purpose of the Study:
- To investigate the distribution and extent of fibrosis and cellular hypertrophy in the hearts of patients with dilated cardiomyopathy.
- To compare these structural changes between DC patients and control subjects.
Main Methods:
- Human heart tissue samples from 9 DC patients and 6 controls were analyzed.
- Transmural sections from ventricular free walls and septum were stained for fibrosis (trichrome) and cell size (hematoxylin-eosin).
- Fibrosis and cell diameter were quantified across different myocardial regions.
Main Results:
- Patients with DC exhibited significantly higher overall fibrosis (20% vs. 4%) and larger myocardial cell diameter (22µm vs. 17µm) compared to controls.
- A distinct pattern of increasing fibrosis from epicardium to endocardium was observed in the left ventricular free wall of DC hearts.
- The left side of the septum showed greater fibrosis than the right side in DC patients.
Conclusions:
- Increased myocardial fibrosis and cellular hypertrophy are characteristic features of dilated cardiomyopathy.
- Specific patterns of fibrosis within the left ventricle and septum are associated with DC.
- These histological findings contribute to a better characterization of dilated cardiomyopathy.
Abstract:
The distribution of fibrosis and cellular hypertrophy was studied in the hearts of patients with dilated cardiomyopathy (DC). Transmural sections were removed from the left and right ventricular free walls and the ventricular septum of 9 patients with heart failure and 6 control subjects. These sections were stained with hematoxylin-eosin (to determine cell size) and trichrome (to determine percent fibrosis). The sections were separated into equal areas from epicardium to endocardium in the free walls and right to left across the septum. Percent fibrosis was greater in patients with DC (20 +/- 4%) than control subjects (4 +/- 1%, p = 0.0001). A pattern of increasing fibrosis in the left ventricular free wall from epicardium (14 +/- 6%) to endocardium (22 +/- 9%, p less than 0.05) was documented. Fibrosis was greater on the left (21 +/- 12%) than the right (15 +/- 6%, p less than 0.05) side of the septum. No pattern was evident in the right ventricular free wall or in the control group. Myocardial cell diameter was greater in the heart failure group (22 +/- 5 micron) than the control group (17 +/- 2 micron, p less than 0.05), but no pattern of hypertrophy across the walls was seen. The increased fibrosis, the pattern of fibrosis and the increased cell diameter in patients with DC help to characterize DC.