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Dilated cardiomyopathy is associated with an increase in the type I/type III collagen ratio: a quantitative
M M Marijianowski1, P Teeling, J Mann
1Department of Cardiovascular Pathology, Academic Medical Center, Amsterdam, The Netherlands.
Insights
Dilated cardiomyopathy hearts show increased total collagen and a higher type I/type III collagen ratio, particularly in the endomysium and perimysium. These fibrotic changes may impact cardiac compliance.
Area of Science:
- Cardiovascular pathology
- Cardiac fibrosis
- Extracellular matrix remodeling
Background:
- Dilated cardiomyopathy (DCM) is characterized by increased intramyocardial fibrillar collagen.
- Collagen types I and III are the primary collagen types in the heart.
- Altered collagen composition can affect myocardial stiffness and cardiac compliance.
Purpose of the Study:
- To quantify total collagen and the type I/type III collagen ratio in hearts with DCM.
- To determine the localization of collagen types I and III within the myocardium of DCM hearts.
- To investigate the potential impact of collagen changes on cardiac function.
Main Methods:
- Study included 19 DCM hearts (17 explants, 2 autopsy) and control hearts.
- Total collagen measured via hydroxyproline analysis.
- Collagen types I and III quantified using cyanogen bromide method and immunohistochemistry with microdensitophotometry.
- Collagen localization analyzed using light and electron microscopy, including immunoelectron microscopy.
Main Results:
- Hearts with DCM exhibited significantly increased total collagen and a higher type I/type III collagen ratio (p < 0.05).
- Electron microscopy revealed diffuse endomysial collagen fibril increase and inhomogeneous perimysial changes.
- Collagen fibrils were thicker in DCM hearts, with fibrous long-spacing collagen observed in the endomysium.
- Immunoelectron microscopy confirmed an increase in type I collagen deposition.
Conclusions:
- DCM hearts demonstrate a significant elevation in the collagen type I/type III ratio.
- Collagen alterations are distributed within the endomysium and perimysium.
- These fibrotic changes in intramyocardial collagen may increase cardiac rigidity, reducing compliance.
- Further research is required to understand the temporal development of these collagen changes in DCM progression.
Objectives:
The aim of this study was to quantify total collagen and the type I/type III collagen ratio and their localization in hearts with dilated cardiomyopathy.
Background:
Patients with dilated cardiomyopathy have an increase in intramyocardial fibrillar collagen. Types I and III are the main constituents and have different physical properties that may affect cardiac compliance.
Methods:
Nineteen hearts with dilated cardiomyopathy were studied (17 cardiac explants, 2 hearts obtained at autopsy) and compared with reference hearts. Total collagen was determined by hydroxyproline analysis. Collagen types I and III were analyzed using the cyanogen bromide method and immunohistochemical analysis followed by microdensitophotometric quantification. Localization of collagen types I and III was established at the light and electron microscopic levels. Immunoelectron microscopy provided information regarding their localization.
Results:
Total collagen and the collagen type I/type III ratio were increased in hearts with dilated cardiomyopathy (p < 0.05). Electron microscopy showed a diffuse increase in collagen fibrils in the endomysium; the perimysium showed an inhomogeneous increase. Collagen fibrils were thicker, and fibrous long-spacing collagen occurred in the endomysium. Immunoelectron microscopic findings confirmed an increase in type I collagen.
Conclusions:
Hearts with dilated cardiomyopathy have a statistically significant increase in the collagen type I/type III ratio. The changes occur in the endomysium and perimysium, although with differences in distribution. These changes in intramyocardial collagen may be clinically relevant because they may affect cardiac rigidity and, therefore, eventually may render the heart less compliant. Further studies are needed to evaluate at what point in the course of the disease these changes appear.