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Diastolic dysfunction and collagen structure in canine pacing-induced heart failure
T Neumann1, A Vollmer, T Schaffner
1Department of Pathophysiology, Center of Internal Medicine, University of Essen, FRG.
Journal of Molecular and Cellular Cardiology
|March 12, 1999
Summary
Heart failure increases left ventricular stiffness due to altered collagen structure. This study found increased collagen fiber disorientation, not volume, correlates with stiffness in heart failure.
Area of Science:
- Cardiology
- Biomedical Engineering
- Pathology
Background:
- Heart failure presents with both systolic and diastolic dysfunction.
- Diastolic dysfunction, a key feature, impacts cardiac tissue properties and collagen structure.
- Understanding these changes is crucial for diagnosing and treating heart failure.
Purpose of the Study:
- To investigate the association between diastolic dysfunction and changes in cardiac tissue properties.
- To analyze alterations in the collagen network structure in heart failure.
- To determine the relationship between collagen structure and left ventricular stiffness.
Main Methods:
- Heart failure was induced in dogs via rapid left ventricular pacing.
- Hemodynamic parameters and left ventricular dimensions were monitored using sonomicrometry.
- Collagen structure was analyzed using picrosirius red staining and polarized light microscopy.
Main Results:
- Heart failure led to increased left ventricular stiffness, indicated by a steeper end-diastolic pressure-strain relation.
- Collagen volume fraction remained unchanged, but collagen fiber orientation became significantly more nonuniform.
- Increased collagen fiber orientation nonuniformity correlated strongly with increased left ventricular stiffness.
Conclusions:
- Diastolic dysfunction in heart failure is associated with increased left ventricular stiffness.
- The structural basis for this stiffness involves altered collagen network organization, specifically increased disorientation.
- These findings highlight the role of collagen remodeling in the mechanical dysfunction of the failing heart.