Related Experiment Videos
[Ultrastructural morphometric analysis of hypertrophied human myocardial left ventricles (author's transl)]
Insights
Hypertrophied heart muscle cells in aortic valve disease show increased volume due to more myofibrils and fewer mitochondria. This cellular remodeling occurs in enlarged human hearts, impacting cardiac function.
Area of Science:
- Cardiovascular Pathology
- Cellular Biology
- Human Physiology
Context:
- Investigated hypertrophied human myocardial left ventricles from patients with aortic valve stenosis, insufficiency, or both.
- Compared findings with normally loaded human left ventricles.
Purpose:
- To morphometrically investigate cellular and subcellular changes in hypertrophied human myocardial left ventricles due to aortic valve disease.
- To compare these changes with normal myocardial tissue.
Summary:
- No light microscopic differences in interstitial tissue or heart muscle cell volume density were found between patient groups and controls.
- Significant reduction in nuclear volume density and number per area suggests increased individual heart muscle cell volume.
- Ultrastructural analysis revealed increased myofibril volume density and decreased mitochondrial volume density, surface area, and cristae, indicating mitochondrial destruction (cristolysis).
Impact:
- Demonstrates significant cellular and subcellular remodeling in hypertrophied ventricles associated with aortic valve disease.
- Highlights mitochondrial damage and loss as a key feature of cardiac hypertrophy in this context.
- Provides morphological evidence for impaired cardiac function in severe heart enlargement beyond critical weight.
Abstract:
Biopsies of hypertrophied human myocardial left ventricles were investigated morphometrically. The diagnoses of the patients were stenosis of the aortic valve, aortic insufficiency or a combination of both lesions. The results were compared with those from normally loaded human left ventricles. There are no differences on light microscopical level between the volume densities of interstitial tissue and of heart muscle cells in the three groups of patients. A significant diminution of the volume density of the nuclei (P less than 0.001) and the number of nuclei per test area (P less than 0.001) when compared with normal groups suggests an increase in volume of the single heart muscle cell. The ultrastructural study shows marked increase in volume density of myofibrils (P less than 0.0001), with accompanying decrease in the volume densities of mitochondria (P less than 0.0001) and the remaining cytoplasm (P less than 0.001). A gross decrease in the surface area of mitochondria (P less than 0.001) and of cristae mitochondriales (P less than 0.0001) is found. The morphological equivalents of this result are numerous stages of mithochondrial destruction including cristolysis. All myocardial weights were beyond the "critical heart weight".