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Cellular hypertrophy in cardiomyopathic patients is associated with lower creatine-stimulated mitochondrial
M Popovich1, S Kostin, T Branishte
1Institute of Preventive and Clinical Cardiology, Kishinev Moldova and Cardiology Research Center, Moscow, Russia.
Insights
In dilated cardiomyopathy, larger heart cells (hypertrophy) correlate with reduced mitochondrial respiration and poorer cardiac function. This suggests energy supply issues may stem from cellular genetic problems.
Area of Science:
- Cardiology
- Mitochondrial Physiology
- Cell Biology
Background:
- Dilated cardiomyopathy (DCM) is a complex heart condition affecting muscle function.
- Mitochondrial dysfunction is implicated in various heart diseases.
- Cellular and nuclear hypertrophy are observed in some cardiomyopathies.
Purpose of the Study:
- To investigate the relationship between morphometric indices (cell size) and mitochondrial respiration in DCM patients.
- To explore potential links between cellular hypertrophy, energy metabolism, and cardiac function severity.
Main Methods:
- Endomyocardial biopsies from 43 DCM patients were analyzed.
- Mitochondrial respiration rates in saponin-skinned fibers were measured.
- Morphometric indices (myocyte and nuclear diameter) were quantified.
- Cardiac function parameters (left ventricular end-diastolic pressure, ejection fraction) were assessed.
Main Results:
- Patients with significantly larger myocyte (30 ± 4 µm) and nuclear (57 ± 5 µm) diameters showed markedly lower creatine-stimulated mitochondrial respiration (36 ± 4%).
- This group also exhibited higher left ventricular end-diastolic pressure and volume index, with decreased ejection fraction.
- In contrast, patients with smaller cell sizes had higher mitochondrial respiration (90 ± 12%) and better cardiac function.
Conclusions:
- Marked nuclear and cellular hypertrophy in DCM is associated with impaired mitochondrial respiration.
- These findings suggest a link between severe cardiac failure and reduced energy supply to myofibrils.
- Disturbances in the cellular genetic apparatus may underlie these energy supply problems in DCM.
Abstract:
The mitochondrial respiration rate and morphometric indices in endomyocardial biopsy samples were measured in 43 patients with dilated cardiomyopathy selected in accordance to WHO criteria by endomyocardial biopsy studies after excluding of various forms of myocarditis, alcoholic cardiomyopathy and other specific diseases of the heart. A group of 13 patients with unusually high mean myocyte diameter, 30 +/- 4 microns, and nuclear size, 57 +/- 5 microns, was selected. The remainder of patients (n = 30) had significantly lower mean myocyte diameter and nuclear size, 23 +/- 3 and 42 +/- 6 microns, respectively, (p < 0.01). Creatine-stimulated elevation in mitochondrial respiration rate as measured in saponin-skinned fibers was found in the former group to be much lower (36 +/- 4%) as compared with the remainder (90 +/- 12%). Also, the former group of patients had higher left ventricular enddiastolic pressure and volume index with concomitantly decreased ejection fraction. The results indicate that marked nuclear and cellular hypertrophy is associated with lower creatine-stimulated mitochondrial respiration rate and more severe cardiac failure. They suggest that disorders in energy supply to myofibrils may be related to disturbances in cellular genetic apparatus.